nach oben

Cancer and Metastasis Reviews

Erschienen in:

01.03.2010

Biological and clinical significance of KRAS mutations in lung cancer: an oncogenic driver that contrasts with EGFR mutation

verfasst von: Kenichi Suda, Kenji Tomizawa, Tetsuya Mitsudomi

Erschienen in: Cancer and Metastasis Reviews | Ausgabe 1/2010

Einloggen, um Zugang zu erhalten

Abstract

KRAS and epidermal growth factor receptor (EGFR) are the two most frequently mutated proto-oncogenes in adenocarcinoma of the lung. The occurrence of these two oncogenic mutations is mutually exclusive, and they exhibit many contrasting characteristics such as clinical background, pathological features of patients harboring each mutation, and prognostic or predictive implications. Lung cancers harboring the EGFR mutations are remarkably sensitive to EGFR tyrosine kinase inhibitors such as gefitinib or erlotinib. This discovery has dramatically changed the clinical treatment of lung cancer in that it almost doubled the duration of survival for lung cancer patients with an EGFR mutation. In this review, we describe the features of KRAS mutations in lung cancer and contrast these with the features of EGFR mutations. Recent strategies to combat lung cancer harboring KRAS mutations are also reviewed.

Shih, C., Padhy, L. C., Murray, M., & Weinberg, R. A. (1981). Transforming genes of carcinomas and neuroblastomas introduced into mouse fibroblasts. Nature, 290, 261–264.CrossRefPubMed

Perucho, M., Goldfarb, M., Shimizu, K., Lama, C., Fogh, J., & Wigler, M. (1981). Human-tumor-derived cell lines contain common and different transforming genes. Cell, 27, 467–476.CrossRefPubMed

Krontiris, T. G., & Cooper, G. M. (1981). Transforming activity of human tumor DNAs. Proceedings of the National Academy of Sciences of the United States of America, 78, 1181–1184.CrossRefPubMed

Der, C. J., Krontiris, T. G., & Cooper, G. M. (1982). Transforming genes of human bladder and lung carcinoma cell lines are homologous to the ras genes of Harvey and Kirsten sarcoma viruses. Proceedings of the National Academy of Sciences of the United States of America, 79, 3637–3640.CrossRefPubMed

Goldfarb, M., Shimizu, K., Perucho, M., & Wigler, M. (1982). Isolation and preliminary characterization of a human transforming gene from T24 bladder carcinoma cells. Nature, 296, 404–409.CrossRefPubMed

Parada, L. F., Tabin, C. J., Shih, C., & Weinberg, R. A. (1982). Human EJ bladder carcinoma oncogene is homologue of Harvey sarcoma virus ras gene. Nature, 297, 474–478.CrossRefPubMed

Tabin, C. J., Bradley, S. M., Bargmann, C. I., Weinberg, R. A., Papageorge, A. G., Scolnick, E. M., et al. (1982). Mechanism of activation of a human oncogene. Nature, 300, 143–149.CrossRefPubMed

Reddy, E. P., Reynolds, R. K., Santos, E., & Barbacid, M. (1982). A point mutation is responsible for the acquisition of transforming properties by the T24 human bladder carcinoma oncogene. Nature, 300, 149–152.CrossRefPubMed

Taparowsky, E., Suard, Y., Fasano, O., Shimizu, K., Goldfarb, M., & Wigler, M. (1982). Activation of the T24 bladder carcinoma transforming gene is linked to a single amino acid change. Nature, 300, 762–765.CrossRefPubMed

10.

Bos, J. (1988). The ras gene family and human carcinogenesis. Mutation Research, 195, 255–271.PubMed

11.

Shimizu, K., Goldfarb, M., Suard, Y., Perucho, M., Li, Y., Kamata, T., et al. (1983). Three human transforming genes are related to the viral ras oncogenes. Proceedings of the National Academy of Sciences of the United States of America, 80, 2112–2116.CrossRefPubMed

12.

Hall, A., Marshall, C. J., Spurr, N. K., & Weiss, R. A. (1983). Identification of transforming gene in two human sarcoma cell lines as a new member of the ras gene family located on chromosome 1. Nature, 303, 396–400.CrossRefPubMed

13.

DeClue, J. E., Papageorge, A. G., Fletcher, J. A., Diehl, S. R., Ratner, N., Vass, W. C., et al. (1992). Abnormal regulation of mammalian p21ras contributes to malignant tumor growth in von Recklinghausen (type 1) neurofibromatosis. Cell, 69, 265–273.CrossRefPubMed

14.

Trahey, M., & McCormick, F. (1987). A cytoplasmic protein stimulates normal N-ras p21 GTPase, but does not affect oncogenic mutants. Science, 1987(238), 542–545.CrossRef

15.

Willumsen, B. M., Norris, K., Papageorge, A. G., Hubbert, N. L., & Lowy, D. R. (1984). Harvey murine sarcoma virus p21 ras protein: biological and biochemical significance of the cysteine nearest the carboxy terminus. The EMBO Journal, 3, 2581–2585.PubMed

16.

Casey, P. J., Solski, P. A., Der, C. J., & Buss, J. E. (1989). p21ras is modified by a farnesyl isoprenoid. Proceedings of the National Academy of Sciences of the United States of America, 86, 8323–8327.CrossRefPubMed

17.

Schaber, M. D., O'Hara, M. B., Garsky, V. M., Mosser, S. C., Bergstrom, J. D., Moores, S. L., et al. (1990). Polyisoprenylation of Ras in vitro by a farnesyl-protein transferase. The Journal of Biological Chemistry, 265, 14701–14704.PubMed

18.

Hancock, J. F., Paterson, H., & Marshall, C. J. (1990). A polybasic domain or palmitoylation is required in addition to the CAAX motif to localize p21ras to the plasma membrane. Cell, 63, 133–139.CrossRefPubMed

19.

Patek, C. E., Arends, M. J., Wallace, W. A., Luo, F., Hagan, S., Brownstein, D. G., et al. (2008). Mutationally activated K-ras 4A and 4B both mediate lung carcinogenesis. Experimental Cell Research, 314, 1105–1114.CrossRefPubMed

20.

To, M. D., Wong, C. E., Karnezis, A. N., Del Rosario, R., Di Lauro, R., & Balmain, A. (2008). Kras regulatory elements and exon 4A determine mutation specificity in lung cancer. Nature Genetics, 40, 1240–1244.CrossRefPubMed

21.

Newbold, R. F., & Overell, R. W. (1983). Fibroblast immortality is a prerequisite for transformation by EJ c-Ha-ras oncogene. Nature, 304, 648–651.CrossRefPubMed

22.

Land, H., Parada, L. F., & Weinberg, R. A. (1983). Tumorigenic conversion of primary embryo fibroblasts requires at least two cooperating oncogenes. Nature, 304, 596–602.CrossRefPubMed

23.

Ruley, H. E. (1983). Adenovirus early region 1A enables viral and cellular transforming genes to transform primary cells in culture. Nature, 304, 602–606.CrossRefPubMed

24.

Serrano, M., Lin, A. W., McCurrach, M. E., Beach, D., & Lowe, S. W. (1997). Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a. Cell, 88, 593–602.CrossRefPubMed

25.

Karnoub, A. E., & Weinberg, R. A. (2008). Ras oncogenes: split personalities. Nature Reviews Molecular Cell Biology, 9, 517–531.CrossRefPubMed

26.

Sun, P., Yoshizuka, N., New, L., Moser, B. A., Li, Y., Liao, R., et al. (2007). PRAK is essential for ras-induced senescence and tumor suppression. Cell, 128, 295–308.CrossRefPubMed

27.

Tuveson, D. A., Shaw, A. T., Willis, N. A., Silver, D. P., Jackson, E. L., Chang, S., et al. (2004). Endogenous oncogenic K-ras(G12D) stimulates proliferation and widespread neoplastic and developmental defects. Cancer Cell, 5, 375–387.CrossRefPubMed

28.

Collado, M., Gil, J., Efeyan, A., Guerra, C., Schuhmacher, A. J., Barradas, M., et al. (2005). Tumour biology: senescence in premalignant tumours. Nature, 436, 642.CrossRefPubMed

29.

Santos, E., Martin-Zanca, D., Reddy, E. P., Pierotti, M. A., Della Porta, G., & Barbacid, M. (1984). Malignant activation of a K-ras oncogene in lung carcinoma but not in normal tissue of the same patient. Science, 223, 661–664.CrossRefPubMed

30.

Rodenhuis, S., van de Wetering, M. L., Mooi, W. J., Evers, S. G., van Zandwijk, N., & Bos, J. L. (1987). Mutational activation of the K-ras oncogene. A possible pathogenetic factor in adenocarcinoma of the lung. The New England Journal of Medicine, 317, 929–935.PubMed

31.

Mitsudomi, T., Viallet, J., Linnoila, R. I., Mulshine, J. L., Minna, J. D., & Gazdar, A. F. (1991). Mutations of ras genes distinguish a subset of non-small cell lung cancer cell lines from small cell lung cancer cell lines. Oncogene, 6, 1353–1362.PubMed

32.

Shigematsu, H., Takahashi, T., Nomura, M., Majmudar, K., Suzuki, M., Lee, H., et al. (2005). Somatic mutations of the HER2 kinase domain in lung adenocarcinomas. Cancer Research, 65, 1642–1646.CrossRefPubMed

33.

Shigematsu, H., Lin, L., Takahashi, T., Nomura, M., Suzuki, M., Wistuba, I. I., et al. (2005). Clinical and biological features associated with epidermal growth factor receptor gene mutations in lung cancers. Journal of the National Cancer Institute, 97, 339–346.PubMed

34.

Slebos, R. J., Hruban, R. H., Dalesio, O., Mooi, W. J., Offerhaus, G. J., & Rodenhuis, S. (1991). Relationship between K-ras oncogene activation and smoking in adenocarcinoma of the human lung. Journal of the National Cancer Institute, 83, 1024–1027.CrossRefPubMed

35.

Kosaka, T., Yatabe, Y., Endoh, H., Kuwano, H., Takahashi, T., & Mitsudomi, T. (2004). Mutations of the epidermal growth factor receptor gene in lung cancer: biological and clinical implications. Cancer Research, 64, 8919–8923.CrossRefPubMed

36.

Ding, L., Getz, G., Wheeler, D. A., Mardis, E. R., McLellan, M. D., Cibulskis, K., et al. (2008). Somatic mutations affect key pathways in lung adenocarcinoma. Nature, 455, 1069–1075.CrossRefPubMed

37.

Gealy, R., Zhang, L., Siegfried, J. M., Luketich, J. D., & Keohavong, P. (1999). Comparison of mutations in the p53 and K-ras genes in lung carcinomas from smoking and nonsmoking women. Cancer Epidemiology, Biomarkers & Prevention, 8, 297–302.

38.

Vahakangas, K. H., Bennett, W. P., Castren, K., Welsh, J. A., Khan, M. A., Blomeke, B., et al. (2001). p53 and K-ras mutations in lung cancers from former and never-smoking women. Cancer Research, 61, 4350–4356.PubMed

39.

Riely, G. J., Kris, M. G., Rosenbaum, D., Marks, J., Li, A., Chitale, D. A., et al. (2008). Frequency and distinctive spectrum of KRAS mutations in never smokers with lung adenocarcinoma. Clinical Cancer Research, 14, 5731–5734.CrossRefPubMed

40.

Bos, J. L. (1989). ras oncogenes in human cancer: a review. Cancer Research, 49, 4682–4689.PubMed

41.

Weir, B. A., Woo, M. S., Getz, G., Perner, S., Ding, L., Beroukhim, R., et al. (2007). Characterizing the cancer genome in lung adenocarcinoma. Nature, 450, 893–898.CrossRefPubMed

42.

Kendall, J., Liu, Q., Bakleh, A., Krasnitz, A., Nguyen, K. C., Lakshmi, B., et al. (2007). Oncogenic cooperation and coamplification of developmental transcription factor genes in lung cancer. Proceedings of the National Academy of Sciences of the United States of America, 104, 16663–16668.CrossRefPubMed

43.

Soh, J., Okumura, N., Lockwood, W. W., Yamamoto, H., Shigematsu, H., Zhang, W., et al. (2009). Oncogene mutations, copy number gains and mutant allele specific imbalance (MASI) frequently occur together in tumor cells. PLoS One, 4, e7464.CrossRefPubMed

44.

Zhang, Z., Wang, Y., Vikis, H. G., Johnson, L., Liu, G., Li, J., et al. (2001). Wildtype Kras2 can inhibit lung carcinogenesis in mice. Nature Genetics, 29, 25–33.CrossRefPubMed

45.

Diaz, R., Lue, J., Mathews, J., Yoon, A., Ahn, D., Garcia-Espana, A., et al. (2005). Inhibition of Ras oncogenic activity by Ras protooncogenes. International Journal of Cancer, 113, 241–248.CrossRef

46.

To, M. D., Perez-Losada, J., Mao, J. H., Hsu, J., Jacks, T., & Balmain, A. (2006). A functional switch from lung cancer resistance to susceptibility at the Pas1 locus in Kras2LA2 mice. Nature Genetics, 38, 926–930.CrossRefPubMed

47.

Kobayashi, T., Tsuda, H., Noguchi, M., Hirohashi, S., Shimosato, Y., Goya, T., et al. (1990). Association of point mutation in c-Ki-ras oncogene in lung adenocarcinoma with particular reference to cytologic subtypes. Cancer, 66, 289–294.CrossRefPubMed

48.

Tsuchiya, E., Furuta, R., Wada, N., Nakagawa, K., Ishikawa, Y., Kawabuchi, B., et al. (1995). High K-ras mutation rates in goblet-cell-type adenocarcinomas of the lungs. Journal of Cancer Research and Clinical Oncology, 121, 577–581.CrossRefPubMed

49.

Marchetti, A., Buttitta, F., Pellegrini, S., Chella, A., Bertacca, G., Filardo, A., et al. (1996). Bronchioloalveolar lung carcinomas: K-ras mutations are constant events in the mucinous subtype. The Journal of Pathology, 179, 254–259.CrossRefPubMed

50.

Yatabe, Y., Koga, T., Mitsudomi, T., & Takahashi, T. (2004). CK20 expression, CDX2 expression, K-ras mutation, and goblet cell morphology in a subset of lung adenocarcinomas. The Journal of Pathology, 203, 645–652.CrossRefPubMed

51.

Paez, J. G., Janne, P. A., Lee, J. C., Tracy, S., Greulich, H., Gabriel, S., et al. (2004). EGFR mutations in lung cancer: correlation with clinical response to gefitinib therapy. Science, 304, 1497–1500.CrossRefPubMed

52.

Lynch, T. J., Bell, D. W., Sordella, R., Gurubhagavatula, S., Okimoto, R. A., Brannigan, B. W., et al. (2004). Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefitinib. The New England Journal of Medicine, 350, 2129–2139.CrossRefPubMed

53.

Pao, W., Miller, V., Zakowski, M., Doherty, J., Politi, K., Sarkaria, I., et al. (2004). EGF receptor gene mutations are common in lung cancers from “never smokers” and are associated with sensitivity of tumors to gefitinib and erlotinib. Proceedings of the National Academy of Sciences of the United States of America, 101, 13306–13311.CrossRefPubMed

54.

Mitsudomi, T., & Yatabe, Y. (2007). Mutations of the epidermal growth factor receptor gene and related genes as determinants of epidermal growth factor receptor tyrosine kinase inhibitors sensitivity in lung cancer. Cancer Science, 98, 1817–1824.CrossRefPubMed

55.

Leidner, R. S., Fu, P., Clifford, B., Hamdan, A., Jin, C., Eisenberg, R., et al. (2009). Genetic abnormalities of the EGFR pathway in African American patients with non-small-cell lung cancer. Journal of Clinical Oncology, 27, 5620–5626.CrossRefPubMed

56.

Matsuo, K., Ito, H., Yatabe, Y., Hiraki, A., Hirose, K., Wakai, K., et al. (2007). Risk factors differ for non-small-cell lung cancers with and without EGFR mutation: assessment of smoking and sex by a case-control study in Japanese. Cancer Science, 98, 96–101.CrossRefPubMed

57.

Slebos, R. J., Kibbelaar, R. E., Dalesio, O., Kooistra, A., Stam, J., Meijer, C. J., et al. (1990). K-ras oncogene activation as a prognostic marker in adenocarcinoma of the lung. The New England Journal of Medicine, 323, 561–565.PubMedCrossRef

58.

Mascaux, C., Iannino, N., Martin, B., Paesmans, M., Berghmans, T., Dusart, M., et al. (2005). The role of RAS oncogene in survival of patients with lung cancer: a systematic review of the literature with meta-analysis. British Journal of Cancer, 92, 131–139.CrossRefPubMed

59.

Kosaka, T., Yatabe, Y., Onozato, R., Kuwano, H., & Mitsudomi, T. (2009). Prognostic implication of EGFR, KRAS, and TP53 gene mutations in a large cohort of Japanese patients with surgically treated lung adenocarcinoma. Journal of Thoracic Oncology, 4, 22–29.PubMed

60.

Fukuoka, M., Yano, S., Giaccone, G., Tamura, T., Nakagawa, K., Douillard, J. Y., et al. (2003). Multi-institutional randomized phase II trial of gefitinib for previously treated patients with advanced non-small-cell lung cancer. Journal of Clinical Oncology, 21, 2237–2246.CrossRefPubMed

61.

Kris, M. G., Natale, R. B., Herbst, R. S., Lynch, T. J., Jr., Prager, D., Belani, C. P., et al. (2003). Efficacy of gefitinib, an inhibitor of the epidermal growth factor receptor tyrosine kinase, in symptomatic patients with non-small cell lung cancer: a randomized trial. The Journal of the American Medical Association, 290, 2149–2158.CrossRef

62.

Sordella, R., Bell, D. W., Haber, D. A., & Settleman, J. (2004). Gefitinib-sensitizing EGFR mutations in lung cancer activate anti-apoptotic pathways. Science, 305, 1163–1167.CrossRefPubMed

63.

Mitsudomi, T., Kosaka, T., Endoh, H., Horio, Y., Hida, T., Mori, S., et al. (2005). Mutations of the epidermal growth factor receptor gene predict prolonged survival after gefitinib treatment in patients with non-small-cell lung cancer with postoperative recurrence. Journal of Clinical Oncology, 23, 2513–2520.CrossRefPubMed

64.

Takano, T., Fukui, T., Ohe, Y., Tsuta, K., Yamamoto, S., Nokihara, H., et al. (2008). EGFR mutations predict survival benefit from gefitinib in patients with advanced lung adenocarcinoma: a historical comparison of patients treated before and after gefitinib approval in Japan. Journal of Clinical Oncology, 26, 5589–5595.CrossRefPubMed

65.

Cappuzzo, F., Hirsch, F. R., Rossi, E., Bartolini, S., Ceresoli, G. L., Bemis, L., et al. (2005). Epidermal growth factor receptor gene and protein and gefitinib sensitivity in non-small-cell lung cancer. Journal of the National Cancer Institute, 97, 643–655.PubMedCrossRef

66.

Mok, T. S., Wu, Y. L., Thongprasert, S., Yang, C. H., Chu, D. T., Saijo, N., et al. (2009). Gefitinib or carboplatin-paclitaxel in pulmonary adenocarcinoma. The New England Journal of Medicine, 361, 947–957.CrossRefPubMed

67.

Kobayashi, K., Inoue, A., Maemondo, M., Sugawara, S., Isobe, H., Oizumi, S., et al. (2009). First-line gefitinib versus first-line chemotherapy by carboplatin (CBDCA) plus paclitaxel (TXL) in non-small cell lung cancer (NSCLC) patients (pts) with EGFR mutations: a phase III study (002) by North East Japan Gefitinib Study Group. Journal of Clinical Oncology, 27, 15s (suppl; abstr 8016).CrossRef

68.

Tsurutani, J., Mitsudomi, T., Mori, S., Okamoto, I., Nozaki, K., Tada, H., et al. (2009). A phase III, first-line trial of gefitinib versus cisplatin plus docetaxel for patients with advanced or recurrent non-small cell lungcancer (NSCLC) harboring activating mutation of the epidermal growthfactor receptor (EGFR) gene: a preliminary results of WJTOG 3405. European Journal of Cancer, 7(Suppl), 505(abstr O-9002).

69.

Pao, W., Wang, T. Y., Riely, G. J., Miller, V. A., Pan, Q., Ladanyi, M., et al. (2005). KRAS mutations and primary resistance of lung adenocarcinomas to gefitinib or erlotinib. PLoS Medicine, 2, e17.CrossRefPubMed

70.

Murray, S., Dahabreh, I. J., Linardou, H., Manoloukos, M., Bafaloukos, D., & Kosmidis, P. (2008). Somatic mutations of the tyrosine kinase domain of epidermal growth factor receptor and tyrosine kinase inhibitor response to TKIs in non-small cell lung cancer: an analytical database. Journal of Thoracic Oncology, 3, 832–839.CrossRefPubMed

71.

Jackman, D. M., Miller, V. A., Cioffredi, L. A., Yeap, B. Y., Janne, P. A., Riely, G. J., et al. (2009). Impact of epidermal growth factor receptor and KRAS mutations on clinical outcomes in previously untreated non-small cell lung cancer patients: results of an online tumor registry of clinical trials. Clinical Cancer Research, 15, 5267–5273.CrossRefPubMed

72.

O'Byrne, K. J., Bondarenko, I., Barrios, C., Eschbach, C., Martens, U., Hotko, Y., et al. (2009). Molecular and clinical predictors of outcome for cetuximab in non-small cell lung cancer (NSCLC): Data from the FLEX study. Journal of Clinical Oncology, 27, 15s (suppl; abstr 8007).CrossRef

73.

Lynch, T. J., Patel, T., Dreisbach, L., McCleod, M., Heim, W. J., Robert, H., et al. (2007). A randomized multicenter phase III study of cetuximab in combination with taxane/carboplatin versus taxane/carboplatin alone as first-line treatment for patients with advanced/metastatic non-small cell lung cancer. Journal of Thoracic Oncology, 2, s340.CrossRef

74.

Cutsem, E.V., Lang, I., D'haens, G., Moiseyenko, V., Zaluski J., Folprecht G., et al. (2008). KRAS status and efficacy in the first-line treatment of patients with metastatic colorectal cancer (mCRC) treated with FOLFIRI with or without cetuximab: The CRYSTAL experience. Journal of Clinical Oncology, 26, abstr 2.

75.

Downward, J. (2003). Targeting RAS signalling pathways in cancer therapy. Nature Reviews Cancer, 3, 11–22.CrossRefPubMed

76.

Weinstein, I. B., & Joe, A. (2008). Oncogene addiction. Cancer Research, 68, 3077–80. discussion 80.CrossRefPubMed

77.

Singh, A., Greninger, P., Rhodes, D., Koopman, L., Violette, S., Bardeesy, N., et al. (2009). A gene expression signature associated with “K-Ras addiction” reveals regulators of EMT and tumor cell survival. Cancer Cell, 15, 489–500.CrossRefPubMed

78.

Horiguchi, K., Shirakihara, T., Nakano, A., Imamura, T., Miyazono, K., & Saitoh, M. (2009). Role of Ras signaling in the induction of snail by transforming growth factor-beta. The Journal of Biological Chemistry, 284, 245–253.CrossRefPubMed

79.

Gupta, S., Ramjaun, A. R., Haiko, P., Wang, Y., Warne, P. H., Nicke, B., et al. (2007). Binding of ras to phosphoinositide 3-kinase p110alpha is required for ras-driven tumorigenesis in mice. Cell, 129, 957–968.CrossRefPubMed

80.

Yang, Y., Iwanaga, K., Raso, M. G., Wislez, M., Hanna, A. E., Wieder, E. D., et al. (2008). Phosphatidylinositol 3-kinase mediates bronchioalveolar stem cell expansion in mouse models of oncogenic K-ras-induced lung cancer. PLoS One, 3, e2220.CrossRefPubMed

81.

Engelman, J. A., Chen, L., Tan, X., Crosby, K., Guimaraes, A. R., Upadhyay, R., et al. (2008). Effective use of PI3K and MEK inhibitors to treat mutant Kras G12D and PIK3CA H1047R murine lung cancers. Nature Medicine, 14, 1351–1356.CrossRefPubMed

82.

Wee, S., Jagani, Z., Xiang, K. X., Loo, A., Dorsch, M., Yao, Y. M., et al. (2009). PI3K pathway activation mediates resistance to MEK inhibitors in KRAS mutant cancers. Cancer Research, 69, 4286–4293.CrossRefPubMed

83.

Sos, M. L., Michel, K., Zander, T., Weiss, J., Frommolt, P., Peifer, M., et al. (2009). Predicting drug susceptibility of non-small cell lung cancers based on genetic lesions. The Journal of Clinical Investigation, 119, 1727–1740.CrossRefPubMed

84.

Scholl, C., Frohling, S., Dunn, I. F., Schinzel, A. C., Barbie, D. A., Kim, S. Y., et al. (2009). Synthetic lethal interaction between oncogenic KRAS dependency and STK33 suppression in human cancer cells. Cell, 137, 821–834.CrossRefPubMed

85.

Luo, J., Emanuele, M. J., Li, D., Creighton, C. J., Schlabach, M. R., Westbrook, T. F., et al. (2009). A genome-wide RNAi screen identifies multiple synthetic lethal interactions with the Ras oncogene. Cell, 137, 835–848.CrossRefPubMed

86.

Barbie, D. A., Tamayo, P., Boehm, J. S., Kim, S. Y., Moody, S. E., Dunn, I. F., et al. (2009). Systematic RNA interference reveals that oncogenic KRAS-driven cancers require TBK1. Nature, 462, 108–112.CrossRefPubMed

87.

Chien, Y., Kim, S., Bumeister, R., Loo, Y. M., Kwon, S. W., Johnson, C. L., et al. (2006). RalB GTPase-mediated activation of the IkappaB family kinase TBK1 couples innate immune signaling to tumor cell survival. Cell, 127, 157–170.CrossRefPubMed

88.

Meylan, E., Dooley, A. L., Feldser, D. M., Shen, L., Turk, E., Ouyang, C., et al. (2009). Requirement for NF-kappaB signalling in a mouse model of lung adenocarcinoma. Nature, 462, 104–107.CrossRefPubMed

89.

Shimamura, T., Ji, H., Minami, Y., Thomas, R. K., Lowell, A. M., Shah, K., et al. (2006). Non-small-cell lung cancer and Ba/F3 transformed cells harboring the ERBB2 G776insV_G/C mutation are sensitive to the dual-specific epidermal growth factor receptor and ERBB2 inhibitor HKI-272. Cancer Research, 66, 6487–6491.CrossRefPubMed

90.

Soda, M., Choi, Y. L., Enomoto, M., Takada, S., Yamashita, Y., Ishikawa, S., et al. (2007). Identification of the transforming EML4-ALK fusion gene in non-small-cell lung cancer. Nature, 448, 561–566.CrossRefPubMed

91.

Koivunen, J. P., Mermel, C., Zejnullahu, K., Murphy, C., Lifshits, E., Holmes, A. J., et al. (2008). EML4-ALK fusion gene and efficacy of an ALK kinase inhibitor in lung cancer. Clinical Cancer Research, 14, 4275–4283.CrossRefPubMed

92.

Morita, S., Okamoto, I., Kobayashi, K., Yamazaki, K., Asahina, H., Inoue, A., et al. (2009). Combined Survival Analysis of Prospective Clinical Trials of Gefitinib for Non-Small Cell Lung Cancer with EGFR Mutations. Clinical Cancer Research, 15, 4493–4498.CrossRefPubMed

93.

Kim, E. S., Hirsh, V., Mok, T., Socinski, M. A., Gervais, R., Wu, Y. L., et al. (2008). Gefitinib versus docetaxel in previously treated non-small-cell lung cancer (INTEREST): a randomised phase III trial. Lancet, 372, 1809–1818.CrossRefPubMed

94.

Maruyama, R., Nishiwaki, Y., Tamura, T., Yamamoto, N., Tsuboi, M., Nakagawa, K., et al. (2008). Phase III study, V-15-32, of gefitinib versus docetaxel in previously treated Japanese patients with non-small-cell lung cancer. Journal of Clinical Oncology, 26, 4244–4252.CrossRefPubMed

95.

Lee, J. C., Vivanco, I., Beroukhim, R., Huang, J. H., Feng, W. L., DeBiasi, R. M., et al. (2006). Epidermal growth factor receptor activation in glioblastoma through novel missense mutations in the extracellular domain. PLoS Medicine, 3, e485.CrossRefPubMed

96.

Hynes, N. E., & Lane, H. A. (2005). ERBB receptors and cancer: the complexity of targeted inhibitors. Nature Reviews Cancer, 5, 341–354.CrossRefPubMed

97.

Mitin, N., Rossman, K. L., & Der, C. J. (2005). Signaling interplay in Ras superfamily function. Current Biology, 15, R563–574.CrossRefPubMed

98.

Repasky, G. A., Chenette, E. J., & Der, C. J. (2004). Renewing the conspiracy theory debate: does Raf function alone to mediate Ras oncogenesis? Trends in Cell Biology, 14, 639–647.CrossRefPubMed

99.

Schubbert, S., Shannon, K., & Bollag, G. (2007). Hyperactive Ras in developmental disorders and cancer. Nature Reviews Cancer, 7, 295–308.CrossRefPubMed

100.

Downward, J. (2009). Cancer: A tumour gene's fatal flaws. Nature, 462, 44–45.CrossRefPubMed

101.

Tam, I. Y., Chung, L. P., Suen, W. S., Wang, E., Wong, M. C., Ho, K. K., et al. (2006). Distinct epidermal growth factor receptor and KRAS mutation patterns in non-small cell lung cancer patients with different tobacco exposure and clinicopathologic features. Clinical Cancer Research, 12, 1647–1653.CrossRefPubMed

102.

Rudin, C. M., Avila-Tang, E., Harris, C. C., Herman, J. G., Hirsch, F. R., Pao, W., et al. (2009). Lung cancer in never smokers: molecular profiles and therapeutic implications. Clinical Cancer Research, 15, 5646–5661.CrossRefPubMed

Titel: Biological and clinical significance of KRAS mutations in lung cancer: an oncogenic driver that contrasts with EGFR mutation
verfasst von: Kenichi Suda
Kenji Tomizawa
Tetsuya Mitsudomi
Publikationsdatum: 01.03.2010
Verlag: Springer US
Erschienen in: Cancer and Metastasis Reviews / Ausgabe 1/2010
Print ISSN: 0167-7659
Elektronische ISSN: 1573-7233
DOI: https://doi.org/10.1007/s10555-010-9209-4

Neu im Fachgebiet Onkologie

25.04.2024 | Nierenkarzinom | Nachrichten

Springer Medizin

Biological and clinical significance of KRAS mutations in lung cancer: an oncogenic driver that contrasts with EGFR mutation

Abstract

Neu im Fachgebiet Onkologie

Adjuvante Immuntherapie verlängert Leben bei RCC

Alectinib verbessert krankheitsfreies Überleben bei ALK-positivem NSCLC

Bei Senioren mit Prostatakarzinom auf Anämie achten!

ICI-Therapie in der Schwangerschaft wird gut toleriert

Update Onkologie

Springer Medizin

Abstract

Bitte loggen Sie sich ein, um Zugang zu diesem Inhalt zu erhalten

Weitere Artikel der Ausgabe 1/2010

microRNAs and lung cancer: tumors and 22-mers

Evidence for self-renewing lung cancer stem cells and their implications in tumor initiation, progression, and targeted therapy

Preface

Modeling prostate cancer: a perspective on transgenic mouse models

Biography—Adi Gazdar

EGFR mutations and the terminal respiratory unit

Neu im Fachgebiet Onkologie

Adjuvante Immuntherapie verlängert Leben bei RCC

Alectinib verbessert krankheitsfreies Überleben bei ALK-positivem NSCLC

Bei Senioren mit Prostatakarzinom auf Anämie achten!

ICI-Therapie in der Schwangerschaft wird gut toleriert

Update Onkologie