Skip to main content
Erschienen in: Cancer and Metastasis Reviews 2/2017

13.07.2017

Platelet-targeted pharmacologic treatments as anti-cancer therapy

verfasst von: P. Gresele, S. Momi, M. Malvestiti, M. Sebastiano

Erschienen in: Cancer and Metastasis Reviews | Ausgabe 2/2017

Einloggen, um Zugang zu erhalten

Abstract

Platelets act as multifunctional cells participating in immune response, inflammation, allergy, tissue regeneration, and lymphoangiogenesis. Among the best-established aspects of a role of platelets in non-hemostatic or thrombotic disorders, there is their participation in cancer invasion and metastasis. The interaction of many different cancer cells with platelets leads to platelet activation, and on the other hand platelet activation is strongly instrumental to the pro-carcinogenic and pro-metastatic activities of platelets. It is thus obvious that over the last years a lot of interest has focused on the possible chemopreventive effect of platelet-targeted pharmacologic treatments. This article gives an overview of the platelet-targeted pharmacologic approaches that have been attempted in the prevention of cancer development, progression, and metastasis, including the application of anti-platelet drugs currently used for cardiovascular disease and of new and novel pharmacologic strategies. Despite the fact that very promising results have been obtained with some of these approaches in pre-clinical models, with the exclusion of aspirin, clinical evidence of a beneficial effect of anti-platelet agents in cancer is however still largely missing. Future studies with platelet-targeted drugs in cancer must carefully deal with design issues, and in particular with the careful selection of patients, and/or explore novel platelet targets in order to provide a solution to the critical issue of the risk/benefit profile of long-term anti-platelet therapy in the prevention of cancer progression and dissemination.
Literatur
1.
Zurück zum Zitat Simmons, D. L., Botting, R. M., & Hla, T. (2004). Cyclooxygenase isozymes: the biology of prostaglandin synthesis and inhibition. Pharmacological Reviews, 56(3), 387–437.PubMedCrossRef Simmons, D. L., Botting, R. M., & Hla, T. (2004). Cyclooxygenase isozymes: the biology of prostaglandin synthesis and inhibition. Pharmacological Reviews, 56(3), 387–437.PubMedCrossRef
2.
Zurück zum Zitat Iniguez, M. A., Cacheiro-Llaguno, C., Cuesta, N., Diaz-Munoz, M. D., & Fresno, M. (2008). Prostanoid function and cardiovascular disease. Archives of Physiology and Biochemistry, 114(3), 201–209.PubMedCrossRef Iniguez, M. A., Cacheiro-Llaguno, C., Cuesta, N., Diaz-Munoz, M. D., & Fresno, M. (2008). Prostanoid function and cardiovascular disease. Archives of Physiology and Biochemistry, 114(3), 201–209.PubMedCrossRef
3.
Zurück zum Zitat Gresele, P., Deckmyn, H., Nenci, G. G., & Vermylen, J. (1991). Thromboxane synthase inhibitors, thromboxane receptor antagonists and dual blockers in thrombotic disorders. Trends in Pharmacological Sciences, 12(4), 158–163.PubMedCrossRef Gresele, P., Deckmyn, H., Nenci, G. G., & Vermylen, J. (1991). Thromboxane synthase inhibitors, thromboxane receptor antagonists and dual blockers in thrombotic disorders. Trends in Pharmacological Sciences, 12(4), 158–163.PubMedCrossRef
4.
Zurück zum Zitat Nakahata, N. (2008). Thromboxane A2: physiology/pathophysiology, cellular signal transduction and pharmacology. Pharmacological Therapy, 118(1), 18–35.CrossRef Nakahata, N. (2008). Thromboxane A2: physiology/pathophysiology, cellular signal transduction and pharmacology. Pharmacological Therapy, 118(1), 18–35.CrossRef
5.
Zurück zum Zitat Vane, J. R. (1972). Inhibition of prostaglandin synthesis as a mechanism of action for aspirin-like drugs. Nature: New Biology, 231(25), 232–235. Vane, J. R. (1972). Inhibition of prostaglandin synthesis as a mechanism of action for aspirin-like drugs. Nature: New Biology, 231(25), 232–235.
6.
Zurück zum Zitat Roth, G. J., Stanford, N., & Majerus, P. W. (1975). Acetylation of prostaglandin synthase by aspirin. Proceedings of the National Academy of Sciences USA, 72(8), 3073–3076.CrossRef Roth, G. J., Stanford, N., & Majerus, P. W. (1975). Acetylation of prostaglandin synthase by aspirin. Proceedings of the National Academy of Sciences USA, 72(8), 3073–3076.CrossRef
7.
Zurück zum Zitat Gasic, G. J., Gasic, T. B., & Murphy, S. (1972). Anti-metastatic effect of aspirin. Lancet, 2(7783), 932–933.PubMedCrossRef Gasic, G. J., Gasic, T. B., & Murphy, S. (1972). Anti-metastatic effect of aspirin. Lancet, 2(7783), 932–933.PubMedCrossRef
8.
Zurück zum Zitat Gasic, G. J., Gasic, T. B., & Stewart, C. C. (1968). Anti-metastatic effect associated with platelet reduction. Proceeding of the National Academy of Science USA, 61(1), 46–52.CrossRef Gasic, G. J., Gasic, T. B., & Stewart, C. C. (1968). Anti-metastatic effect associated with platelet reduction. Proceeding of the National Academy of Science USA, 61(1), 46–52.CrossRef
9.
10.
Zurück zum Zitat Bennett, A., & Del Tacca, M. (1975). Proceedings: prostaglandins in human colonic carcinoma. Gut, 16(5), 409.PubMed Bennett, A., & Del Tacca, M. (1975). Proceedings: prostaglandins in human colonic carcinoma. Gut, 16(5), 409.PubMed
11.
Zurück zum Zitat Reddy, B. S., Rao, C. V., Rivenson, A., & Kelloff, G. (1993). Inhibitory effect of aspirin on azoxymethane-induced colon carcinogenesis in F344 rats. Carcinogenesis, 14(8), 1493–1497.PubMedCrossRef Reddy, B. S., Rao, C. V., Rivenson, A., & Kelloff, G. (1993). Inhibitory effect of aspirin on azoxymethane-induced colon carcinogenesis in F344 rats. Carcinogenesis, 14(8), 1493–1497.PubMedCrossRef
12.
Zurück zum Zitat Duperron, C., & Castonguay, A. (1997). Chemopreventive efficacies of aspirin and sulindac against lung tumorigenesis in A/J mice. Carcinogenesis, 18(5), 1001–1006.PubMedCrossRef Duperron, C., & Castonguay, A. (1997). Chemopreventive efficacies of aspirin and sulindac against lung tumorigenesis in A/J mice. Carcinogenesis, 18(5), 1001–1006.PubMedCrossRef
13.
Zurück zum Zitat Tian, Y., Ye, Y., Gao, W., et al. (2011). Aspirin promotes apoptosis in a murine model of colorectal cancer by mechanisms involving downregulation of IL-6-STAT3 signaling pathway. International Journal of Colorectal Disease, 26(1), 13–22.PubMedCrossRef Tian, Y., Ye, Y., Gao, W., et al. (2011). Aspirin promotes apoptosis in a murine model of colorectal cancer by mechanisms involving downregulation of IL-6-STAT3 signaling pathway. International Journal of Colorectal Disease, 26(1), 13–22.PubMedCrossRef
14.
Zurück zum Zitat Vad, N. M., Kudugunti, S. K., Wang, H., Bhat, G. J., & Moridani, M. Y. (2014). Efficacy of acetylsalicylic acid (aspirin) in skin B16-F0 melanoma tumor-bearing C57BL/6 mice. Tumour Biology, 35(5), 4967–4976.PubMedCrossRef Vad, N. M., Kudugunti, S. K., Wang, H., Bhat, G. J., & Moridani, M. Y. (2014). Efficacy of acetylsalicylic acid (aspirin) in skin B16-F0 melanoma tumor-bearing C57BL/6 mice. Tumour Biology, 35(5), 4967–4976.PubMedCrossRef
15.
Zurück zum Zitat Cathomas, G. (2014). PIK3CA in colorectal cancer. Frontiers in Oncology, 4, 1–4.CrossRef Cathomas, G. (2014). PIK3CA in colorectal cancer. Frontiers in Oncology, 4, 1–4.CrossRef
16.
Zurück zum Zitat Okumura, H., Uchikado, Y., Setoyama, T., et al. (2014). Biomarkers for predicting the response of esophageal squamous cell carcinoma to neoadjuvant chemoradiation therapy. Surgery Today, 44(3), 421–428.PubMedCrossRef Okumura, H., Uchikado, Y., Setoyama, T., et al. (2014). Biomarkers for predicting the response of esophageal squamous cell carcinoma to neoadjuvant chemoradiation therapy. Surgery Today, 44(3), 421–428.PubMedCrossRef
17.
Zurück zum Zitat Reimers, M. S., Bastiaannet, E., Langley, R. E., et al. (2014). Expression of HLA class I antigen, aspirin use, and survival after a diagnosis of colon cancer. JAMA International Medicine, 174(5), 732–739.CrossRef Reimers, M. S., Bastiaannet, E., Langley, R. E., et al. (2014). Expression of HLA class I antigen, aspirin use, and survival after a diagnosis of colon cancer. JAMA International Medicine, 174(5), 732–739.CrossRef
18.
Zurück zum Zitat Henrich, K. O., Bauer, T., Schulte, J., et al. (2011). CAMTA1, a 1p36 tumor suppressor candidate, inhibits growth and activates differentiation programs in neuroblastoma cells. Cancer Research, 71(8), 3142–3151.PubMedCrossRef Henrich, K. O., Bauer, T., Schulte, J., et al. (2011). CAMTA1, a 1p36 tumor suppressor candidate, inhibits growth and activates differentiation programs in neuroblastoma cells. Cancer Research, 71(8), 3142–3151.PubMedCrossRef
19.
Zurück zum Zitat Mikami, J., Kurokawa, Y., Takahashi, T., et al. (2016). Antitumor effect of antiplatelet agents in gastric cancer cells: an in vivo and in vitro study. Gastric Cancer, 19(3), 817–826.PubMedCrossRef Mikami, J., Kurokawa, Y., Takahashi, T., et al. (2016). Antitumor effect of antiplatelet agents in gastric cancer cells: an in vivo and in vitro study. Gastric Cancer, 19(3), 817–826.PubMedCrossRef
20.
Zurück zum Zitat Guillem-Llobat, P., Dovizio, M., Bruno, A., et al. (2016). Aspirin prevents colorectal cancer metastasis in mice by splitting the crosstalk between platelets and tumor cells. Oncotarget, 7(22), 32462–32477.PubMedPubMedCentralCrossRef Guillem-Llobat, P., Dovizio, M., Bruno, A., et al. (2016). Aspirin prevents colorectal cancer metastasis in mice by splitting the crosstalk between platelets and tumor cells. Oncotarget, 7(22), 32462–32477.PubMedPubMedCentralCrossRef
21.
Zurück zum Zitat Uluçkan, O., Eagleton, M. C., Floyd, D. H., et al. (2008). APT102, a novel adpase, cooperates with aspirin to disrupt bone metastasis in mice. Journal of Cellular Biochemistry, 104(4), 1311–1323.PubMedPubMedCentralCrossRef Uluçkan, O., Eagleton, M. C., Floyd, D. H., et al. (2008). APT102, a novel adpase, cooperates with aspirin to disrupt bone metastasis in mice. Journal of Cellular Biochemistry, 104(4), 1311–1323.PubMedPubMedCentralCrossRef
22.
Zurück zum Zitat Kune, G. A., Kune, S., & Watson, L. F. (1988). Colorectal cancer risk, chronic illnesses, operations, and medications: case control results from the Melbourne Colorectal Cancer Study. Cancer Research, 48(15), 4399–4404.PubMed Kune, G. A., Kune, S., & Watson, L. F. (1988). Colorectal cancer risk, chronic illnesses, operations, and medications: case control results from the Melbourne Colorectal Cancer Study. Cancer Research, 48(15), 4399–4404.PubMed
23.
Zurück zum Zitat Algra, A. M., & Rothwell, P. M. (2012). Effects of regular aspirin on long-term cancer incidence and metastasis: a systematic comparison of evidence from observational studies versus randomised trials. Lancet Oncology, 13(5), 518–527.PubMedCrossRef Algra, A. M., & Rothwell, P. M. (2012). Effects of regular aspirin on long-term cancer incidence and metastasis: a systematic comparison of evidence from observational studies versus randomised trials. Lancet Oncology, 13(5), 518–527.PubMedCrossRef
24.
Zurück zum Zitat Baron, J. A., Cole, B. F., & Sandler, R. S. (2003). A randomized trial of aspirin to prevent colorectal adenomas. New England Journal of Medicine, 348(10), 891–899.PubMedCrossRef Baron, J. A., Cole, B. F., & Sandler, R. S. (2003). A randomized trial of aspirin to prevent colorectal adenomas. New England Journal of Medicine, 348(10), 891–899.PubMedCrossRef
25.
Zurück zum Zitat Sandler, R. S., Halabi, S., & Baron, J. A. (2003). A randomized trial of aspirin to prevent colorectal adenomas in patients with previous colorectal cancer. New England Journal of Medicine, 348(10), 883–890.PubMedCrossRef Sandler, R. S., Halabi, S., & Baron, J. A. (2003). A randomized trial of aspirin to prevent colorectal adenomas in patients with previous colorectal cancer. New England Journal of Medicine, 348(10), 883–890.PubMedCrossRef
26.
Zurück zum Zitat Logan, R.F., Grainge, M.J., & Shepherd, V.C., et al.; (2008) ukCAP Trial Group. Aspirin and folic acid for the prevention of recurrent colorectal adenomas. Gastroenterology, 134(1), 29–38. Logan, R.F., Grainge, M.J., & Shepherd, V.C., et al.; (2008) ukCAP Trial Group. Aspirin and folic acid for the prevention of recurrent colorectal adenomas. Gastroenterology, 134(1), 29–38.
27.
Zurück zum Zitat Benamouzig, R., Deyra, J., Martin, A., et al. (2003). Daily soluble aspirin and prevention of colorectal adenoma recurrence: one-year results of the APACC trial. Gastroenterology, 125(2), 328–336.PubMedCrossRef Benamouzig, R., Deyra, J., Martin, A., et al. (2003). Daily soluble aspirin and prevention of colorectal adenoma recurrence: one-year results of the APACC trial. Gastroenterology, 125(2), 328–336.PubMedCrossRef
28.
Zurück zum Zitat Cole, B. F., Logan, R. F., Halabi, S., et al. (2009). Aspirin for the chemoprevention of colorectal adenomas: meta-analysis of the randomized trials. Journal of the National Cancer Institute, 101(4), 256–266.PubMedCrossRef Cole, B. F., Logan, R. F., Halabi, S., et al. (2009). Aspirin for the chemoprevention of colorectal adenomas: meta-analysis of the randomized trials. Journal of the National Cancer Institute, 101(4), 256–266.PubMedCrossRef
29.
Zurück zum Zitat Burn, J., Bishop, D. T., Mecklin, J. P., & CAPP2 Investigators. (2008). Effect of aspirin or resistant starch on colorectal neoplasia in the Lynch syndrome. New England Journal of Medicine, 359(24), 2567–2578.PubMedCrossRef Burn, J., Bishop, D. T., Mecklin, J. P., & CAPP2 Investigators. (2008). Effect of aspirin or resistant starch on colorectal neoplasia in the Lynch syndrome. New England Journal of Medicine, 359(24), 2567–2578.PubMedCrossRef
30.
Zurück zum Zitat Cooke, N. M., Spillane, C. D., Sheils, O., O'Leary, J., & Kenny, D. (2015). Aspirin and P2Y12 inhibition attenuate platelet-induced ovarian cancer cell invasion. BMC Cancer, 15, 627.PubMedPubMedCentralCrossRef Cooke, N. M., Spillane, C. D., Sheils, O., O'Leary, J., & Kenny, D. (2015). Aspirin and P2Y12 inhibition attenuate platelet-induced ovarian cancer cell invasion. BMC Cancer, 15, 627.PubMedPubMedCentralCrossRef
31.
Zurück zum Zitat Antithrombotic Trialists’ Collaboration. (2002). Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients. British Medical Journal, 324(7329), 71–86.CrossRef Antithrombotic Trialists’ Collaboration. (2002). Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients. British Medical Journal, 324(7329), 71–86.CrossRef
32.
Zurück zum Zitat Gresele, P. (2013). Antiplatelet agents in clinical practice and their haemorrhagic risk. Blood Transfusion, 11(3), 349–356.PubMedPubMedCentral Gresele, P. (2013). Antiplatelet agents in clinical practice and their haemorrhagic risk. Blood Transfusion, 11(3), 349–356.PubMedPubMedCentral
33.
Zurück zum Zitat Stürmer, T., Glynn, R. J., Lee, I. M., Manson, J. E., Buring, J. E., & Hennekens, C. H. (1998). Aspirin use and colorectal cancer: post-trial follow-up data from the Physicians’ Health Study. Annals of Internal Medicine, 128(9), 713–720.PubMedCrossRef Stürmer, T., Glynn, R. J., Lee, I. M., Manson, J. E., Buring, J. E., & Hennekens, C. H. (1998). Aspirin use and colorectal cancer: post-trial follow-up data from the Physicians’ Health Study. Annals of Internal Medicine, 128(9), 713–720.PubMedCrossRef
34.
Zurück zum Zitat Rothwell, P. M., Wilson, M., & Elwin, C. E. (2010). Long-term effect of aspirin on colorectal cancer incidence and mortality: 20-year follow-up of five randomised trials. Lancet, 376(9754), 1741–1750.PubMedCrossRef Rothwell, P. M., Wilson, M., & Elwin, C. E. (2010). Long-term effect of aspirin on colorectal cancer incidence and mortality: 20-year follow-up of five randomised trials. Lancet, 376(9754), 1741–1750.PubMedCrossRef
35.
Zurück zum Zitat Rothwell, P. M., Fowkes, F. G., Belch, J. F., Ogawa, H., Warlow, C. P., & Meade, T. W. (2011). Effect of daily aspirin on long-term risk of death due to cancer: analysis of individual patient data from randomised trials. Lancet, 377(9759), 31–41.PubMedCrossRef Rothwell, P. M., Fowkes, F. G., Belch, J. F., Ogawa, H., Warlow, C. P., & Meade, T. W. (2011). Effect of daily aspirin on long-term risk of death due to cancer: analysis of individual patient data from randomised trials. Lancet, 377(9759), 31–41.PubMedCrossRef
36.
Zurück zum Zitat Rothwell, P. M., Wilson, M., Price, J. F., Belch, J. F., Meade, T. W., & Mehta, Z. (2012). Effect of daily aspirin on risk of cancer metastasis: a study of incident cancers during randomised controlled trials. Lancet, 379(9826), 1591–1601.PubMedCrossRef Rothwell, P. M., Wilson, M., Price, J. F., Belch, J. F., Meade, T. W., & Mehta, Z. (2012). Effect of daily aspirin on risk of cancer metastasis: a study of incident cancers during randomised controlled trials. Lancet, 379(9826), 1591–1601.PubMedCrossRef
37.
Zurück zum Zitat Rothwell, P. M., Price, J. F., Fowkes, F. G., et al. (2012). Short-term effects of daily aspirin on cancer incidence, mortality, and non-vascular death: analysis of the time course of risks and benefits in 51 randomised controlled trials. Lancet, 379(9826), 1602–1612.PubMedCrossRef Rothwell, P. M., Price, J. F., Fowkes, F. G., et al. (2012). Short-term effects of daily aspirin on cancer incidence, mortality, and non-vascular death: analysis of the time course of risks and benefits in 51 randomised controlled trials. Lancet, 379(9826), 1602–1612.PubMedCrossRef
38.
Zurück zum Zitat Thun, M. J., Jacobs, E. J., & Patrono, C. (2012). The role of aspirin in cancer prevention. Nature Reviews Clinical Oncology, 9(5), 259–267.PubMedCrossRef Thun, M. J., Jacobs, E. J., & Patrono, C. (2012). The role of aspirin in cancer prevention. Nature Reviews Clinical Oncology, 9(5), 259–267.PubMedCrossRef
39.
Zurück zum Zitat Chubak, J., Whitlock, E. P., Williams, S. B., et al. (2016). Aspirin for the prevention of cancer incidence and mortality: systematic evidence reviews for the U.S. Preventive Services Task Force. Annals of Internal Medicine, 164(12), 814–825.PubMedCrossRef Chubak, J., Whitlock, E. P., Williams, S. B., et al. (2016). Aspirin for the prevention of cancer incidence and mortality: systematic evidence reviews for the U.S. Preventive Services Task Force. Annals of Internal Medicine, 164(12), 814–825.PubMedCrossRef
40.
Zurück zum Zitat Gresele, P., Momi, S., & Falcinelli, E. (2011). Anti-platelet therapy: phosphodiesterase inhibitors. British Journal of Clinical Pharmacology, 72(4), 634–646.PubMedPubMedCentralCrossRef Gresele, P., Momi, S., & Falcinelli, E. (2011). Anti-platelet therapy: phosphodiesterase inhibitors. British Journal of Clinical Pharmacology, 72(4), 634–646.PubMedPubMedCentralCrossRef
41.
Zurück zum Zitat Faxon, D.P., Creager, M.A., Smith, S.C., et al., (2004) American Heart Association. Atherosclerotic vascular disease conference: executive summary: atherosclerotic vascular disease conference proceeding for healthcare professionals from a special writing group of the American Heart Association. Circulation, 109(21), 2595–2604. Faxon, D.P., Creager, M.A., Smith, S.C., et al., (2004) American Heart Association. Atherosclerotic vascular disease conference: executive summary: atherosclerotic vascular disease conference proceeding for healthcare professionals from a special writing group of the American Heart Association. Circulation, 109(21), 2595–2604.
42.
Zurück zum Zitat Murata, K., Kameyama, M., Fukui, F., et al. (1999). Phosphodiesterase type III inhibitor, cilostazol, inhibits colon cancer cell motility. Clinical and Experimental Metastasis, 17(6), 525–530.PubMedCrossRef Murata, K., Kameyama, M., Fukui, F., et al. (1999). Phosphodiesterase type III inhibitor, cilostazol, inhibits colon cancer cell motility. Clinical and Experimental Metastasis, 17(6), 525–530.PubMedCrossRef
43.
Zurück zum Zitat Uzawa, K., Kasamatsu, A., Baba, T., et al. (2013). Targeting phosphodiesterase 3B enhances cisplatin sensitivity in human cancer cells. Cancer Medicine, 2(1), 40–49.PubMedPubMedCentralCrossRef Uzawa, K., Kasamatsu, A., Baba, T., et al. (2013). Targeting phosphodiesterase 3B enhances cisplatin sensitivity in human cancer cells. Cancer Medicine, 2(1), 40–49.PubMedPubMedCentralCrossRef
44.
Zurück zum Zitat Okoshi, H., Hakomori, S., Nisar, M., et al. (1991). Cell membrane signaling as target in cancer therapy II: inhibitory effect of N,N,N-trimethylsphingosine on metastatic potential of murine B16 melanoma cell line through blocking of tumor cell-dependent platelet aggregation. Cancer Research, 51(22), 6019–6025.PubMed Okoshi, H., Hakomori, S., Nisar, M., et al. (1991). Cell membrane signaling as target in cancer therapy II: inhibitory effect of N,N,N-trimethylsphingosine on metastatic potential of murine B16 melanoma cell line through blocking of tumor cell-dependent platelet aggregation. Cancer Research, 51(22), 6019–6025.PubMed
45.
Zurück zum Zitat Inufusa, H., Adachi, T., Nakamura, M., Shindo, K., Yasutomi, M., & Kimura, Y. (1995). Inhibition of experimental metastasis of human adenocarcinoma by cilostazol, a platelet phosphodiesterase inhibitor. Oncology Report, 2(6), 1079–1083. Inufusa, H., Adachi, T., Nakamura, M., Shindo, K., Yasutomi, M., & Kimura, Y. (1995). Inhibition of experimental metastasis of human adenocarcinoma by cilostazol, a platelet phosphodiesterase inhibitor. Oncology Report, 2(6), 1079–1083.
46.
Zurück zum Zitat Akcan, A., Kucuk, C., Ok, E., Canoz, O., Muhtaroglu, S., et al. (2006). The effect of amrinone on liver regeneration in experimental hepatic resection model. The Journal of Surgical Research, 130(1), 66–72.PubMedCrossRef Akcan, A., Kucuk, C., Ok, E., Canoz, O., Muhtaroglu, S., et al. (2006). The effect of amrinone on liver regeneration in experimental hepatic resection model. The Journal of Surgical Research, 130(1), 66–72.PubMedCrossRef
47.
Zurück zum Zitat Savai, R., Pullamsetti, S. S., Banat, G. A., et al. (2010). Targeting cancer with phosphodiesterase inhibitors. Expert Opinion on Investigational Drugs, 19(1), 117–131.PubMedCrossRef Savai, R., Pullamsetti, S. S., Banat, G. A., et al. (2010). Targeting cancer with phosphodiesterase inhibitors. Expert Opinion on Investigational Drugs, 19(1), 117–131.PubMedCrossRef
48.
Zurück zum Zitat Strowitzki, M. J., Dold, S., von Heesen, M., et al. (2014). The phosphodiesterase 3 inhibitor cilostazol does not stimulate growth of colorectal liver metastases after major hepatectomy. Clinical and Experimental Metastasis, 31(7), 795–803.PubMedCrossRef Strowitzki, M. J., Dold, S., von Heesen, M., et al. (2014). The phosphodiesterase 3 inhibitor cilostazol does not stimulate growth of colorectal liver metastases after major hepatectomy. Clinical and Experimental Metastasis, 31(7), 795–803.PubMedCrossRef
49.
Zurück zum Zitat Gresele, P., Zoja, C., Deckmyn, H., Arnout, J., Vermylen, J., & Verstraete, M. (1983). Dipyridamole inhibits platelet aggregation in whole blood. Thrombosis and Haemostasis, 50(4), 852–856.PubMed Gresele, P., Zoja, C., Deckmyn, H., Arnout, J., Vermylen, J., & Verstraete, M. (1983). Dipyridamole inhibits platelet aggregation in whole blood. Thrombosis and Haemostasis, 50(4), 852–856.PubMed
50.
Zurück zum Zitat Gresele, P., Arnout, J., Deckmyn, H., & Vermylen, J. (1986). Mechanism of the antiplatelet action of dipyridamole in whole blood: modulation of adenosine concentration and activity. Thrombosis and Haemostasis, 55(1), 12–18.PubMed Gresele, P., Arnout, J., Deckmyn, H., & Vermylen, J. (1986). Mechanism of the antiplatelet action of dipyridamole in whole blood: modulation of adenosine concentration and activity. Thrombosis and Haemostasis, 55(1), 12–18.PubMed
51.
Zurück zum Zitat Gresele, P., Arnout, J., & Vermylen, J. (1987). Dipyridamole inhibits leukotriene B4 synthesis. Thrombosis and Haemostasis, 57(2), 235.PubMed Gresele, P., Arnout, J., & Vermylen, J. (1987). Dipyridamole inhibits leukotriene B4 synthesis. Thrombosis and Haemostasis, 57(2), 235.PubMed
52.
Zurück zum Zitat Deckmyn, H., Gresele, P., Arnout, J., Todisco, A., & Vermylen, J. (1984). Prolonging prostacyclin production by nafazatrom or dipyridamole. Lancet, 2(8399), 410–411.PubMedCrossRef Deckmyn, H., Gresele, P., Arnout, J., Todisco, A., & Vermylen, J. (1984). Prolonging prostacyclin production by nafazatrom or dipyridamole. Lancet, 2(8399), 410–411.PubMedCrossRef
53.
Zurück zum Zitat Tzanakakis, G. N., Agarwal, K. C., & Vezeridis, M. P. (1993). Prevention of human pancreatic cancer cell-induced hepatic metastasis in nude mice by dipyridamole and its analog RA-233. Cancer, 71(8), 2466–2471.PubMedCrossRef Tzanakakis, G. N., Agarwal, K. C., & Vezeridis, M. P. (1993). Prevention of human pancreatic cancer cell-induced hepatic metastasis in nude mice by dipyridamole and its analog RA-233. Cancer, 71(8), 2466–2471.PubMedCrossRef
54.
Zurück zum Zitat Desai, P. B., Duan, J., Sridhar, R., & Damle, B. D. (1997). Reversal of doxorubicin resistance in multidrug resistant melanoma cells in vitro and in vivo by dipyridamole. Methods and Findings in Experimental Clinical Pharmacology, 19(4), 231–239. Desai, P. B., Duan, J., Sridhar, R., & Damle, B. D. (1997). Reversal of doxorubicin resistance in multidrug resistant melanoma cells in vitro and in vivo by dipyridamole. Methods and Findings in Experimental Clinical Pharmacology, 19(4), 231–239.
55.
Zurück zum Zitat Spano, D., Marshall, J. C., Marino, N., et al. (2013). Dipyridamole prevents triple-negative breast-cancer progression. Clinical and Experimental Metastasis, 30(1), 47–68.PubMedCrossRef Spano, D., Marshall, J. C., Marino, N., et al. (2013). Dipyridamole prevents triple-negative breast-cancer progression. Clinical and Experimental Metastasis, 30(1), 47–68.PubMedCrossRef
56.
Zurück zum Zitat Goda, A. E., Yoshida, T., Horinaka, M., et al. (2008). Mechanisms of enhancement of TRAIL tumoricidal activity against human cancer cells of different origin by dipyridamole. Oncogene, 27(24), 3435–3445.PubMedCrossRef Goda, A. E., Yoshida, T., Horinaka, M., et al. (2008). Mechanisms of enhancement of TRAIL tumoricidal activity against human cancer cells of different origin by dipyridamole. Oncogene, 27(24), 3435–3445.PubMedCrossRef
57.
Zurück zum Zitat Shalinsky, D. R., Andreeff, M., & Howell, S. B. (1990). Modulation of drug sensitivity by dipyridamole in multidrug resistant tumor cells in vitro. Cancer Research, 50(23), 7537–7543.PubMed Shalinsky, D. R., Andreeff, M., & Howell, S. B. (1990). Modulation of drug sensitivity by dipyridamole in multidrug resistant tumor cells in vitro. Cancer Research, 50(23), 7537–7543.PubMed
58.
Zurück zum Zitat Rhodes, E. L., Misch, K. J., Edwards, J. M., & Jarrett, P. E. (1985). Dipyridamole for treatment of melanoma. Lancet, 1(8430), 693.PubMedCrossRef Rhodes, E. L., Misch, K. J., Edwards, J. M., & Jarrett, P. E. (1985). Dipyridamole for treatment of melanoma. Lancet, 1(8430), 693.PubMedCrossRef
59.
Zurück zum Zitat Kohnoe, S., Maehara, Y., Takahashi, I., Emi, Y., Baba, H., & Sugimachi, K. (1998). Treatment of advanced gastric cancer with 5-fluorouracil and cisplatin in combination with dipyridamole. International Journal of Oncology, 13(6), 1203–1206.PubMed Kohnoe, S., Maehara, Y., Takahashi, I., Emi, Y., Baba, H., & Sugimachi, K. (1998). Treatment of advanced gastric cancer with 5-fluorouracil and cisplatin in combination with dipyridamole. International Journal of Oncology, 13(6), 1203–1206.PubMed
60.
Zurück zum Zitat Todd, K. E., Gloor, B., Lane, J. S., Isacoff, W. H., & Reber, H. A. (1998). Resection of locally advanced pancreatic cancer after downstaging with continuous-infusion 5-fluorouracil, mitomycin-C, leucovorin, and dipyridamole. Journal of Gastrointestinal Surgery, 2(2), 159–166.PubMedCrossRef Todd, K. E., Gloor, B., Lane, J. S., Isacoff, W. H., & Reber, H. A. (1998). Resection of locally advanced pancreatic cancer after downstaging with continuous-infusion 5-fluorouracil, mitomycin-C, leucovorin, and dipyridamole. Journal of Gastrointestinal Surgery, 2(2), 159–166.PubMedCrossRef
61.
Zurück zum Zitat Isacoff, W. H., Bendetti, J. K., Barstis, J. J., Jazieh, A. R., Macdonald, J. S., & Philip, P. A. (2007). Phase II trial of infusional fluorouracil, leucovorin, mitomycin, and dipyridamole in locally advanced unresectable pancreatic adenocarcinoma: SWOG S9700. Journal of Clinical Oncology, 25(13), 1665–1669.PubMedCrossRef Isacoff, W. H., Bendetti, J. K., Barstis, J. J., Jazieh, A. R., Macdonald, J. S., & Philip, P. A. (2007). Phase II trial of infusional fluorouracil, leucovorin, mitomycin, and dipyridamole in locally advanced unresectable pancreatic adenocarcinoma: SWOG S9700. Journal of Clinical Oncology, 25(13), 1665–1669.PubMedCrossRef
62.
Zurück zum Zitat Cusack, N. J., & Hourani, S. M. O. (2000). Platelet P2 receptors: from curiosity to clinical targets. Journal of Autonomous Nervous System, 81(1–3), 37–43.CrossRef Cusack, N. J., & Hourani, S. M. O. (2000). Platelet P2 receptors: from curiosity to clinical targets. Journal of Autonomous Nervous System, 81(1–3), 37–43.CrossRef
63.
Zurück zum Zitat Burnstock, G. (1972). Purinergic nerves. Pharmacological Reviews, 24(3), 509–581.PubMed Burnstock, G. (1972). Purinergic nerves. Pharmacological Reviews, 24(3), 509–581.PubMed
64.
Zurück zum Zitat Hollopeter, G., Jantzen, H. M., Vincent, D., et al. (2001). Identification of the platelet ADP receptor targeted by antithrombotic drugs. Nature, 409(6817), 202–207.PubMedCrossRef Hollopeter, G., Jantzen, H. M., Vincent, D., et al. (2001). Identification of the platelet ADP receptor targeted by antithrombotic drugs. Nature, 409(6817), 202–207.PubMedCrossRef
65.
Zurück zum Zitat Andre, P., Delaney, S. M., La Rocca, T., et al. (2003). P2Y12 regulates platelet adhesion/activation, thrombus growth, and thrombus stability in injured arteries. Journal of Clinical Investigation, 112(3), 398–406.PubMedPubMedCentralCrossRef Andre, P., Delaney, S. M., La Rocca, T., et al. (2003). P2Y12 regulates platelet adhesion/activation, thrombus growth, and thrombus stability in injured arteries. Journal of Clinical Investigation, 112(3), 398–406.PubMedPubMedCentralCrossRef
66.
Zurück zum Zitat Dangelmaier, C., Jin, J., Smith, J. B., & Kunapuli, S. P. (2001). Potentiation of thromboxane A2-induced platelet secretion by Gi signaling through the phosphoinositide-3 kinase pathway. Thrombosis and Haemostasis, 85(2), 341–348.PubMed Dangelmaier, C., Jin, J., Smith, J. B., & Kunapuli, S. P. (2001). Potentiation of thromboxane A2-induced platelet secretion by Gi signaling through the phosphoinositide-3 kinase pathway. Thrombosis and Haemostasis, 85(2), 341–348.PubMed
67.
Zurück zum Zitat Dorsam, R. T., Kim, S., Jin, J., & Kunapuli, S. P. (2002). Coordinated signaling through both G12/13 and G(i) pathways is sufficient to activate GPIIb/IIIa in human platelets. Journal of Biological Chemistry, 277(49), 47588–47595.PubMedCrossRef Dorsam, R. T., Kim, S., Jin, J., & Kunapuli, S. P. (2002). Coordinated signaling through both G12/13 and G(i) pathways is sufficient to activate GPIIb/IIIa in human platelets. Journal of Biological Chemistry, 277(49), 47588–47595.PubMedCrossRef
68.
Zurück zum Zitat Dorsam, R. T., & Kunapuli, S. P. (2004). Central role of the P2Y12 receptor in platelet activation. Journal of Clinical Investigation, 113(3), 340–345.PubMedPubMedCentralCrossRef Dorsam, R. T., & Kunapuli, S. P. (2004). Central role of the P2Y12 receptor in platelet activation. Journal of Clinical Investigation, 113(3), 340–345.PubMedPubMedCentralCrossRef
69.
Zurück zum Zitat van Gestel, M. A., Heemskerk, J. W., Slaaf, D. W., et al. (2003). In vivo blockade of platelet ADP receptor P2Y12 reduces embolus and thrombus formation but not thrombus stability. Arteriosclerosis Thrombosis and Vascular Biology, 23(3), 518–523.CrossRef van Gestel, M. A., Heemskerk, J. W., Slaaf, D. W., et al. (2003). In vivo blockade of platelet ADP receptor P2Y12 reduces embolus and thrombus formation but not thrombus stability. Arteriosclerosis Thrombosis and Vascular Biology, 23(3), 518–523.CrossRef
70.
Zurück zum Zitat Woulfe, D., Jiang, H., Mortensen, R., Yang, J., & Brass, L. F. (2002). Activation of Rap1B by G(i) family members in platelets. Journal of Biological Chemistry, 277(26), 23382–23390.PubMedCrossRef Woulfe, D., Jiang, H., Mortensen, R., Yang, J., & Brass, L. F. (2002). Activation of Rap1B by G(i) family members in platelets. Journal of Biological Chemistry, 277(26), 23382–23390.PubMedCrossRef
71.
72.
Zurück zum Zitat Di Virgilio, F. (2012). Purines, purinergic receptors, and cancer. Cancer Research, 72(21), 5441–5447.PubMedCrossRef Di Virgilio, F. (2012). Purines, purinergic receptors, and cancer. Cancer Research, 72(21), 5441–5447.PubMedCrossRef
73.
Zurück zum Zitat Aymeric, L., Apetoh, L., Ghiringhelli, F., et al. (2010). Tumor cell death and ATP release prime dendritic cells and efficient anticancer immunity. Cancer Research, 70(3), 855–858.PubMedCrossRef Aymeric, L., Apetoh, L., Ghiringhelli, F., et al. (2010). Tumor cell death and ATP release prime dendritic cells and efficient anticancer immunity. Cancer Research, 70(3), 855–858.PubMedCrossRef
74.
Zurück zum Zitat Boukerche, H., Berthier-Vergnes, O., Penin, F., et al. (1994). Human melanoma cell lines differ in their capacity to release ADP and aggregate platelets. British Journal of Haematology, 87(4), 763–772.PubMedCrossRef Boukerche, H., Berthier-Vergnes, O., Penin, F., et al. (1994). Human melanoma cell lines differ in their capacity to release ADP and aggregate platelets. British Journal of Haematology, 87(4), 763–772.PubMedCrossRef
75.
Zurück zum Zitat Ordinas, A., Díaz-Ricart, M., Almirall, L., & Bastida, E. (1990). The role of platelets in cancer metastasis. Blood Coagulation and Fibrinolysis, 1(6), 707–711.PubMed Ordinas, A., Díaz-Ricart, M., Almirall, L., & Bastida, E. (1990). The role of platelets in cancer metastasis. Blood Coagulation and Fibrinolysis, 1(6), 707–711.PubMed
77.
Zurück zum Zitat Coupland, L. A., & Parish, C. R. (2014). Platelets, selectins, and the control of tumor metastasis. Seminars in Oncology, 41(3), 422–434.PubMedCrossRef Coupland, L. A., & Parish, C. R. (2014). Platelets, selectins, and the control of tumor metastasis. Seminars in Oncology, 41(3), 422–434.PubMedCrossRef
78.
Zurück zum Zitat Johansson, J., Tabor, V., Wikell, A., Jalkanen, S., & Fuxe, J. (2015). TGF-β1-induced epithelial-mesenchymal transition promotes monocyte/macrophage properties in breast cancer cells. Frontiers in Oncology, 5, 3.PubMedPubMedCentralCrossRef Johansson, J., Tabor, V., Wikell, A., Jalkanen, S., & Fuxe, J. (2015). TGF-β1-induced epithelial-mesenchymal transition promotes monocyte/macrophage properties in breast cancer cells. Frontiers in Oncology, 5, 3.PubMedPubMedCentralCrossRef
79.
Zurück zum Zitat Contractor, H., & Ruparelia, N. (2012). Advances in antiplatelet therapy for acute coronary syndromes. Postgraduate Medical Journal, 88(1041), 391–396.PubMedCrossRef Contractor, H., & Ruparelia, N. (2012). Advances in antiplatelet therapy for acute coronary syndromes. Postgraduate Medical Journal, 88(1041), 391–396.PubMedCrossRef
80.
Zurück zum Zitat Collet, J. P., Hulot, J. S., Pena, A., et al. (2009). Cytochrome P450 2C19 polymorphism in young patients treated with clopidogrel after myocardial infarction: a cohort study. Lancet, 373(9660), 309–317.PubMedCrossRef Collet, J. P., Hulot, J. S., Pena, A., et al. (2009). Cytochrome P450 2C19 polymorphism in young patients treated with clopidogrel after myocardial infarction: a cohort study. Lancet, 373(9660), 309–317.PubMedCrossRef
81.
Zurück zum Zitat Herbert, J. M., & Savi, P. (2003). P2Y12, a new platelet ADP receptor, target of clopidogrel. Seminars in Vascular Medicine, 3(2), 113–122.PubMedCrossRef Herbert, J. M., & Savi, P. (2003). P2Y12, a new platelet ADP receptor, target of clopidogrel. Seminars in Vascular Medicine, 3(2), 113–122.PubMedCrossRef
82.
Zurück zum Zitat Kazui, M., Nishiya, Y., Ishizuka, T., et al. (2010). Identification of the human cytochrome P450 enzymes involved in the two oxidative steps in the bioactivation of clopidogrel to its pharmacologically active metabolite. Drug Metabolism and Disposition, 38(1), 92–99.PubMedCrossRef Kazui, M., Nishiya, Y., Ishizuka, T., et al. (2010). Identification of the human cytochrome P450 enzymes involved in the two oxidative steps in the bioactivation of clopidogrel to its pharmacologically active metabolite. Drug Metabolism and Disposition, 38(1), 92–99.PubMedCrossRef
83.
Zurück zum Zitat Pereillo, J. M., Maftouh, M., Andrieu, A., et al. (2002). Structure and stereochemistry of the active metabolite of clopidogrel. Drug Metabolism and Disposition, 30(11), 1288–1295.PubMedCrossRef Pereillo, J. M., Maftouh, M., Andrieu, A., et al. (2002). Structure and stereochemistry of the active metabolite of clopidogrel. Drug Metabolism and Disposition, 30(11), 1288–1295.PubMedCrossRef
84.
Zurück zum Zitat Bambace, N. M., Levis, J. E., & Holmes, C. E. (2010). The effect of P2Y-mediated platelet activation on the release of VEGF and endostatin from platelets. Platelets, 21(2), 85–93.PubMedCrossRef Bambace, N. M., Levis, J. E., & Holmes, C. E. (2010). The effect of P2Y-mediated platelet activation on the release of VEGF and endostatin from platelets. Platelets, 21(2), 85–93.PubMedCrossRef
85.
Zurück zum Zitat Klein-Soyer, C., Céraline, J., Orvain, C., de la Salle, C., Bergerat, J. P., & Cazenave, J. P. (1997). Angiogenesis inhibitor SR 25989 upregulates thrombospondin-1 expression in human vascular endothelial cells and foreskin fibroblasts. Biology of the Cell, 89(4), 295–307.PubMedCrossRef Klein-Soyer, C., Céraline, J., Orvain, C., de la Salle, C., Bergerat, J. P., & Cazenave, J. P. (1997). Angiogenesis inhibitor SR 25989 upregulates thrombospondin-1 expression in human vascular endothelial cells and foreskin fibroblasts. Biology of the Cell, 89(4), 295–307.PubMedCrossRef
86.
Zurück zum Zitat Ma, H., Hara, A., Xiao, C. Y., et al. (2001). Increased bleeding tendency and decreased susceptibility to thromboembolism in mice lacking the prostaglandin E2 receptor subtype EP3. Circulation, 104(10), 1176–1180.PubMedCrossRef Ma, H., Hara, A., Xiao, C. Y., et al. (2001). Increased bleeding tendency and decreased susceptibility to thromboembolism in mice lacking the prostaglandin E2 receptor subtype EP3. Circulation, 104(10), 1176–1180.PubMedCrossRef
87.
Zurück zum Zitat Sitia, G., Aiolfi, R., Di Lucia, P., et al. (2012). Antiplatelet therapy prevents hepatocellular carcinoma and improves survival in a mouse model of chronic hepatitis B. Proceeding of the National Academy of Sciences U S A, 109(32), E2165–E2172.CrossRef Sitia, G., Aiolfi, R., Di Lucia, P., et al. (2012). Antiplatelet therapy prevents hepatocellular carcinoma and improves survival in a mouse model of chronic hepatitis B. Proceeding of the National Academy of Sciences U S A, 109(32), E2165–E2172.CrossRef
88.
Zurück zum Zitat Pandey, A., Sarangi, S., Chien, K., et al. (2014). Anti-platelet agents augment cisplatin nanoparticle cytotoxicity by enhancing tumor vasculature permeability and drug delivery. Nanotechnology, 25(44), 445101.PubMedCrossRef Pandey, A., Sarangi, S., Chien, K., et al. (2014). Anti-platelet agents augment cisplatin nanoparticle cytotoxicity by enhancing tumor vasculature permeability and drug delivery. Nanotechnology, 25(44), 445101.PubMedCrossRef
89.
Zurück zum Zitat Roop, R. P., Naughton, M. J., Van Poznak, C., et al. (2013). A randomized phase II trial investigating the effect of platelet function inhibition on circulating tumor cells in patients with metastatic breast cancer. Clinical Breast Cancer, 13(6), 409–415.PubMedPubMedCentralCrossRef Roop, R. P., Naughton, M. J., Van Poznak, C., et al. (2013). A randomized phase II trial investigating the effect of platelet function inhibition on circulating tumor cells in patients with metastatic breast cancer. Clinical Breast Cancer, 13(6), 409–415.PubMedPubMedCentralCrossRef
90.
Zurück zum Zitat Choe, K. S., Correa, D., Jani, A. B., & Liauw, S. L. (2010). The use of anticoagulants improves biochemical control of localized prostate cancer treated with radiotherapy. Cancer, 116(7), 1820–1826.PubMedCrossRef Choe, K. S., Correa, D., Jani, A. B., & Liauw, S. L. (2010). The use of anticoagulants improves biochemical control of localized prostate cancer treated with radiotherapy. Cancer, 116(7), 1820–1826.PubMedCrossRef
91.
Zurück zum Zitat Hicks, B. M., Murray, L. J., Hughes, C., & Cardwell, C. R. (2015). Clopidogrel use and cancer-specific mortality: a population-based cohort study of colorectal, breast and prostate cancer patients. Pharmacoepidemiological Drug Safety, 24(8), 830–840.CrossRef Hicks, B. M., Murray, L. J., Hughes, C., & Cardwell, C. R. (2015). Clopidogrel use and cancer-specific mortality: a population-based cohort study of colorectal, breast and prostate cancer patients. Pharmacoepidemiological Drug Safety, 24(8), 830–840.CrossRef
92.
Zurück zum Zitat Husted, S., Emanuelsson, H., Heptinstall, S., et al. (2006). Pharmacodynamics, pharmacokinetics, and safety of the oral reversible P2Y12 antagonist AZD6140 with aspirin in patients with atherosclerosis: a double-blind comparison to clopidogrel with aspirin. European Heart Journal, 27(9), 1038–1047.PubMedCrossRef Husted, S., Emanuelsson, H., Heptinstall, S., et al. (2006). Pharmacodynamics, pharmacokinetics, and safety of the oral reversible P2Y12 antagonist AZD6140 with aspirin in patients with atherosclerosis: a double-blind comparison to clopidogrel with aspirin. European Heart Journal, 27(9), 1038–1047.PubMedCrossRef
93.
Zurück zum Zitat Teng, R., Oliver, S., Hayes, M. A., & Butler, K. (2010). Absorption, distribution, metabolism, and excretion of ticagrelor in healthy subjects. Drug Metabolism and Disposable, 38(9), 1514–1521.CrossRef Teng, R., Oliver, S., Hayes, M. A., & Butler, K. (2010). Absorption, distribution, metabolism, and excretion of ticagrelor in healthy subjects. Drug Metabolism and Disposable, 38(9), 1514–1521.CrossRef
94.
Zurück zum Zitat Gebremeskel, S., LeVatte, T., Liwski, R. S., Johnston, B., & Bezuhly, M. (2015). The reversible P2Y12 inhibitor ticagrelor inhibits metastasis and improves survival in mouse models of cancer. International Journal of Cancer, 136(1), 234–240.PubMedCrossRef Gebremeskel, S., LeVatte, T., Liwski, R. S., Johnston, B., & Bezuhly, M. (2015). The reversible P2Y12 inhibitor ticagrelor inhibits metastasis and improves survival in mouse models of cancer. International Journal of Cancer, 136(1), 234–240.PubMedCrossRef
95.
Zurück zum Zitat Bonaca, M. P., Bhatt, D. L., Cohen, M. P. H., et al. (2015). Long-term use of ticagrelor in patients with prior myocardial infarction. New England Journal of Medicine, 372(19), 1791–1800.PubMedCrossRef Bonaca, M. P., Bhatt, D. L., Cohen, M. P. H., et al. (2015). Long-term use of ticagrelor in patients with prior myocardial infarction. New England Journal of Medicine, 372(19), 1791–1800.PubMedCrossRef
96.
Zurück zum Zitat Serebruany, V. L., Cherepanov, V., Cabrera-Fuentes, H. A., & Kim, M. H. (2015). Solid cancers after antiplatelet therapy: confirmations, controversies, and challenges. Thrombosis and Haemostasis, 114(6), 1104–1112.PubMedCrossRef Serebruany, V. L., Cherepanov, V., Cabrera-Fuentes, H. A., & Kim, M. H. (2015). Solid cancers after antiplatelet therapy: confirmations, controversies, and challenges. Thrombosis and Haemostasis, 114(6), 1104–1112.PubMedCrossRef
97.
Zurück zum Zitat Serebruany, V. L., Dinicolantonio, J. J., Can, M. M., Pershukov, I. V., & Kuliczkowski, W. (2013). Gastrointestinal adverse events after dual antiplatelet therapy: clopidogrel is safer than ticagrelor, but prasugrel data are lacking or inconclusive. Cardiology, 126(1), 35–40.PubMedCrossRef Serebruany, V. L., Dinicolantonio, J. J., Can, M. M., Pershukov, I. V., & Kuliczkowski, W. (2013). Gastrointestinal adverse events after dual antiplatelet therapy: clopidogrel is safer than ticagrelor, but prasugrel data are lacking or inconclusive. Cardiology, 126(1), 35–40.PubMedCrossRef
98.
Zurück zum Zitat Unger, E. F. (2009). Weighing benefits and risks—the FDA’s review of prasugrel. New England Journal of Medicine, 361(10), 942–945.PubMedCrossRef Unger, E. F. (2009). Weighing benefits and risks—the FDA’s review of prasugrel. New England Journal of Medicine, 361(10), 942–945.PubMedCrossRef
99.
Zurück zum Zitat Floyd, J. S., & Serebruany, V. L. (2010). Prasugrel as a potential cancer promoter: review of the unpublished data. Archives of Internal Medicine, 170(12), 1078–1080.PubMedCrossRef Floyd, J. S., & Serebruany, V. L. (2010). Prasugrel as a potential cancer promoter: review of the unpublished data. Archives of Internal Medicine, 170(12), 1078–1080.PubMedCrossRef
100.
Zurück zum Zitat Roe, M.T., Cyr, D.D., Eckart, D., et al.; (2016) TRILOGY ACS Investigators. Ascertainment, classification, and impact of neoplasm detection during prolonged treatment with dual antiplatelet therapy with prasugrel vs clopidogrel following acute coronary syndrome. European Heart Journal, 37(4), 412–422. Roe, M.T., Cyr, D.D., Eckart, D., et al.; (2016) TRILOGY ACS Investigators. Ascertainment, classification, and impact of neoplasm detection during prolonged treatment with dual antiplatelet therapy with prasugrel vs clopidogrel following acute coronary syndrome. European Heart Journal, 37(4), 412–422.
101.
Zurück zum Zitat Mauri, L., Kereiakes, D.J., Yeh, R.W., et al. (2014). DAPT Study Investigators. Twelve or 30 months of dual antiplatelet therapy after drug-eluting stents. New England Journal of Medicine, 371(23), 2155–2166. Mauri, L., Kereiakes, D.J., Yeh, R.W., et al. (2014). DAPT Study Investigators. Twelve or 30 months of dual antiplatelet therapy after drug-eluting stents. New England Journal of Medicine, 371(23), 2155–2166.
102.
Zurück zum Zitat Kotronias, R. A., Kwok, C. S., Wong, C. W., Kinnaird, T., Zaman, A., & Mamas, M. A. (2017). Cancer event rate and mortality with thienopyridines: a systematic review and meta-analysis. Drug Safety, 40(3), 229–240.PubMedCrossRef Kotronias, R. A., Kwok, C. S., Wong, C. W., Kinnaird, T., Zaman, A., & Mamas, M. A. (2017). Cancer event rate and mortality with thienopyridines: a systematic review and meta-analysis. Drug Safety, 40(3), 229–240.PubMedCrossRef
103.
104.
Zurück zum Zitat Shattil, S. J., Kashiwagi, H., & Pampori, N. (1998). Integrin signaling: the platelet paradigm. Blood, 91(8), 2645–2657.PubMed Shattil, S. J., Kashiwagi, H., & Pampori, N. (1998). Integrin signaling: the platelet paradigm. Blood, 91(8), 2645–2657.PubMed
105.
Zurück zum Zitat Schrör, K., & Weber, A. (2003). Comparative pharmacology of GP IIb/IIIa antagonists. Journal of Thrombosis and Thrombolysis, 15(5), 71–80.PubMedCrossRef Schrör, K., & Weber, A. (2003). Comparative pharmacology of GP IIb/IIIa antagonists. Journal of Thrombosis and Thrombolysis, 15(5), 71–80.PubMedCrossRef
106.
Zurück zum Zitat Salame, M., Verheye, S., More, R., King 3rd, S. B., & Chronos, N. (1999). GPIIbIIIa inhibitors as adjunctive therapy in acute myocardial infarction. International Journal of Cardiology, 69(3), 231–236.PubMedCrossRef Salame, M., Verheye, S., More, R., King 3rd, S. B., & Chronos, N. (1999). GPIIbIIIa inhibitors as adjunctive therapy in acute myocardial infarction. International Journal of Cardiology, 69(3), 231–236.PubMedCrossRef
107.
Zurück zum Zitat Ahrens, I., Bode, C., & Zirlik, A. (2014). Anticoagulation during and after acute coronary syndrome. Hämostaseologie, 34(1), 72–77.PubMedCrossRef Ahrens, I., Bode, C., & Zirlik, A. (2014). Anticoagulation during and after acute coronary syndrome. Hämostaseologie, 34(1), 72–77.PubMedCrossRef
108.
Zurück zum Zitat Clezardin, P., Drouin, J., Morel-Kopp, M. C., et al. (1993). Role of platelet membrane glycoproteins Ib/IX and IIb/IIIa, and of platelet alpha-granule proteins in platelet aggregation induced by human osteosarcoma cells. Cancer Research, 53(19), 4695–4700.PubMed Clezardin, P., Drouin, J., Morel-Kopp, M. C., et al. (1993). Role of platelet membrane glycoproteins Ib/IX and IIb/IIIa, and of platelet alpha-granule proteins in platelet aggregation induced by human osteosarcoma cells. Cancer Research, 53(19), 4695–4700.PubMed
109.
Zurück zum Zitat Santos-Martinez, M. J., Medina, C., Jurasz, P., & Radomski, M. W. (2008). Role of metalloproteinases in platelet function. Thrombosis Research, 121(4), 535–542.PubMedCrossRef Santos-Martinez, M. J., Medina, C., Jurasz, P., & Radomski, M. W. (2008). Role of metalloproteinases in platelet function. Thrombosis Research, 121(4), 535–542.PubMedCrossRef
110.
Zurück zum Zitat Bakewell, S. J., Nestor, P., Prasad, S., et al. (2003). Platelet and osteoclast beta3 integrins are critical for bone metastasis. Proceedings of the National Academy of Science U S A, 100(24), 14205–14210.CrossRef Bakewell, S. J., Nestor, P., Prasad, S., et al. (2003). Platelet and osteoclast beta3 integrins are critical for bone metastasis. Proceedings of the National Academy of Science U S A, 100(24), 14205–14210.CrossRef
111.
112.
Zurück zum Zitat Bennett, J. S., Chan, C., Vilaire, G., Mousa, S. A., & DeGrado, W. F. (1997). Agonist-activated alphavbeta3 on platelets and lymphocytes binds to the matrix protein osteopontin. Journal of Biological Chemistry, 272(13), 8137–8140.PubMedCrossRef Bennett, J. S., Chan, C., Vilaire, G., Mousa, S. A., & DeGrado, W. F. (1997). Agonist-activated alphavbeta3 on platelets and lymphocytes binds to the matrix protein osteopontin. Journal of Biological Chemistry, 272(13), 8137–8140.PubMedCrossRef
113.
Zurück zum Zitat Wilder, R. L. (2002). Integrin alpha V beta 3 as a target for treatment of rheumatoid arthritis and related rheumatic diseases. Annals of Rheumatisms Disease, 61(Suppl 2), 96–99.CrossRef Wilder, R. L. (2002). Integrin alpha V beta 3 as a target for treatment of rheumatoid arthritis and related rheumatic diseases. Annals of Rheumatisms Disease, 61(Suppl 2), 96–99.CrossRef
114.
Zurück zum Zitat Brooks, P. C., Clark, R. A., & Cheresh, D. A. (1994). Requirement of vascular integrin alpha v beta 3 for angiogenesis. Science, 264(5158), 569–571.PubMedCrossRef Brooks, P. C., Clark, R. A., & Cheresh, D. A. (1994). Requirement of vascular integrin alpha v beta 3 for angiogenesis. Science, 264(5158), 569–571.PubMedCrossRef
115.
Zurück zum Zitat Kumar, C. C. (2003). Integrin alpha v beta 3 as a therapeutic target for blocking tumor-induced angiogenesis. Current Drug Targets, 4(2), 123–131.PubMedCrossRef Kumar, C. C. (2003). Integrin alpha v beta 3 as a therapeutic target for blocking tumor-induced angiogenesis. Current Drug Targets, 4(2), 123–131.PubMedCrossRef
116.
Zurück zum Zitat Weber, M. R., Zuka, M., Lorger, M., et al. (2016). Activated tumor cell integrin αvβ3 cooperates with platelets to promote extravasation and metastasis from the blood stream. Thrombosis Research, 140(Suppl 1), S27–S36.PubMedPubMedCentralCrossRef Weber, M. R., Zuka, M., Lorger, M., et al. (2016). Activated tumor cell integrin αvβ3 cooperates with platelets to promote extravasation and metastasis from the blood stream. Thrombosis Research, 140(Suppl 1), S27–S36.PubMedPubMedCentralCrossRef
117.
Zurück zum Zitat Tesfamariam, B. (2016). Involvement of platelets in tumor cell metastasis. Pharmacological. Therapy, 157, 112–119.CrossRef Tesfamariam, B. (2016). Involvement of platelets in tumor cell metastasis. Pharmacological. Therapy, 157, 112–119.CrossRef
118.
Zurück zum Zitat Lonsdorf, A. S., Kramer, B. F., Fahrleitner, M., et al. (2012). Engagement of alpha(IIb)beta(3) (GPIIb/IIIa) with alphanubeta3 integrin mediates interaction of melanoma cells with platelets: a connection to hematogenous metastasis. Journal of Biological Chemistry, 287(3), 2168–2178.PubMedCrossRef Lonsdorf, A. S., Kramer, B. F., Fahrleitner, M., et al. (2012). Engagement of alpha(IIb)beta(3) (GPIIb/IIIa) with alphanubeta3 integrin mediates interaction of melanoma cells with platelets: a connection to hematogenous metastasis. Journal of Biological Chemistry, 287(3), 2168–2178.PubMedCrossRef
119.
Zurück zum Zitat Gomes, N., Vassy, J., Lebos, C., Arbeille, B., Legrand, C., & Fauvel-Lafeve, F. (2004). Breast adenocarcinoma cell adhesion to the vascular subendothelium in whole blood and under flow conditions: effects of alphavbeta3 and alphaIIbbeta3 antagonists. Clinical and Experimental Metastasis, 21(6), 553–561.PubMedCrossRef Gomes, N., Vassy, J., Lebos, C., Arbeille, B., Legrand, C., & Fauvel-Lafeve, F. (2004). Breast adenocarcinoma cell adhesion to the vascular subendothelium in whole blood and under flow conditions: effects of alphavbeta3 and alphaIIbbeta3 antagonists. Clinical and Experimental Metastasis, 21(6), 553–561.PubMedCrossRef
120.
Zurück zum Zitat Harris, T. D., Kalogeropoulos, S., Nguyen, T., et al. (2003). Design, synthesis, and evaluation of radiolabeled integrin alpha v beta 3 receptor antagonists for tumor imaging and radiotherapy. Cancer Biotherapy and Radiopharmaceuticals, 18(4), 627–641.PubMedCrossRef Harris, T. D., Kalogeropoulos, S., Nguyen, T., et al. (2003). Design, synthesis, and evaluation of radiolabeled integrin alpha v beta 3 receptor antagonists for tumor imaging and radiotherapy. Cancer Biotherapy and Radiopharmaceuticals, 18(4), 627–641.PubMedCrossRef
121.
Zurück zum Zitat Amirkhosravi, A., Mousa, S. A., Amaya, M., et al. (2003). Inhibition of tumor cell-induced platelet aggregation and lung metastasis by the oral GpIIb/IIIa antagonist XV454. Thrombosis and Haemostasis, 90(3), 549–554.PubMed Amirkhosravi, A., Mousa, S. A., Amaya, M., et al. (2003). Inhibition of tumor cell-induced platelet aggregation and lung metastasis by the oral GpIIb/IIIa antagonist XV454. Thrombosis and Haemostasis, 90(3), 549–554.PubMed
122.
Zurück zum Zitat Sheu, J. R., Lin, C. H., Chung, J.l., Teng, C. M., & Huang, T. F. (1992). Triflavin, an Arg-Gly-Asp containing snake venom peptide, inhibits aggregation of human platelets induced by human hepatoma cell line. Thrombosis Research, 66(6), 679–691. Sheu, J. R., Lin, C. H., Chung, J.l., Teng, C. M., & Huang, T. F. (1992). Triflavin, an Arg-Gly-Asp containing snake venom peptide, inhibits aggregation of human platelets induced by human hepatoma cell line. Thrombosis Research, 66(6), 679–691.
123.
Zurück zum Zitat Chiang, H. S., Swaim, M. W., & Huang, T. F. (1994). Characterization of platelet aggregation induced by human colon adenocarcinoma cells and its inhibition by snake venom peptides, trigramin and rhodostomin. British Journal of Haematology, 87(2), 325–331.PubMedCrossRef Chiang, H. S., Swaim, M. W., & Huang, T. F. (1994). Characterization of platelet aggregation induced by human colon adenocarcinoma cells and its inhibition by snake venom peptides, trigramin and rhodostomin. British Journal of Haematology, 87(2), 325–331.PubMedCrossRef
124.
Zurück zum Zitat Borsig, L., Wong, R., Feramisco, J., Nadeau, D. R., Varki, N. M., & Varki, A. (2001). Heparin and cancer revisited: mechanistic connections involving platelets, P-selectin, carcinoma mucins, and tumor metastasis. Proceedings of the National Academy of Science U S A, 98(6), 3352–3357.CrossRef Borsig, L., Wong, R., Feramisco, J., Nadeau, D. R., Varki, N. M., & Varki, A. (2001). Heparin and cancer revisited: mechanistic connections involving platelets, P-selectin, carcinoma mucins, and tumor metastasis. Proceedings of the National Academy of Science U S A, 98(6), 3352–3357.CrossRef
125.
Zurück zum Zitat Sobel, M., Fish, W. R., Toma, N., et al. (2001). Heparin modulates integrin function in human platelets. Journal of Vascular Surgery, 33(3), 587–594.PubMedCrossRef Sobel, M., Fish, W. R., Toma, N., et al. (2001). Heparin modulates integrin function in human platelets. Journal of Vascular Surgery, 33(3), 587–594.PubMedCrossRef
126.
Zurück zum Zitat Zhang, C., Liu, Y., Gao, Y., et al. (2009). Modified heparins inhibit integrin alpha(IIb)beta(3) mediated adhesion of melanoma cells to platelets in vitro and in vivo. International Journal of Cancer, 125(9), 2058–2065.PubMedCrossRef Zhang, C., Liu, Y., Gao, Y., et al. (2009). Modified heparins inhibit integrin alpha(IIb)beta(3) mediated adhesion of melanoma cells to platelets in vitro and in vivo. International Journal of Cancer, 125(9), 2058–2065.PubMedCrossRef
127.
Zurück zum Zitat Gutheil, J. C., Campbell, T. N., Pierce, P. R., et al. (2000). Targeted antiangiogenic therapy for cancer using vitaxin: a humanized monoclonal antibody to the integrin alphavbeta3. Clinical and Cancer Research, 6(8), 3056–3061. Gutheil, J. C., Campbell, T. N., Pierce, P. R., et al. (2000). Targeted antiangiogenic therapy for cancer using vitaxin: a humanized monoclonal antibody to the integrin alphavbeta3. Clinical and Cancer Research, 6(8), 3056–3061.
128.
Zurück zum Zitat Patel, S., Jenkins, J., Papadopolous, N., et al. (2001). Pilot study of vitaxin—an angiogenesis inhibitor—in patients with advanced leiomyosarcomas. Cancer, 92(5), 1347–1348.PubMedCrossRef Patel, S., Jenkins, J., Papadopolous, N., et al. (2001). Pilot study of vitaxin—an angiogenesis inhibitor—in patients with advanced leiomyosarcomas. Cancer, 92(5), 1347–1348.PubMedCrossRef
129.
Zurück zum Zitat Posey, J., Khazaeli, M., Del Grosso, A., et al. (2001). A pilot trial of vitaxin, a humanized anti-vitronectin receptor (anti-αvβ3) antibody in patients with metastatic cancer. Cancer Biotherapy and Radiopharmaceuticals, 16(2), 125–132.PubMedCrossRef Posey, J., Khazaeli, M., Del Grosso, A., et al. (2001). A pilot trial of vitaxin, a humanized anti-vitronectin receptor (anti-αvβ3) antibody in patients with metastatic cancer. Cancer Biotherapy and Radiopharmaceuticals, 16(2), 125–132.PubMedCrossRef
130.
Zurück zum Zitat Cai, W., Wu, Y., Chen, K., Cao, Q., Tice, D., & Chen, X. (2006). In vitro and in vivo characterization of 64Cu-labeled Abegrin, a humanized monoclonal antibody against integrin αvβ3. Cancer Research, 66(19), 9673–9681.PubMedCrossRef Cai, W., Wu, Y., Chen, K., Cao, Q., Tice, D., & Chen, X. (2006). In vitro and in vivo characterization of 64Cu-labeled Abegrin, a humanized monoclonal antibody against integrin αvβ3. Cancer Research, 66(19), 9673–9681.PubMedCrossRef
131.
Zurück zum Zitat Hersey, P., Sosman, J., O'Day, S., et al. (2010). A randomized phase 2 study of etaracizumab, a monoclonal antibody against integrin αvβ3, +/− dacarbazine in patients with stage IV metastatic melanoma. Cancer, 116(6), 1526–1534.PubMedCrossRef Hersey, P., Sosman, J., O'Day, S., et al. (2010). A randomized phase 2 study of etaracizumab, a monoclonal antibody against integrin αvβ3, +/− dacarbazine in patients with stage IV metastatic melanoma. Cancer, 116(6), 1526–1534.PubMedCrossRef
132.
Zurück zum Zitat Delbaldo, C., Raymond, E., Vera, K., et al. (2008). Phase I and pharmacokinetic study of etaracizumab (Abegrin), a humanized monoclonal antibody against αvβ3 integrin receptor, in patients with advanced solid tumors. Investigational New Drugs, 26(1), 35–43.PubMedCrossRef Delbaldo, C., Raymond, E., Vera, K., et al. (2008). Phase I and pharmacokinetic study of etaracizumab (Abegrin), a humanized monoclonal antibody against αvβ3 integrin receptor, in patients with advanced solid tumors. Investigational New Drugs, 26(1), 35–43.PubMedCrossRef
133.
Zurück zum Zitat Dyke, C. M. (1999). Safety of glycoprotein IIb-IIIa inhibitors: a heart surgeon’s perspective. American Heart Journal, 138(4 pt 2), 307–316.PubMedCrossRef Dyke, C. M. (1999). Safety of glycoprotein IIb-IIIa inhibitors: a heart surgeon’s perspective. American Heart Journal, 138(4 pt 2), 307–316.PubMedCrossRef
134.
Zurück zum Zitat Gulba, D. C., Huber, K., Moll, S., & Dietz, R. (1998). Platelet inhibition: new agents, new strategies, new trials. Fibrinolysis and Proteolysis, 12(Suppl2), 13–23. Gulba, D. C., Huber, K., Moll, S., & Dietz, R. (1998). Platelet inhibition: new agents, new strategies, new trials. Fibrinolysis and Proteolysis, 12(Suppl2), 13–23.
135.
Zurück zum Zitat Tam, S., Sassoli, P., Jordan, R., & Nakada, M. (1998). Abciximab (ReoPro, chimeric 7E3 Fab) demonstrates equivalent affinity and functional blockade of lycoprotein IIb/IIIa αvβ3 integrins. Circulation, 98(11), 1085–1091.PubMedCrossRef Tam, S., Sassoli, P., Jordan, R., & Nakada, M. (1998). Abciximab (ReoPro, chimeric 7E3 Fab) demonstrates equivalent affinity and functional blockade of lycoprotein IIb/IIIa αvβ3 integrins. Circulation, 98(11), 1085–1091.PubMedCrossRef
136.
Zurück zum Zitat Antoniucci, D. (2007). Differences among GP IIb/IIIa inhibitors: different clinical benefits in non-ST-segment elevation acute coronary syndrome percutaneous coronary intervention patients. European Heart Journal, 9, A32–A36.CrossRef Antoniucci, D. (2007). Differences among GP IIb/IIIa inhibitors: different clinical benefits in non-ST-segment elevation acute coronary syndrome percutaneous coronary intervention patients. European Heart Journal, 9, A32–A36.CrossRef
137.
Zurück zum Zitat Casserly, I., & Topol, E. (2002). Glycoprotein IIb/IIIa-antagonists—from bench to practice. Cellular and Molecular Life Sciences, 59(3), 478–500.PubMedCrossRef Casserly, I., & Topol, E. (2002). Glycoprotein IIb/IIIa-antagonists—from bench to practice. Cellular and Molecular Life Sciences, 59(3), 478–500.PubMedCrossRef
138.
Zurück zum Zitat Amirkhosravi, A., Amaya, M., Siddiqui, F., Biggerstaff, J. P., Meyer, T. V., & Francis, J. L. (1999). Blockade of GPIIb/IIIa inhibits the release of vascular endothelial growth factor (VEGF) from tumor cell-activated platelets and experimental metastasis. Platelets, 10(5), 285–292.PubMedCrossRef Amirkhosravi, A., Amaya, M., Siddiqui, F., Biggerstaff, J. P., Meyer, T. V., & Francis, J. L. (1999). Blockade of GPIIb/IIIa inhibits the release of vascular endothelial growth factor (VEGF) from tumor cell-activated platelets and experimental metastasis. Platelets, 10(5), 285–292.PubMedCrossRef
139.
Zurück zum Zitat Trikha, M., Zhou, Z., Timar, J., et al. (2002). Multiple roles for platelet GPIIb/IIIa and alphavbeta3 integrins in tumor growth, angiogenesis, and metastasis. Cancer Research, 62(10), 2824–2833.PubMed Trikha, M., Zhou, Z., Timar, J., et al. (2002). Multiple roles for platelet GPIIb/IIIa and alphavbeta3 integrins in tumor growth, angiogenesis, and metastasis. Cancer Research, 62(10), 2824–2833.PubMed
140.
Zurück zum Zitat Tcheng, J. (2000). Clinical challenges of platelet glycoprotein IIb/IIIa receptor inhibitor therapy: bleeding, reversal, thrombocytopenia, and retreatment. American Heart Journal, 139(2 pt 2), S38–S45.PubMedCrossRef Tcheng, J. (2000). Clinical challenges of platelet glycoprotein IIb/IIIa receptor inhibitor therapy: bleeding, reversal, thrombocytopenia, and retreatment. American Heart Journal, 139(2 pt 2), S38–S45.PubMedCrossRef
141.
Zurück zum Zitat Kononczuk, J., Surazynski, A., Czyzewska, U., et al. (2015). αIIbβ3-integrin ligands: abciximab and eptifibatide as proapoptotic factors in MCF-7 human breast cancer cells. Current Drug Targets, 16(13), 1429–1437.PubMedCrossRef Kononczuk, J., Surazynski, A., Czyzewska, U., et al. (2015). αIIbβ3-integrin ligands: abciximab and eptifibatide as proapoptotic factors in MCF-7 human breast cancer cells. Current Drug Targets, 16(13), 1429–1437.PubMedCrossRef
142.
Zurück zum Zitat Karlheinz, P. (2005). Antiplatelet drugs. In M. S. Runge (Ed.), Principles of molecular cardiology (Vol. 105, pp. 203–218). Totowa: Human Press. Karlheinz, P. (2005). Antiplatelet drugs. In M. S. Runge (Ed.), Principles of molecular cardiology (Vol. 105, pp. 203–218). Totowa: Human Press.
143.
Zurück zum Zitat Peter, K. (2005). Principles of molecular cardiology. Totowa: Humana Press. Peter, K. (2005). Principles of molecular cardiology. Totowa: Humana Press.
144.
Zurück zum Zitat Davì, G., Santilli, F., & Vazzana, N. (2012). Thromboxane receptors antagonists and/or synthase inhibitors. Handbook of Experimental Pharmacology, 210, 261–286.CrossRef Davì, G., Santilli, F., & Vazzana, N. (2012). Thromboxane receptors antagonists and/or synthase inhibitors. Handbook of Experimental Pharmacology, 210, 261–286.CrossRef
145.
Zurück zum Zitat Honn, K. V. (1983). Inhibition of tumor cell metastasis by modulation of the vascular prostacyclin/thromboxane A2 system. Clinical and Experimental Metastasis, 1(2), 103–114.PubMedCrossRef Honn, K. V. (1983). Inhibition of tumor cell metastasis by modulation of the vascular prostacyclin/thromboxane A2 system. Clinical and Experimental Metastasis, 1(2), 103–114.PubMedCrossRef
146.
Zurück zum Zitat Ogletree, M. L. (1987). Overview of physiological and pathophysiological effects of thromboxane A2. Federation Proceedings, 46(1), 133–138.PubMed Ogletree, M. L. (1987). Overview of physiological and pathophysiological effects of thromboxane A2. Federation Proceedings, 46(1), 133–138.PubMed
147.
Zurück zum Zitat Nie, D., Lamberti, M., Zacharek, A., et al. (2000). Thromboxane A2 regulation of endothelial cell migration, angiogenesis, and tumor metastasis. Biochemical and Biophysical Research Communication, 267, 245–251.CrossRef Nie, D., Lamberti, M., Zacharek, A., et al. (2000). Thromboxane A2 regulation of endothelial cell migration, angiogenesis, and tumor metastasis. Biochemical and Biophysical Research Communication, 267, 245–251.CrossRef
148.
Zurück zum Zitat de Leval, X., Benoit, V., Delarge, J., et al. (2003). Pharmacological evaluation of the novel thromboxane modulator BM-567 (II/II). Effects of BM-567 on osteogenic sarcoma-cell-induced platelet aggregation. Prostaglandins and Leukotriene Essential Fatty Acids, 68(1), 55–59.CrossRef de Leval, X., Benoit, V., Delarge, J., et al. (2003). Pharmacological evaluation of the novel thromboxane modulator BM-567 (II/II). Effects of BM-567 on osteogenic sarcoma-cell-induced platelet aggregation. Prostaglandins and Leukotriene Essential Fatty Acids, 68(1), 55–59.CrossRef
149.
Zurück zum Zitat Mehta, P., Lawson, D., Ward, M. B., Lee-Ambrose, L., & Kimura, A. (1986). Effects of thromboxane A2 inhibition on osteogenic sarcoma cell-induced platelet aggregation. Cancer Research, 46(10), 5061–5063.PubMed Mehta, P., Lawson, D., Ward, M. B., Lee-Ambrose, L., & Kimura, A. (1986). Effects of thromboxane A2 inhibition on osteogenic sarcoma cell-induced platelet aggregation. Cancer Research, 46(10), 5061–5063.PubMed
150.
Zurück zum Zitat Yokoyama, I., Hayashi, S., Kobayashi, T., et al. (1995). Prevention of experimental hepatic metastasis with thromboxane synthase inhibitor. Research and Experimental Medicine, 195(4), 209–215.CrossRef Yokoyama, I., Hayashi, S., Kobayashi, T., et al. (1995). Prevention of experimental hepatic metastasis with thromboxane synthase inhibitor. Research and Experimental Medicine, 195(4), 209–215.CrossRef
151.
Zurück zum Zitat Vezza, R., Roberti, R., Nenci, G. G., & Gresele, P. (1993). Prostaglandin E2 potentiates platelet aggregation by priming protein kinase C. Blood, 82(9), 2704–2713.PubMed Vezza, R., Roberti, R., Nenci, G. G., & Gresele, P. (1993). Prostaglandin E2 potentiates platelet aggregation by priming protein kinase C. Blood, 82(9), 2704–2713.PubMed
152.
Zurück zum Zitat Fabre, J. E., Nguyen, M. T., Athirakul, K., et al. (2001). Activation of the murine EP3 receptor for PGE2 inhibits cAMP production and promotes platelet aggregation. Journal of Clinical Investigation, 107(5), 603–610.PubMedPubMedCentralCrossRef Fabre, J. E., Nguyen, M. T., Athirakul, K., et al. (2001). Activation of the murine EP3 receptor for PGE2 inhibits cAMP production and promotes platelet aggregation. Journal of Clinical Investigation, 107(5), 603–610.PubMedPubMedCentralCrossRef
153.
Zurück zum Zitat Gross, S., Tilly, P., Hentsch, D., et al. (2007). Vascular-wall produced prostaglandin E2 exacerbates arterial thrombosis and atherothrombosis through platelet EP3 receptors. Journal of Experimental Medicine, 204(2), 311–320.PubMedPubMedCentralCrossRef Gross, S., Tilly, P., Hentsch, D., et al. (2007). Vascular-wall produced prostaglandin E2 exacerbates arterial thrombosis and atherothrombosis through platelet EP3 receptors. Journal of Experimental Medicine, 204(2), 311–320.PubMedPubMedCentralCrossRef
154.
Zurück zum Zitat Gresele, P., Blockmans, D., Deckmyn, H., & Vermylen, J. (1988). Adenylate cyclase activation determines the effect of thromboxane synthase inhibitors on platelet aggregation in vitro. Comparison of platelets from responders and nonresponders. Journal of Pharmacological and Experimental Therapeutics, 246(1), 301–307. Gresele, P., Blockmans, D., Deckmyn, H., & Vermylen, J. (1988). Adenylate cyclase activation determines the effect of thromboxane synthase inhibitors on platelet aggregation in vitro. Comparison of platelets from responders and nonresponders. Journal of Pharmacological and Experimental Therapeutics, 246(1), 301–307.
155.
Zurück zum Zitat Singh, J., Zeller, W., Zhou, N., et al. (2009). Antagonists of the EP3 receptor for prostaglandin E2 are novel antiplatelet agents that do not prolong bleeding. ACS Chemical Biology, 4(2), 115–126.PubMedCrossRef Singh, J., Zeller, W., Zhou, N., et al. (2009). Antagonists of the EP3 receptor for prostaglandin E2 are novel antiplatelet agents that do not prolong bleeding. ACS Chemical Biology, 4(2), 115–126.PubMedCrossRef
156.
Zurück zum Zitat Fox, S. C., May, J. A., Johnson, A., et al. (2013). Effects on platelet function of an EP3 receptor antagonist used alone and in combination with a P2Y12 antagonist both in vitro and ex vivo in human volunteers. Platelets, 24(5), 392–400.PubMedCrossRef Fox, S. C., May, J. A., Johnson, A., et al. (2013). Effects on platelet function of an EP3 receptor antagonist used alone and in combination with a P2Y12 antagonist both in vitro and ex vivo in human volunteers. Platelets, 24(5), 392–400.PubMedCrossRef
157.
Zurück zum Zitat Honn, K. V., Cicone, B., & Skoff, A. (1981). Prostacyclin: a potent antimetastatic agent. Science, 212(4500), 1270–1272.PubMedCrossRef Honn, K. V., Cicone, B., & Skoff, A. (1981). Prostacyclin: a potent antimetastatic agent. Science, 212(4500), 1270–1272.PubMedCrossRef
158.
Zurück zum Zitat Dogne, J. M., Hanson, J., & Pratico, D. (2005). Thromboxane, prostacyclin and isoprostanes: therapeutic targets in atherogenesis. Trends in Pharmacological Science, 26(12), 639–644.CrossRef Dogne, J. M., Hanson, J., & Pratico, D. (2005). Thromboxane, prostacyclin and isoprostanes: therapeutic targets in atherogenesis. Trends in Pharmacological Science, 26(12), 639–644.CrossRef
159.
Zurück zum Zitat Fetalvero, K. M., Martin, K. A., & Hwa, J. (2007). Cardioprotective prostacyclin signaling in vascular smooth muscle. Prostaglandins and Other Lipid Mediators, 82(1–4), 109–118.PubMedCrossRef Fetalvero, K. M., Martin, K. A., & Hwa, J. (2007). Cardioprotective prostacyclin signaling in vascular smooth muscle. Prostaglandins and Other Lipid Mediators, 82(1–4), 109–118.PubMedCrossRef
160.
Zurück zum Zitat Keith, R. L., & Geraci, M. W. (2006). Prostacyclin in lung cancer. J Thoracic Oncology, 1(6), 503–505.CrossRef Keith, R. L., & Geraci, M. W. (2006). Prostacyclin in lung cancer. J Thoracic Oncology, 1(6), 503–505.CrossRef
161.
Zurück zum Zitat Grommes, C., Landreth, G. E., & Heneka, M. T. (2004). Antineoplastic effects of peroxisome proliferator-activated receptor gamma agonists. Lancet Oncology, 5(7), 419–429.PubMedCrossRef Grommes, C., Landreth, G. E., & Heneka, M. T. (2004). Antineoplastic effects of peroxisome proliferator-activated receptor gamma agonists. Lancet Oncology, 5(7), 419–429.PubMedCrossRef
162.
Zurück zum Zitat Nemenoff, R. A., Meyer, A. M., Hudish, T. M., et al. (2008). Prostacyclin prevents murine lung cancer independent of the membrane receptor by activation of peroxisomal proliferator-activated receptor gamma. Cancer Prevention Research, 1(5), 349–356.PubMedPubMedCentralCrossRef Nemenoff, R. A., Meyer, A. M., Hudish, T. M., et al. (2008). Prostacyclin prevents murine lung cancer independent of the membrane receptor by activation of peroxisomal proliferator-activated receptor gamma. Cancer Prevention Research, 1(5), 349–356.PubMedPubMedCentralCrossRef
163.
Zurück zum Zitat He, P., Borland, M. G., Zhu, B., et al. (2008). Effect of ligand activation of peroxisome proliferator-activated receptor-beta/delta (PPARbeta/delta) in human lung cancer cell lines. Toxicology, 254(1–2), 112–117 26.PubMedPubMedCentralCrossRef He, P., Borland, M. G., Zhu, B., et al. (2008). Effect of ligand activation of peroxisome proliferator-activated receptor-beta/delta (PPARbeta/delta) in human lung cancer cell lines. Toxicology, 254(1–2), 112–117 26.PubMedPubMedCentralCrossRef
164.
Zurück zum Zitat Pedchenko, T. V., Gonzalez, A. L., Wang, D., DuBois, R. N., & Massion, P. P. (2008). Peroxisome proliferator-activated receptor beta/delta expression and activation in lung cancer. American Journal of Respiratory Cell and Molecular Biology, 39(6), 689–696.PubMedPubMedCentralCrossRef Pedchenko, T. V., Gonzalez, A. L., Wang, D., DuBois, R. N., & Massion, P. P. (2008). Peroxisome proliferator-activated receptor beta/delta expression and activation in lung cancer. American Journal of Respiratory Cell and Molecular Biology, 39(6), 689–696.PubMedPubMedCentralCrossRef
165.
Zurück zum Zitat Menter, D. G., Onoda, J. M., Taylor, J. D., & Honn, K. V. (1984). Effects of prostacyclin on tumor cell-induced platelet aggregation. Cancer Research, 44(2), 450–456.PubMed Menter, D. G., Onoda, J. M., Taylor, J. D., & Honn, K. V. (1984). Effects of prostacyclin on tumor cell-induced platelet aggregation. Cancer Research, 44(2), 450–456.PubMed
166.
Zurück zum Zitat Menter, D. G., Onoda, J. M., Moilanen, D., Sloane, B. F., Taylor, J. D., & Honn, K. V. (1987). Inhibition by prostacyclin of the tumor cell-induced platelet release reaction and platelet aggregation. Journal of the National Cancer Institute, 78(5), 961–969.PubMed Menter, D. G., Onoda, J. M., Moilanen, D., Sloane, B. F., Taylor, J. D., & Honn, K. V. (1987). Inhibition by prostacyclin of the tumor cell-induced platelet release reaction and platelet aggregation. Journal of the National Cancer Institute, 78(5), 961–969.PubMed
167.
Zurück zum Zitat Honn, V. H., Cicone, B., & Skoff, A. (1980). Prostacyclin: a potent antimetastatic agent. Science, 212(4500), 1270–1272.CrossRef Honn, V. H., Cicone, B., & Skoff, A. (1980). Prostacyclin: a potent antimetastatic agent. Science, 212(4500), 1270–1272.CrossRef
168.
Zurück zum Zitat Cuneo, K. C., Fu, A., Osusky, K. L., & Geng, L. (2007). Effects of vascular endothelial growth factor receptor inhibitor SU5416 and prostacyclin on murine lung metastasis. Anti-Cancer Drugs, 18(3), 349–355.PubMedCrossRef Cuneo, K. C., Fu, A., Osusky, K. L., & Geng, L. (2007). Effects of vascular endothelial growth factor receptor inhibitor SU5416 and prostacyclin on murine lung metastasis. Anti-Cancer Drugs, 18(3), 349–355.PubMedCrossRef
169.
Zurück zum Zitat Keith, R. L., Miller, Y. E., Hoshikawa, Y., et al. (2002). Manipulation of pulmonary prostacyclin synthase expression prevents murine lung cancer. Cancer Research, 62(3), 734–740.PubMed Keith, R. L., Miller, Y. E., Hoshikawa, Y., et al. (2002). Manipulation of pulmonary prostacyclin synthase expression prevents murine lung cancer. Cancer Research, 62(3), 734–740.PubMed
170.
Zurück zum Zitat Keith, R. L., Miller, Y. E., Hudish, T. M., et al. (2004). Pulmonary prostacyclin synthase overexpression chemoprevents tobacco smoke lung carcinogenesis in mice. Cancer Research, 64(16), 5897–5904.PubMedCrossRef Keith, R. L., Miller, Y. E., Hudish, T. M., et al. (2004). Pulmonary prostacyclin synthase overexpression chemoprevents tobacco smoke lung carcinogenesis in mice. Cancer Research, 64(16), 5897–5904.PubMedCrossRef
171.
Zurück zum Zitat Honn, K. V., Meyer, J., Neagos, G., Henderson, T., Westley, C., & Ratanatharathorn, V. (1982). Control of tumor growth and metastasis with prostacyclin and thromboxane synthetase inhibitors: evidence for a new antitumor and antimetastatic agent (BAY G 6575). In G. A. Jamieson (Ed.), Interaction of platelets and tumor cells (pp. 295–331). New York: Alan R. Uss. Honn, K. V., Meyer, J., Neagos, G., Henderson, T., Westley, C., & Ratanatharathorn, V. (1982). Control of tumor growth and metastasis with prostacyclin and thromboxane synthetase inhibitors: evidence for a new antitumor and antimetastatic agent (BAY G 6575). In G. A. Jamieson (Ed.), Interaction of platelets and tumor cells (pp. 295–331). New York: Alan R. Uss.
172.
Zurück zum Zitat Bren-Mattison, Y., Van Putten, V., Chan, D., Winn, R., Geraci, M. W., & Nemenoff, R. A. (2005). Peroxisome proliferator-activated receptor-gamma (PPAR(gamma)) inhibits tumorigenesis by reversing the undifferentiated phenotype of metastatic non-small-cell lung cancer cells (NSCLC). Oncogene, 24, 1412–1422.PubMedCrossRef Bren-Mattison, Y., Van Putten, V., Chan, D., Winn, R., Geraci, M. W., & Nemenoff, R. A. (2005). Peroxisome proliferator-activated receptor-gamma (PPAR(gamma)) inhibits tumorigenesis by reversing the undifferentiated phenotype of metastatic non-small-cell lung cancer cells (NSCLC). Oncogene, 24, 1412–1422.PubMedCrossRef
173.
Zurück zum Zitat Keith, R. L., Blatchford, P. J., Kittelson, J., et al. (2011). Oral iloprost improves endobronchial dysplasia in former smokers. Cancer Prevention Research, 4(6), 793–802.PubMedPubMedCentralCrossRef Keith, R. L., Blatchford, P. J., Kittelson, J., et al. (2011). Oral iloprost improves endobronchial dysplasia in former smokers. Cancer Prevention Research, 4(6), 793–802.PubMedPubMedCentralCrossRef
174.
Zurück zum Zitat Mascaux, C., Feser, W. J., Lewis, M. T., et al. (2013). Endobronchial miRNAs as biomarkers in lung cancer chemoprevention. Cancer Prevention Research, 6(2), 100–108.PubMedCrossRef Mascaux, C., Feser, W. J., Lewis, M. T., et al. (2013). Endobronchial miRNAs as biomarkers in lung cancer chemoprevention. Cancer Prevention Research, 6(2), 100–108.PubMedCrossRef
175.
Zurück zum Zitat Gibbins, J. M., Okuma, M., Farndale, R., Barnes, M., & Watson, S. P. (1997). Glycoprotein VI is the collagen receptor in platelets which underlies tyrosine phosphorylation of the Fc receptor gamma-chain. FEBS Letters, 413, 255–259.PubMedCrossRef Gibbins, J. M., Okuma, M., Farndale, R., Barnes, M., & Watson, S. P. (1997). Glycoprotein VI is the collagen receptor in platelets which underlies tyrosine phosphorylation of the Fc receptor gamma-chain. FEBS Letters, 413, 255–259.PubMedCrossRef
176.
Zurück zum Zitat Nieswandt, B., Bergmeier, W., Schulte, V., Rackebrandt, K., Gessner, J. E., & Zirngibl, H. (2000). Expression and function of the mouse collagen receptor glycoprotein VI is strictly dependent on its association with the FcRgamma chain. Journal of Biological Chemistry, 275(31), 23998–24002.PubMedCrossRef Nieswandt, B., Bergmeier, W., Schulte, V., Rackebrandt, K., Gessner, J. E., & Zirngibl, H. (2000). Expression and function of the mouse collagen receptor glycoprotein VI is strictly dependent on its association with the FcRgamma chain. Journal of Biological Chemistry, 275(31), 23998–24002.PubMedCrossRef
177.
Zurück zum Zitat Nieswandt, B., Schulte, V., Bergmeier, W., et al. (2001). Long-term antithrombotic protection by in vivo depletion of platelet glycoprotein VI in mice. Journal of Experimental Medicine, 193(4), 459–469.PubMedPubMedCentralCrossRef Nieswandt, B., Schulte, V., Bergmeier, W., et al. (2001). Long-term antithrombotic protection by in vivo depletion of platelet glycoprotein VI in mice. Journal of Experimental Medicine, 193(4), 459–469.PubMedPubMedCentralCrossRef
178.
Zurück zum Zitat Nieswandt, B., Brakebusch, C., Bergmeier, W., et al. (2001). Glycoprotein VI but not alpha2beta1 integrin is essential for platelet interaction with collagen. EMBO Journal, 20(9), 2120–2130.PubMedPubMedCentralCrossRef Nieswandt, B., Brakebusch, C., Bergmeier, W., et al. (2001). Glycoprotein VI but not alpha2beta1 integrin is essential for platelet interaction with collagen. EMBO Journal, 20(9), 2120–2130.PubMedPubMedCentralCrossRef
179.
Zurück zum Zitat Clemetson, J. M., Polgar, J., Magnenat, E., Wells, T. N., & Clemetson, K. J. (1999). The platelet collagen receptor glycoprotein VI is a member of the immunoglobulin superfamily closely related to FcalphaR and the natural killer receptors. Journal of Biological Chemistry, 274(8), 29019–29024.PubMedCrossRef Clemetson, J. M., Polgar, J., Magnenat, E., Wells, T. N., & Clemetson, K. J. (1999). The platelet collagen receptor glycoprotein VI is a member of the immunoglobulin superfamily closely related to FcalphaR and the natural killer receptors. Journal of Biological Chemistry, 274(8), 29019–29024.PubMedCrossRef
180.
Zurück zum Zitat Jandrot-Perrus, M., Busfield, S., Lagrue, A. H., et al. (2000). Cloning, characterization, and functional studies of human and mouse glycoprotein VI: a platelet-specific collagen receptor from the immunoglobulin superfamily. Blood, 96(5), 1798–1807.PubMed Jandrot-Perrus, M., Busfield, S., Lagrue, A. H., et al. (2000). Cloning, characterization, and functional studies of human and mouse glycoprotein VI: a platelet-specific collagen receptor from the immunoglobulin superfamily. Blood, 96(5), 1798–1807.PubMed
181.
Zurück zum Zitat Moroi, M., Jung, S. M., Okuma, M., & Shinmyozu, K. (1989). A patient with platelets deficient in glycoprotein VI that lack both collagen-induced aggregation and adhesion. Journal of Clinical Investigation, 84(5), 1440–1445.PubMedPubMedCentralCrossRef Moroi, M., Jung, S. M., Okuma, M., & Shinmyozu, K. (1989). A patient with platelets deficient in glycoprotein VI that lack both collagen-induced aggregation and adhesion. Journal of Clinical Investigation, 84(5), 1440–1445.PubMedPubMedCentralCrossRef
182.
Zurück zum Zitat Watson, S. P., Asazuma, N., Atkinson, B., et al. (2001). The role of ITAM- and ITIM-coupled receptors in platelet activation by collagen. Thrombosis and Haemostasis, 86, 276–288.PubMed Watson, S. P., Asazuma, N., Atkinson, B., et al. (2001). The role of ITAM- and ITIM-coupled receptors in platelet activation by collagen. Thrombosis and Haemostasis, 86, 276–288.PubMed
183.
Zurück zum Zitat Jain, S., Russell, S., & Ware, J. (2009). Platelet glycoprotein VI facilitates experimental lung metastasis in syngenic mouse models. Journal of Thrombosis and Haemostasis, 7(10), 1713–1717.PubMedCrossRef Jain, S., Russell, S., & Ware, J. (2009). Platelet glycoprotein VI facilitates experimental lung metastasis in syngenic mouse models. Journal of Thrombosis and Haemostasis, 7(10), 1713–1717.PubMedCrossRef
184.
Zurück zum Zitat Ungerer, M., Rosport, K., Bultmann, A., et al. (2011). Novel antiplatelet drug revacept (dimeric glycoprotein VI-Fc) specifically and efficiently inhibited collagen-induced platelet aggregation without affecting general hemostasis in humans. Circulation, 123(17), 891–1899.CrossRef Ungerer, M., Rosport, K., Bultmann, A., et al. (2011). Novel antiplatelet drug revacept (dimeric glycoprotein VI-Fc) specifically and efficiently inhibited collagen-induced platelet aggregation without affecting general hemostasis in humans. Circulation, 123(17), 891–1899.CrossRef
185.
Zurück zum Zitat Dovizio, M., Maier, T. J., Alberti, S., et al. (2013). Pharmacological inhibition of platelet–tumor cell cross-talk prevents platelet-induced overexpression of cyclooxygenase-2 in HT29 human colon carcinoma cells. Molecular Pharmacology, 84(1), 25–40.PubMedCrossRef Dovizio, M., Maier, T. J., Alberti, S., et al. (2013). Pharmacological inhibition of platelet–tumor cell cross-talk prevents platelet-induced overexpression of cyclooxygenase-2 in HT29 human colon carcinoma cells. Molecular Pharmacology, 84(1), 25–40.PubMedCrossRef
186.
Zurück zum Zitat Nangia-Makker, P., Balan, V., & Raz, A. (2008). Regulation of tumor progression by extracellular galectin-3. Cancer Microenvironment, 1(1), 43–51.PubMedPubMedCentralCrossRef Nangia-Makker, P., Balan, V., & Raz, A. (2008). Regulation of tumor progression by extracellular galectin-3. Cancer Microenvironment, 1(1), 43–51.PubMedPubMedCentralCrossRef
187.
Zurück zum Zitat Coughlin, S. R. (2000). Thrombin signalling and protease-activated receptors. Nature, 407(6801), 258–264.PubMedCrossRef Coughlin, S. R. (2000). Thrombin signalling and protease-activated receptors. Nature, 407(6801), 258–264.PubMedCrossRef
188.
189.
Zurück zum Zitat Daniel, T., Gibbs, V. C., Milfay, D., et al. (1986). Thrombin stimulates c-sis gene expression in microvascular endothelial cells. Journal of Biological Chemistry, 261(21), 9579–9582.PubMed Daniel, T., Gibbs, V. C., Milfay, D., et al. (1986). Thrombin stimulates c-sis gene expression in microvascular endothelial cells. Journal of Biological Chemistry, 261(21), 9579–9582.PubMed
190.
Zurück zum Zitat DeMichele, M., & Minnear, F. (1992). Modulation of vascular endothelial permeability by thrombin. Seminars in Thrombosis and Hemostasis, 18(3), 287–295.PubMedCrossRef DeMichele, M., & Minnear, F. (1992). Modulation of vascular endothelial permeability by thrombin. Seminars in Thrombosis and Hemostasis, 18(3), 287–295.PubMedCrossRef
191.
Zurück zum Zitat Wojtukiewicz, M. Z., Tang, D. G., Ciarelli, J. J., et al. (1993). Thrombin increases the metastatic potential of tumor cells. International Journal of Cancer, 54(5), 793–806.PubMedCrossRef Wojtukiewicz, M. Z., Tang, D. G., Ciarelli, J. J., et al. (1993). Thrombin increases the metastatic potential of tumor cells. International Journal of Cancer, 54(5), 793–806.PubMedCrossRef
192.
Zurück zum Zitat Nierodzik, M., Kajumo, F., & Karpatkin, S. (1992). Effect of thrombin treatment of tumor cells on adhesion of tumor cells to platelets in vitro and metastasis in vivo. Cancer Research, 52(12), 3267–3272.PubMed Nierodzik, M., Kajumo, F., & Karpatkin, S. (1992). Effect of thrombin treatment of tumor cells on adhesion of tumor cells to platelets in vitro and metastasis in vivo. Cancer Research, 52(12), 3267–3272.PubMed
193.
Zurück zum Zitat Chen, L. B., & Buchanan, J. M. (1975). Mitogenic activity of blood components. I. Thrombin and prothrombin. Proceedings of the National Academy of Science U S A, 72(1), 131–135.CrossRef Chen, L. B., & Buchanan, J. M. (1975). Mitogenic activity of blood components. I. Thrombin and prothrombin. Proceedings of the National Academy of Science U S A, 72(1), 131–135.CrossRef
194.
Zurück zum Zitat Szaba, F. M., & Smiley, S. T. (2002). Roles for thrombin and fibrin(ogen) in cytokine/chemokine production and macrophage adhesion in vivo. Blood, 99, 1053–1059.PubMedPubMedCentralCrossRef Szaba, F. M., & Smiley, S. T. (2002). Roles for thrombin and fibrin(ogen) in cytokine/chemokine production and macrophage adhesion in vivo. Blood, 99, 1053–1059.PubMedPubMedCentralCrossRef
195.
Zurück zum Zitat Sugama, Y., Tiruppathi, C., Offakidevi, K., Andersen, T. T., Fenton 2nd, J. W., & Malik, A. B. (1992). Thrombin-induced expression of endothelial P-selectin and intercellular adhesion molecule-1: a mechanism for stabilizing neutrophil adhesion. Journal of Cell Biology, 119(4), 935–944.PubMedCrossRef Sugama, Y., Tiruppathi, C., Offakidevi, K., Andersen, T. T., Fenton 2nd, J. W., & Malik, A. B. (1992). Thrombin-induced expression of endothelial P-selectin and intercellular adhesion molecule-1: a mechanism for stabilizing neutrophil adhesion. Journal of Cell Biology, 119(4), 935–944.PubMedCrossRef
196.
Zurück zum Zitat Chiang, H. S., Yang, R. S., & Huang, T. F. (1996). Thrombin enhances the adhesion and migration of human colon adenocarcinoma cells via increased beta 3-integrin expression on the tumour cell surface and their inhibition by the snake venom peptide, rhodostomin. British Journal of Cancer, 73(7), 902–908.PubMedPubMedCentralCrossRef Chiang, H. S., Yang, R. S., & Huang, T. F. (1996). Thrombin enhances the adhesion and migration of human colon adenocarcinoma cells via increased beta 3-integrin expression on the tumour cell surface and their inhibition by the snake venom peptide, rhodostomin. British Journal of Cancer, 73(7), 902–908.PubMedPubMedCentralCrossRef
197.
Zurück zum Zitat Radjabi, A. R., Sawada, K., Jagadeeswaran, S., et al. (2008). Thrombin induces tumor invasion through the induction and association of matrix metalloproteinase-9 and beta1-integrin on the cell surface. Journal of Biological Chemistry, 283(5), 2822–2834.PubMedCrossRef Radjabi, A. R., Sawada, K., Jagadeeswaran, S., et al. (2008). Thrombin induces tumor invasion through the induction and association of matrix metalloproteinase-9 and beta1-integrin on the cell surface. Journal of Biological Chemistry, 283(5), 2822–2834.PubMedCrossRef
198.
Zurück zum Zitat Nierodzik, M. L., & Karpatkin, S. (2006). Thrombin induces tumor growth, metastasis, and angiogenesis: evidence for a thrombin-regulated dormant tumor phenotype. Cancer Cell, 110(5), 355–362.CrossRef Nierodzik, M. L., & Karpatkin, S. (2006). Thrombin induces tumor growth, metastasis, and angiogenesis: evidence for a thrombin-regulated dormant tumor phenotype. Cancer Cell, 110(5), 355–362.CrossRef
199.
Zurück zum Zitat Coughlin, S. R. (2005). Protease-activated receptors in hemostasis, thrombosis and vascular biology. Journal of Thrombosis and Haemostasis, 3(8), 1800–1814.PubMedCrossRef Coughlin, S. R. (2005). Protease-activated receptors in hemostasis, thrombosis and vascular biology. Journal of Thrombosis and Haemostasis, 3(8), 1800–1814.PubMedCrossRef
200.
Zurück zum Zitat Huang, Z., Miao, X., Luan, Y., et al. (2015). PAR1-stimulated platelet releasate promotes angiogenic activities of endothelial progenitor cells more potently than PAR4-stimulated platelet releasate. Thrombosis and Haemostasis, 13(3), 465–476.CrossRef Huang, Z., Miao, X., Luan, Y., et al. (2015). PAR1-stimulated platelet releasate promotes angiogenic activities of endothelial progenitor cells more potently than PAR4-stimulated platelet releasate. Thrombosis and Haemostasis, 13(3), 465–476.CrossRef
201.
Zurück zum Zitat Sedda, S., Marafini, I., Caruso, R., Pallone, F., & Monteleone, G. (2014). Proteinase activated-receptors-associated signaling in the control of gastric cancer. World Journal of Gastroenterology, 20(34), 11977–11984.PubMedPubMedCentralCrossRef Sedda, S., Marafini, I., Caruso, R., Pallone, F., & Monteleone, G. (2014). Proteinase activated-receptors-associated signaling in the control of gastric cancer. World Journal of Gastroenterology, 20(34), 11977–11984.PubMedPubMedCentralCrossRef
202.
Zurück zum Zitat Albrektsen, T., Sorensen, B. B., Hjorto, G. M., Fleckner, J., Rao, L. V., & Petersen, L. C. (2007). Transcriptional program induced by factor VIIa tissue factor, PAR1 and PAR2 in MDA-MB-231 cells. Journal of Thrombosis and Haemostasis, 5(8), 1588–1597.PubMedPubMedCentralCrossRef Albrektsen, T., Sorensen, B. B., Hjorto, G. M., Fleckner, J., Rao, L. V., & Petersen, L. C. (2007). Transcriptional program induced by factor VIIa tissue factor, PAR1 and PAR2 in MDA-MB-231 cells. Journal of Thrombosis and Haemostasis, 5(8), 1588–1597.PubMedPubMedCentralCrossRef
203.
Zurück zum Zitat Zhou, W., Hashimoto, K., Goleniewska, K., et al. (2007). Prostaglandin I2 analogs inhibit proinflammatory cytokine production and T cell stimulatory function of dendritic cells. Journal of Immunology, 178(2), 702–710.CrossRef Zhou, W., Hashimoto, K., Goleniewska, K., et al. (2007). Prostaglandin I2 analogs inhibit proinflammatory cytokine production and T cell stimulatory function of dendritic cells. Journal of Immunology, 178(2), 702–710.CrossRef
204.
Zurück zum Zitat Otsuki, T., Fujimoto, D., Hirono, Y., Goi, T., & Yamaguchi, A. (2014). Thrombin conducts epithelial mesenchymal transition via protease activated receptor 1 in human gastric cancer. International Journal of Oncology, 45(6), 2287–2294.PubMed Otsuki, T., Fujimoto, D., Hirono, Y., Goi, T., & Yamaguchi, A. (2014). Thrombin conducts epithelial mesenchymal transition via protease activated receptor 1 in human gastric cancer. International Journal of Oncology, 45(6), 2287–2294.PubMed
205.
Zurück zum Zitat Fujimoto, D., Hirono, Y., Goi, T., Katayama, K., Matsukawa, S., & Yamaguchi, A. (2010). The activation of proteinase-activated receptor-1 (PAR1) mediates gastric cancer cell proliferation and invasion. Biomedical Central Cancer, 10, 443–458. Fujimoto, D., Hirono, Y., Goi, T., Katayama, K., Matsukawa, S., & Yamaguchi, A. (2010). The activation of proteinase-activated receptor-1 (PAR1) mediates gastric cancer cell proliferation and invasion. Biomedical Central Cancer, 10, 443–458.
206.
Zurück zum Zitat Uzunoglu, F. G., Yavari, N., Bohn, B. A., et al. (2013). C-X-C motif receptor 2, endostatin and proteinase-activated receptor 1 polymorphisms as prognostic factors in NSCLC. Lung Cancer, 81(1), 123–129.PubMedCrossRef Uzunoglu, F. G., Yavari, N., Bohn, B. A., et al. (2013). C-X-C motif receptor 2, endostatin and proteinase-activated receptor 1 polymorphisms as prognostic factors in NSCLC. Lung Cancer, 81(1), 123–129.PubMedCrossRef
207.
Zurück zum Zitat Kaufmann, R., Junker, U., Junker, K., et al. (2002). The serine proteinase thrombin promotes migration of human renal carcinoma cells by a PKA-dependent mechanism. Cancer Letters, 180(2), 183–190.PubMedCrossRef Kaufmann, R., Junker, U., Junker, K., et al. (2002). The serine proteinase thrombin promotes migration of human renal carcinoma cells by a PKA-dependent mechanism. Cancer Letters, 180(2), 183–190.PubMedCrossRef
208.
Zurück zum Zitat Tsopanoglou, N. E., & Maragoudakis, M. E. (2004). Role of thrombin in angiogenesis and tumor progression. Seminars in Thrombosis and Hemostasis, 30(1), 63–69.PubMedCrossRef Tsopanoglou, N. E., & Maragoudakis, M. E. (2004). Role of thrombin in angiogenesis and tumor progression. Seminars in Thrombosis and Hemostasis, 30(1), 63–69.PubMedCrossRef
209.
Zurück zum Zitat Wojtukiewicz, M. Z., Tang, D. G., Nelson, K. K., Walz, D. A., Diglio, C. A., & Honn, K. V. (1992). Thrombin enhances tumor cell adhesive and metastatic properties via increased alpha IIb beta 3 expression on the cell surface. Thrombosis Research, 68(3), 233–245.PubMedCrossRef Wojtukiewicz, M. Z., Tang, D. G., Nelson, K. K., Walz, D. A., Diglio, C. A., & Honn, K. V. (1992). Thrombin enhances tumor cell adhesive and metastatic properties via increased alpha IIb beta 3 expression on the cell surface. Thrombosis Research, 68(3), 233–245.PubMedCrossRef
210.
Zurück zum Zitat Zhu, Q., Luo, J., Wang, T., Ren, J., Hu, K., & Wu, G. (2012). The activation of protease-activated receptor 1 mediates proliferation and invasion of nasopharyngeal carcinoma cells. Oncology Reports, 28(1), 255–261.PubMed Zhu, Q., Luo, J., Wang, T., Ren, J., Hu, K., & Wu, G. (2012). The activation of protease-activated receptor 1 mediates proliferation and invasion of nasopharyngeal carcinoma cells. Oncology Reports, 28(1), 255–261.PubMed
211.
Zurück zum Zitat Even-Ram, S. C., Maoz, M., et al. (2001). Tumor cell invasion is promoted by activation of protease activated receptor-1 in cooperation with the alpha vbeta 5 integrin. Journal of Biological Chemistry, 276(14), 10952–10962.PubMedCrossRef Even-Ram, S. C., Maoz, M., et al. (2001). Tumor cell invasion is promoted by activation of protease activated receptor-1 in cooperation with the alpha vbeta 5 integrin. Journal of Biological Chemistry, 276(14), 10952–10962.PubMedCrossRef
212.
Zurück zum Zitat Bai, S. Y., Xu, N., Chen, C., Song, Y. L., Hu, J., & Bai, C. X. (2015). Integrin αvβ5 as a biomarker for the assessment of nonsmall cell lung cancer metastasis and overall survival. Clinical Respiratory Journal, 9(4), 457–467.PubMedCrossRef Bai, S. Y., Xu, N., Chen, C., Song, Y. L., Hu, J., & Bai, C. X. (2015). Integrin αvβ5 as a biomarker for the assessment of nonsmall cell lung cancer metastasis and overall survival. Clinical Respiratory Journal, 9(4), 457–467.PubMedCrossRef
213.
Zurück zum Zitat Fujimoto, D., Hirono, Y., Goi, T., Katayama, K., & Yamaguchi, A. (2008). Prognostic value of protease-activated receptor-1 (PAR-1) and matrix metalloproteinase-1 (MMP-1) in gastric cancer. Anticancer Research, 28(2A), 847–854.PubMed Fujimoto, D., Hirono, Y., Goi, T., Katayama, K., & Yamaguchi, A. (2008). Prognostic value of protease-activated receptor-1 (PAR-1) and matrix metalloproteinase-1 (MMP-1) in gastric cancer. Anticancer Research, 28(2A), 847–854.PubMed
214.
Zurück zum Zitat Boire, A., Covic, L., Agarwal, A., Jacques, S., Sherifi, S., & Kuliopulos, A. (2005). PAR1 is a matrix metalloprotease-1 receptor that promotes invasion and tumorigenesis of breast cancer cells. Cell, 120(3), 303–313.PubMedCrossRef Boire, A., Covic, L., Agarwal, A., Jacques, S., Sherifi, S., & Kuliopulos, A. (2005). PAR1 is a matrix metalloprotease-1 receptor that promotes invasion and tumorigenesis of breast cancer cells. Cell, 120(3), 303–313.PubMedCrossRef
215.
Zurück zum Zitat Nierodzik, M., Plotkin, A., Kajumo, F., & Karpatkin, S. (1991). Thrombin stimulates tumor-platelet adhesion in vitro and metastasis in vivo. Journal of Clinical Investigation, 87(1), 229–236.PubMedPubMedCentralCrossRef Nierodzik, M., Plotkin, A., Kajumo, F., & Karpatkin, S. (1991). Thrombin stimulates tumor-platelet adhesion in vitro and metastasis in vivo. Journal of Clinical Investigation, 87(1), 229–236.PubMedPubMedCentralCrossRef
216.
Zurück zum Zitat Wojtukiewicz, M. Z., Tang, D. G., Ben-Josef, E., Renaud, C., Walz, D. A., & Honn, K. V. (1995). Solid tumor cells express functional “tethered ligand” thrombin receptor. Cancer Research, 55(3), 698–704.PubMed Wojtukiewicz, M. Z., Tang, D. G., Ben-Josef, E., Renaud, C., Walz, D. A., & Honn, K. V. (1995). Solid tumor cells express functional “tethered ligand” thrombin receptor. Cancer Research, 55(3), 698–704.PubMed
217.
Zurück zum Zitat Nierodzik, M. L., Klepfish, A., & Karpatkin, S. (1995). Role of platelets, thrombin, integrin IIb-IIIa, fibronectin and von Willebrand factor on tumor adhesion in vitro and metastasis in vivo. Thrombosis and Haemostasis, 74(1), 282–290.PubMed Nierodzik, M. L., Klepfish, A., & Karpatkin, S. (1995). Role of platelets, thrombin, integrin IIb-IIIa, fibronectin and von Willebrand factor on tumor adhesion in vitro and metastasis in vivo. Thrombosis and Haemostasis, 74(1), 282–290.PubMed
218.
Zurück zum Zitat Huang, Y. Q., Li, J.-J., Hu, L., & Karpatkin, S. (2002). Thrombin induces the synthesis of VEGF and angiopoietin-2 (Ang-2). Blood, 99(5), 1646–1650.PubMedCrossRef Huang, Y. Q., Li, J.-J., Hu, L., & Karpatkin, S. (2002). Thrombin induces the synthesis of VEGF and angiopoietin-2 (Ang-2). Blood, 99(5), 1646–1650.PubMedCrossRef
219.
Zurück zum Zitat Mohle, R., Green, D., Moore, M., Nachman, R., & Rafii, S. (1997). Constitutive production and thrombin-induced release of VEGF by human megakaryocytes and platelets. Proceeding of the National Academy of Sciences USA, 94(2), 663–668.CrossRef Mohle, R., Green, D., Moore, M., Nachman, R., & Rafii, S. (1997). Constitutive production and thrombin-induced release of VEGF by human megakaryocytes and platelets. Proceeding of the National Academy of Sciences USA, 94(2), 663–668.CrossRef
220.
Zurück zum Zitat Li, J.-J., Huang, Y.-Q., Basch, R., & Karpatkin, S. (2001). Thrombin induces the release of angiopoietin-1 from platelets. Thrombosis and Haemostasis, 85(2), 204–206.PubMed Li, J.-J., Huang, Y.-Q., Basch, R., & Karpatkin, S. (2001). Thrombin induces the release of angiopoietin-1 from platelets. Thrombosis and Haemostasis, 85(2), 204–206.PubMed
221.
Zurück zum Zitat Belting, M., Dorrell, M. I., Sandgren, S., et al. (2004). Regulation of angiogenesis by tissue factor cytoplasmic domain signaling. Nature Medicine, 10(5), 502–509.PubMedCrossRef Belting, M., Dorrell, M. I., Sandgren, S., et al. (2004). Regulation of angiogenesis by tissue factor cytoplasmic domain signaling. Nature Medicine, 10(5), 502–509.PubMedCrossRef
222.
Zurück zum Zitat Trivedi, V., Boire, A., Tchernychev, B., et al. (2009). Platelet matrix metalloprotease-1 mediates thrombogenesis by activating PAR1 at a cryptic ligand site. Cell, 137(2), 332–343.PubMedPubMedCentralCrossRef Trivedi, V., Boire, A., Tchernychev, B., et al. (2009). Platelet matrix metalloprotease-1 mediates thrombogenesis by activating PAR1 at a cryptic ligand site. Cell, 137(2), 332–343.PubMedPubMedCentralCrossRef
223.
Zurück zum Zitat Sebastiano, M., Momi, S., Falcinelli, E., Bury, L., Hoylaerts, M. F., & Gresele, P. (2017). A novel mechanism regulating human platelet activation by MMP-2-mediated PAR1 biased signaling. Blood, 129(7), 883–895.PubMedCrossRef Sebastiano, M., Momi, S., Falcinelli, E., Bury, L., Hoylaerts, M. F., & Gresele, P. (2017). A novel mechanism regulating human platelet activation by MMP-2-mediated PAR1 biased signaling. Blood, 129(7), 883–895.PubMedCrossRef
224.
Zurück zum Zitat Jurasz, P., Sawicki, G., Duszyk, M., et al. (2001). Matrix metalloproteinase 2 in tumor cell-induced platelet aggregation: regulation by nitric oxide. Cancer Research, 61(1), 376–382.PubMed Jurasz, P., Sawicki, G., Duszyk, M., et al. (2001). Matrix metalloproteinase 2 in tumor cell-induced platelet aggregation: regulation by nitric oxide. Cancer Research, 61(1), 376–382.PubMed
225.
Zurück zum Zitat Martin, C., Mahon, G., Klinger, M. B., et al. (2001). The thrombin receptor, PAR-1, causes transformation by activation of Rho-mediated signaling pathways. Oncogene, 20(16), 1953–1963.PubMedCrossRef Martin, C., Mahon, G., Klinger, M. B., et al. (2001). The thrombin receptor, PAR-1, causes transformation by activation of Rho-mediated signaling pathways. Oncogene, 20(16), 1953–1963.PubMedCrossRef
226.
Zurück zum Zitat Nierodzik, M. L., & Karpatkin, S. (2006). Thrombin induces tumor growth, metastasis, and angiogenesis: evidence for a thrombin-regulated dormant tumor phenotype. Cancer Cell, 10(5), 355–362.PubMedCrossRef Nierodzik, M. L., & Karpatkin, S. (2006). Thrombin induces tumor growth, metastasis, and angiogenesis: evidence for a thrombin-regulated dormant tumor phenotype. Cancer Cell, 10(5), 355–362.PubMedCrossRef
227.
Zurück zum Zitat Even-Ram, S., Uziely, B., Cohen, P., et al. (1998). Thrombin receptor overexpression in malignant and physiological invasion processes. Nature Medicine, 4(8), 909–914.PubMedCrossRef Even-Ram, S., Uziely, B., Cohen, P., et al. (1998). Thrombin receptor overexpression in malignant and physiological invasion processes. Nature Medicine, 4(8), 909–914.PubMedCrossRef
228.
Zurück zum Zitat Bar-Shavit, R., Turm, H., Salah, Z., Maoz, M., Cohen, I., Weiss, E., et al. (2011). PAR1 plays a role in epithelial malignancies: transcriptional regulation and novel signaling pathway. International Union of Biochemistry and Molecular Biology Life, 63(6), 397–402.PubMedCrossRef Bar-Shavit, R., Turm, H., Salah, Z., Maoz, M., Cohen, I., Weiss, E., et al. (2011). PAR1 plays a role in epithelial malignancies: transcriptional regulation and novel signaling pathway. International Union of Biochemistry and Molecular Biology Life, 63(6), 397–402.PubMedCrossRef
229.
Zurück zum Zitat Yin, Y. J., Salah, Z., Grisaru-Granovsky, S., et al. (2003). Human protease-activated receptor-1 expression in malignant epithelia: a role in invasiveness. Ateriosclerosis Thrombosis and Vascular Biology, 23(6), 940–944.CrossRef Yin, Y. J., Salah, Z., Grisaru-Granovsky, S., et al. (2003). Human protease-activated receptor-1 expression in malignant epithelia: a role in invasiveness. Ateriosclerosis Thrombosis and Vascular Biology, 23(6), 940–944.CrossRef
230.
Zurück zum Zitat Yin, Y. J., Salah, Z., Grisaru-Granovsky, S., et al. (2003). Oncogenic transformation induces tumor angiogenesis: a role for PAR1 activation. Federation of American Societies for Experimental Biology Journal, 17(2), 163–174.PubMedCrossRef Yin, Y. J., Salah, Z., Grisaru-Granovsky, S., et al. (2003). Oncogenic transformation induces tumor angiogenesis: a role for PAR1 activation. Federation of American Societies for Experimental Biology Journal, 17(2), 163–174.PubMedCrossRef
231.
Zurück zum Zitat Zigler, M., Kamiya, T., Brantley, E. C., Villares, G. J., & Bar-Eli, M. (2011). PAR-1 and thrombin: the ties that bind the microenvironment to melanoma metastasis. Cancer Research, 71(21), 6561–6566.PubMedPubMedCentralCrossRef Zigler, M., Kamiya, T., Brantley, E. C., Villares, G. J., & Bar-Eli, M. (2011). PAR-1 and thrombin: the ties that bind the microenvironment to melanoma metastasis. Cancer Research, 71(21), 6561–6566.PubMedPubMedCentralCrossRef
232.
Zurück zum Zitat Morris, D. R., Ding, Y., Ricks, T. K., Gullapalli, A., Wolfe, B. L., & Trejo, J. (2006). Protease-activated receptor-2 is essential for factor VIIa and Xa-induced signaling, migration, and invasion of breast cancer cells. Cancer Research, 66(1), 307–314.PubMedCrossRef Morris, D. R., Ding, Y., Ricks, T. K., Gullapalli, A., Wolfe, B. L., & Trejo, J. (2006). Protease-activated receptor-2 is essential for factor VIIa and Xa-induced signaling, migration, and invasion of breast cancer cells. Cancer Research, 66(1), 307–314.PubMedCrossRef
233.
Zurück zum Zitat Tsopanoglou, N. E., & Maragoudakis, M. E. (2007). Inhibition of angiogenesis by small-molecule antagonists of protease-activated receptor-1. Seminars in Thrombosis and Hemostasis, 33(7), 680–687.PubMedCrossRef Tsopanoglou, N. E., & Maragoudakis, M. E. (2007). Inhibition of angiogenesis by small-molecule antagonists of protease-activated receptor-1. Seminars in Thrombosis and Hemostasis, 33(7), 680–687.PubMedCrossRef
234.
Zurück zum Zitat Zania, P., Kritikou, S., Flordellis, C. S., Maragoudakis, M. E., & Tsopanoglou, N. E. (2006). Blockade of angiogenesis by small molecule antagonists to protease-activated receptor-1: association with endothelial cell growth suppression and induction of apoptosis. Journal of Pharmacology and Experimental Therapy, 318(1), 246–254.CrossRef Zania, P., Kritikou, S., Flordellis, C. S., Maragoudakis, M. E., & Tsopanoglou, N. E. (2006). Blockade of angiogenesis by small molecule antagonists to protease-activated receptor-1: association with endothelial cell growth suppression and induction of apoptosis. Journal of Pharmacology and Experimental Therapy, 318(1), 246–254.CrossRef
235.
Zurück zum Zitat Gurbel, P. A., Bliden, K. P., Turner, S. E., et al. (2016). Cell-penetrating pepducin therapy targeting PAR1 in subjects with coronary artery disease. Arterioscleriosclerosis Thrombosis and Vascular Biology, 36(1), 189–197. Gurbel, P. A., Bliden, K. P., Turner, S. E., et al. (2016). Cell-penetrating pepducin therapy targeting PAR1 in subjects with coronary artery disease. Arterioscleriosclerosis Thrombosis and Vascular Biology, 36(1), 189–197.
236.
Zurück zum Zitat Yang, E., Boire, A., Agarwal, A., et al. (2009). Blockade of PAR1 signaling with cell-penetrating pepducins inhibits Akt survival pathways in breast cancer cells and suppresses tumor survival and metastasis. Cancer Research, 69(15), 6223–6231.PubMedPubMedCentralCrossRef Yang, E., Boire, A., Agarwal, A., et al. (2009). Blockade of PAR1 signaling with cell-penetrating pepducins inhibits Akt survival pathways in breast cancer cells and suppresses tumor survival and metastasis. Cancer Research, 69(15), 6223–6231.PubMedPubMedCentralCrossRef
237.
Zurück zum Zitat Cisowski, J., O'Callaghan, K., Kuliopulos, A., et al. (2011). Targeting protease-activated receptor-1 with cell-penetrating pepducins in lung cancer. American Journal of Pathology, 179(1), 513–523. Cisowski, J., O'Callaghan, K., Kuliopulos, A., et al. (2011). Targeting protease-activated receptor-1 with cell-penetrating pepducins in lung cancer. American Journal of Pathology, 179(1), 513–523.
238.
Zurück zum Zitat Agarwal, A., Covic, L., Sevigny, L. M., Kaneider, N. C., Lazarides, K., Azabdaftari, G., et al. (2008). Targeting a metalloprotease-PAR1 signaling system with cell-penetrating pepducins inhibits angiogenesis, ascites, and progression of ovarian cancer. Molecular Cancer Therapeutics, 7(9), 2746–2757.PubMedPubMedCentralCrossRef Agarwal, A., Covic, L., Sevigny, L. M., Kaneider, N. C., Lazarides, K., Azabdaftari, G., et al. (2008). Targeting a metalloprotease-PAR1 signaling system with cell-penetrating pepducins inhibits angiogenesis, ascites, and progression of ovarian cancer. Molecular Cancer Therapeutics, 7(9), 2746–2757.PubMedPubMedCentralCrossRef
239.
Zurück zum Zitat Justus, C. R., & Yang, L. V. (2015). GPR4 decreases B16F10 melanoma cell spreading and regulates focal adhesion dynamics through the G13/Rho signaling pathway. Experimental Cell Research, 334(1), 100–113.PubMedCrossRef Justus, C. R., & Yang, L. V. (2015). GPR4 decreases B16F10 melanoma cell spreading and regulates focal adhesion dynamics through the G13/Rho signaling pathway. Experimental Cell Research, 334(1), 100–113.PubMedCrossRef
240.
Zurück zum Zitat Bian, D., Mahanivong, C., Yu, J., et al. (2006). The G12/13-RhoA signaling pathway contributes to efficient lysophosphatidic acid-stimulated cell migration. Oncogene, 25(15), 2234–2244.PubMedCrossRef Bian, D., Mahanivong, C., Yu, J., et al. (2006). The G12/13-RhoA signaling pathway contributes to efficient lysophosphatidic acid-stimulated cell migration. Oncogene, 25(15), 2234–2244.PubMedCrossRef
241.
Zurück zum Zitat Lan, T., Wang, H., Zhang, Z., et al. (2017). Downregulation of β-arrestin 1 suppresses glioblastoma cell growth and glycolysis via inhibition of Src signaling. Experimental Cell Research, 4827(17), 30251–30253. Lan, T., Wang, H., Zhang, Z., et al. (2017). Downregulation of β-arrestin 1 suppresses glioblastoma cell growth and glycolysis via inhibition of Src signaling. Experimental Cell Research, 4827(17), 30251–30253.
242.
Zurück zum Zitat Duan, X., Kong, Z., Liu, Y., et al. (2015). β-Arrestin2 contributes to cell viability and proliferation via the down-regulation of FOXO1 in castration-resistant prostate cancer. Journal of Cellular Physiology, 230(10), 2371–2381.PubMedCrossRef Duan, X., Kong, Z., Liu, Y., et al. (2015). β-Arrestin2 contributes to cell viability and proliferation via the down-regulation of FOXO1 in castration-resistant prostate cancer. Journal of Cellular Physiology, 230(10), 2371–2381.PubMedCrossRef
243.
Zurück zum Zitat Kotula, J. W., Sun, J., Li, M., et al. (2014). Targeted disruption of β-arrestin 2-mediated signaling pathways by aptamer chimeras leads to inhibition of leukemic cell growth. PloS One, 9(4), e93441.PubMedPubMedCentralCrossRef Kotula, J. W., Sun, J., Li, M., et al. (2014). Targeted disruption of β-arrestin 2-mediated signaling pathways by aptamer chimeras leads to inhibition of leukemic cell growth. PloS One, 9(4), e93441.PubMedPubMedCentralCrossRef
244.
Zurück zum Zitat Xu, P., Zuo, H., Chen, B., et al. (2017). Doxorubicin-loaded platelets as a smart drug delivery system: an improved therapy for lymphoma. Scientific Reports, 7, 42632.PubMedPubMedCentralCrossRef Xu, P., Zuo, H., Chen, B., et al. (2017). Doxorubicin-loaded platelets as a smart drug delivery system: an improved therapy for lymphoma. Scientific Reports, 7, 42632.PubMedPubMedCentralCrossRef
245.
Zurück zum Zitat Sarkar, S., Alam, M. A., Shaw, J., & Dasgupta, A. K. (2013). Drug delivery using platelet cancer cell interaction. Pharmacological Research, 30(11), 2785–2794.CrossRef Sarkar, S., Alam, M. A., Shaw, J., & Dasgupta, A. K. (2013). Drug delivery using platelet cancer cell interaction. Pharmacological Research, 30(11), 2785–2794.CrossRef
246.
Zurück zum Zitat Xu, P., Zuo, H., Zhou, R., et al. (2017). Doxorubicin-loaded platelets conjugated with anti-CD22 mAbs: a novel targeted delivery system for lymphoma treatment with cardiopulmonary avoidance. Oncotarget. doi:10.18632/oncotarget.16871. Xu, P., Zuo, H., Zhou, R., et al. (2017). Doxorubicin-loaded platelets conjugated with anti-CD22 mAbs: a novel targeted delivery system for lymphoma treatment with cardiopulmonary avoidance. Oncotarget. doi:10.​18632/​oncotarget.​16871.
247.
Zurück zum Zitat Li, J., Sharkey, C. C., Wun, B., Liesveld, J. L., & King, M. R. (2016). Genetic engineering of platelets to neutralize circulating tumor cells. Journal of Controlled Release, 228, 38–47.PubMedPubMedCentralCrossRef Li, J., Sharkey, C. C., Wun, B., Liesveld, J. L., & King, M. R. (2016). Genetic engineering of platelets to neutralize circulating tumor cells. Journal of Controlled Release, 228, 38–47.PubMedPubMedCentralCrossRef
248.
Zurück zum Zitat Li, J., Ai, Y., Wang, L., et al. (2016). Targeted drug delivery to circulating tumor cells via platelet membrane-functionalized particles. Biomaterials, 76, 52–65.PubMedCrossRef Li, J., Ai, Y., Wang, L., et al. (2016). Targeted drug delivery to circulating tumor cells via platelet membrane-functionalized particles. Biomaterials, 76, 52–65.PubMedCrossRef
249.
Zurück zum Zitat Hu, Q., Quian, C., Sun, W., et al. (2016). Engineered nanoplatelets for enhanced treatment of multiple myeloma and thrombus. Advanced Materials, 28(43), 9573–9580. Hu, Q., Quian, C., Sun, W., et al. (2016). Engineered nanoplatelets for enhanced treatment of multiple myeloma and thrombus. Advanced Materials, 28(43), 9573–9580.
250.
Zurück zum Zitat Żmigrodzka, M., Guzera, M., Miśkiewicz, A., Jagielski, D., & Winnicka, A. (2016). The biology of extracellular vesicles with focus on platelet microparticles and their role in cancer development and progression. Tumour Biology, 37(11), 14391–14401.PubMedPubMedCentralCrossRef Żmigrodzka, M., Guzera, M., Miśkiewicz, A., Jagielski, D., & Winnicka, A. (2016). The biology of extracellular vesicles with focus on platelet microparticles and their role in cancer development and progression. Tumour Biology, 37(11), 14391–14401.PubMedPubMedCentralCrossRef
251.
Zurück zum Zitat Amison, R., Page, C., & Pitchford, S. C. (2012). Pharmacological modulation of the inflammatory actions of platelets. Handbook of Experimental Pharmacology, 210, 447–468.CrossRef Amison, R., Page, C., & Pitchford, S. C. (2012). Pharmacological modulation of the inflammatory actions of platelets. Handbook of Experimental Pharmacology, 210, 447–468.CrossRef
252.
Zurück zum Zitat Carboni, E., Tschudi, K., Nam, J., Lu, X., & Ma, A. W. (2014). Particle margination and its implications on intravenous anticancer drug delivery. AAPS PharmSciTech, 15(3), 762–771.PubMedPubMedCentralCrossRef Carboni, E., Tschudi, K., Nam, J., Lu, X., & Ma, A. W. (2014). Particle margination and its implications on intravenous anticancer drug delivery. AAPS PharmSciTech, 15(3), 762–771.PubMedPubMedCentralCrossRef
253.
254.
Zurück zum Zitat Gresele, P., Momi, S., Pitchford, S. C., & Page, C. P. (2008). Platelets in respiratory disorders and inflammatory conditions. In P. Gresele, V. Fuster, J. A. Lòpez, C. P. Page, & J. Vermylen (Eds.), Platelets in hematologic and cardiovascular disorders, A clinical handbook (pp. 323–340). Cambridge, UK: Cambridge University Press. Gresele, P., Momi, S., Pitchford, S. C., & Page, C. P. (2008). Platelets in respiratory disorders and inflammatory conditions. In P. Gresele, V. Fuster, J. A. Lòpez, C. P. Page, & J. Vermylen (Eds.), Platelets in hematologic and cardiovascular disorders, A clinical handbook (pp. 323–340). Cambridge, UK: Cambridge University Press.
255.
Zurück zum Zitat Gresele, P., Falcinelli, E., & Momi, S. (2008). Potentiation and priming of platelet activation: a potential target for antiplatelet therapy. Trends in Pharmacological Sciences, 29(7), 352–360.PubMedCrossRef Gresele, P., Falcinelli, E., & Momi, S. (2008). Potentiation and priming of platelet activation: a potential target for antiplatelet therapy. Trends in Pharmacological Sciences, 29(7), 352–360.PubMedCrossRef
256.
Zurück zum Zitat Menter, D. G., Davis, J. S., Tucker, S. C., et al. (2017). Platelets: “first responders” in cancer progression and metastasis. In P. Gresele, N. Kleiman, J. A. Lopez, & C. P. Page (Eds.), Platelets in thrombotic and non-thrombotic disorders (Vol. 2, pp. 1111–1132). Switzerland: Springer, Cham.CrossRef Menter, D. G., Davis, J. S., Tucker, S. C., et al. (2017). Platelets: “first responders” in cancer progression and metastasis. In P. Gresele, N. Kleiman, J. A. Lopez, & C. P. Page (Eds.), Platelets in thrombotic and non-thrombotic disorders (Vol. 2, pp. 1111–1132). Switzerland: Springer, Cham.CrossRef
257.
Zurück zum Zitat Ware, J., & Post, S. R. (2017). Platelets and inflammatory disorders of connective tissue. In P. Gresele, N. Kleiman, J. A. Lopez, & C. P. Page (Eds.), Platelet in thrombotic and non-thrombotic disorders (Vol. 2, pp. 1133–1137). Switzerland: Springer, Cham.CrossRef Ware, J., & Post, S. R. (2017). Platelets and inflammatory disorders of connective tissue. In P. Gresele, N. Kleiman, J. A. Lopez, & C. P. Page (Eds.), Platelet in thrombotic and non-thrombotic disorders (Vol. 2, pp. 1133–1137). Switzerland: Springer, Cham.CrossRef
258.
Zurück zum Zitat Momi, S., Pitchford, S. C., Gresle, P., & Page, C. P. (2017). Platelets and airway diseases. In P. Gresele, N. Kleiman, J. A. Lopez, & C. P. Page (Eds.), Platelet in thrombotic and non-thrombotic disorders (Vol. 2, pp. 1149–1168). Switzerland: Springer, Cham.CrossRef Momi, S., Pitchford, S. C., Gresle, P., & Page, C. P. (2017). Platelets and airway diseases. In P. Gresele, N. Kleiman, J. A. Lopez, & C. P. Page (Eds.), Platelet in thrombotic and non-thrombotic disorders (Vol. 2, pp. 1149–1168). Switzerland: Springer, Cham.CrossRef
259.
Zurück zum Zitat Andre, P. (2017). Targeting intraplatelet signaling pathways as potential antithrombotic strategy. In P. Gresele, N. Kleiman, J. A. Lopez, & C. P. Page (Eds.), Platelet in thrombotic and non-thrombotic disorders (Vol. 2, pp. 1341–1360). Switzerland: Springer, Cham.CrossRef Andre, P. (2017). Targeting intraplatelet signaling pathways as potential antithrombotic strategy. In P. Gresele, N. Kleiman, J. A. Lopez, & C. P. Page (Eds.), Platelet in thrombotic and non-thrombotic disorders (Vol. 2, pp. 1341–1360). Switzerland: Springer, Cham.CrossRef
Metadaten
Titel
Platelet-targeted pharmacologic treatments as anti-cancer therapy
verfasst von
P. Gresele
S. Momi
M. Malvestiti
M. Sebastiano
Publikationsdatum
13.07.2017
Verlag
Springer US
Erschienen in
Cancer and Metastasis Reviews / Ausgabe 2/2017
Print ISSN: 0167-7659
Elektronische ISSN: 1573-7233
DOI
https://doi.org/10.1007/s10555-017-9679-8

Weitere Artikel der Ausgabe 2/2017

Cancer and Metastasis Reviews 2/2017 Zur Ausgabe

ReviewPaper

Preface

Update Onkologie

Bestellen Sie unseren Fach-Newsletter und bleiben Sie gut informiert.