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Cancer and Metastasis Reviews

01.03.2008

The Met tyrosine kinase receptor in development and cancer

verfasst von: Alessandra Gentile, Livio Trusolino, Paolo M. Comoglio

Erschienen in: Cancer and Metastasis Reviews | Ausgabe 1/2008

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Abstract

Met is a tyrosine kinase receptor, encoded by an oncogene, whose crucial role has been elucidated during the last two decades. The complex biological program triggered by Met has been dissected and its biological relevance in both physiology and pathology has been proven. Met supports a morphogenetic program, known as invasive growth, taking place both during embryogenesis and adulthood. In tumors Met is often aberrantly activated, giving rise to the pathological counterpart of the invasive growth program: cancer progression towards metastasis. Several approaches have been recently developed to interfere with the tumorigenic and metastatic processes triggered by Met.
Literatur
1.
Cooper, C. S., Park, M., Blair, D. G., Tainsky, M. A., Huebner, K., Croce, C. M., et al. (1984). Molecular cloning of a new transforming gene from a chemically transformed human cell line. Nature, 311, 29–33.PubMedCrossRef
2.
Park, M., Testa, J. R., Blair, D. G., Parsa, N. Z., & Vande Woude, G. F. (1988). Two rearranged MET alleles in MNNG-HOS cells reveal the orientation of MET on chromosome 7 to other markers tightly linked to the cystic fibrosis locus. Proceedings of the National Academy of Sciences of the United States of America, 85, 2667–2671.PubMedCrossRef
3.
Park, M., Dean, M., Cooper, C. S., Schmidt, M., O’Brien, S. J., Blair, D. G., et al. (1986). Mechanism of met oncogene activation. Cell, 45, 895–904.PubMedCrossRef
4.
Soman, N. R., Wogan, G. N., & Rhim, J. S. (1990). TPR-MET oncogenic rearrangement: Detection by polymerase chain reaction amplification of the transcript and expression in human tumor cell lines. Proceedings of the National Academy of Sciences of the United States of America, 87, 738–742.PubMedCrossRef
5.
Giordano, S., Ponzetto, C., Di Renzo, M. F., Cooper, C. S., & Comoglio, P. M. (1989). Tyrosine kinase receptor indistinguishable from the c-met protein. Nature, 339, 155–156.PubMedCrossRef
6.
Stoker, M., Gherardi, E., Perryman, M., & Gray, J. (1987). Scatter factor is a fibroblast-derived modulator of epithelial cell mobility. Nature, 327, 239–242.PubMedCrossRef
7.
Nakamura, T., Nishizawa, T., Hagiya, M., Seki, T., Shimonishi, M., Sugimura, A., et al. (1989). Molecular cloning and expression of human hepatocyte growth factor. Nature, 342, 440–443.PubMedCrossRef
8.
Zarnegar, R., & Michalopoulos, G. (1989). Purification and biological characterization of human hepatopoietin A, a polypeptide growth factor for hepatocytes. Cancer Research, 49, 3314–3320.PubMed
9.
10.
Weidner, K. M., Arakaki, N., Hartmann, G., Vandekerckhove, J., Weingart, S., Rieder, H., et al. (1991). Evidence for the identity of human scatter factor and human hepatocyte growth factor. Proceedings of the National Academy of Sciences of the United States of America, 88, 7001–7005.PubMedCrossRef
11.
Naldini, L., Vigna, E., Narsimhan, R. P., Gaudino, G., Zarnegar, R., Michalopoulos, G. K., et al. (1991). Hepatocyte growth factor (HGF) stimulates the tyrosine kinase activity of the receptor encoded by the proto-oncogene c-MET. Oncogene, 6, 501–504.PubMed
12.
Bottaro, D. P., Rubin, J. S., Faletto, D. L., Chan, A. M., Kmiecik, T. E., Vande Woude, G. F., et al. (1991). Identification of the hepatocyte growth factor receptor as the c-met proto-oncogene product. Science, 251, 802–804.PubMedCrossRef
13.
Comoglio, P. M. (2002). Trusolino L: Invasive growth: From development to metastasis. Journal of Clinical Investigation, 109, 857–862.PubMedCrossRef
14.
Montesano, R., Matsumoto, K., Nakamura, T., & Orci, L. (1991). Identification of a fibroblast-derived epithelial morphogen as hepatocyte growth factor. Cell, 67, 901–908.PubMedCrossRef
15.
Trusolino, L., & Comoglio, P. M. (2002). Scatter-factor and semaphorin receptors: Cell signalling for invasive growth. Nature Reviews Cancer, 2, 289–300.PubMedCrossRef
16.
Maina, F., Casagranda, F., Audero, E., Simeone, A., Comoglio, P. M., Klein, R., et al. (1996). Uncoupling of Grb2 from the Met receptor in vivo reveals complex roles in muscle development. Cell, 87, 531–542.PubMedCrossRef
17.
Ponzetto, C., Bardelli, A., Zhen, Z., Maina, F., Dalla, Z. P., Giordano, S., et al. (1994). A multifunctional docking site mediates signaling and transformation by the hepatocyte growth factor/scatter factor receptor family. Cell, 77, 261–271.PubMedCrossRef
18.
Zanetti, A., Stoppacciaro, A., Marzullo, A., Ciabatta, M., Fazioli, F., Prat, M., et al. (1998). Expression of Met protein and urokinase-type plasminogen activator receptor (uPA-R) in papillary carcinoma of the thyroid. Journal of Pathology, 186, 287–291.PubMedCrossRef
19.
Gaudino, G., Follenzi, A., Naldini, L., Collesi, C., Santoro, M., Gallo, K. A., et al. (1994). RON is a heterodimeric tyrosine kinase receptor activated by the HGF homologue MSP. European Molecular Biology Organization Journal, 13, 3524–3532.
20.
Huff, J. L., Jelinek, M. A., Borgman, C. A., Lansing, T. J., & Parsons, J. T. (1993). The protooncogene c-sea encodes a transmembrane protein-tyrosine kinase related to the Met/hepatocyte growth factor/scatter factor receptor. Proceedings of the National Academy of Sciences of the United States of America, 90, 6140–6144.PubMedCrossRef
21.
Birchmeier, C., Birchmeier, W., Gherardi, E., & Vande Woude, G. F. (2003). Met, metastasis, motility and more. Nature Reviews. Molecular Cell Biology, 4, 915–925.PubMedCrossRef
22.
Gandino, L., Longati, P., Medico, E., Prat, M., & Comoglio, P. M. (1994). Phosphorylation of serine 985 negatively regulates the hepatocyte growth factor receptor kinase. Journal of Biological Chemistry, 269, 1815–1820.PubMed
23.
Peschard, P., Fournier, T. M., Lamorte, L., Naujokas, M. A., Band, H., Langdon, W. Y., et al. (2001). Mutation of the c-Cbl TKB domain binding site on the Met receptor tyrosine kinase converts it into a transforming protein. Molecular Cell, 8, 995–1004.PubMedCrossRef
24.
Furge, K. A., Zhang, Y. W., & Vande Woude, G. F. (2000). Met receptor tyrosine kinase: Enhanced signaling through adapter proteins. Oncogene, 19, 5582–5589.PubMedCrossRef
25.
Pelicci, G., Giordano, S., Zhen, Z., Salcini, A. E., Lanfrancone, L., Bardelli, A., et al. (1995). The motogenic and mitogenic responses to HGF are amplified by the Shc adaptor protein. Oncogene, 10, 1631–1638.PubMed
26.
Weidner, K. M., Di, C. S., Sachs, M., Brinkmann, V., Behrens, J., & Birchmeier, W. (1996). Interaction between Gab1 and the c-Met receptor tyrosine kinase is responsible for epithelial morphogenesis. Nature, 384, 173–176.PubMedCrossRef
27.
Gual, P., Giordano, S., Anguissola, S., Parker, P. J., & Comoglio, P. M. (2001). Gab1 phosphorylation: A novel mechanism for negative regulation of HGF receptor signaling. Oncogene, 20, 156–166.PubMedCrossRef
28.
Gual, P., Giordano, S., Williams, T. A., Rocchi, S., Van, O. E., & Comoglio, P. M. (2000). Sustained recruitment of phospholipase C-gamma to Gab1 is required for HGF-induced branching tubulogenesis. Oncogene, 19, 1509–1518.PubMedCrossRef
29.
Maroun, C. R., Naujokas, M. A., Holgado-Madruga, M., Wong, A. J., & Park, M. (2000). The tyrosine phosphatase SHP-2 is required for sustained activation of extracellular signal-regulated kinase and epithelial morphogenesis downstream from the met receptor tyrosine kinase. Molecular Cell Biology, 20, 8513–8525.CrossRef
30.
Fournier, T. M., Kamikura, D., Teng, K., & Park, M. (1996). Branching tubulogenesis but not scatter of Madin–Darby canine kidney cells requires a functional Grb2 binding site in the Met receptor tyrosine kinase. Journal of Biological Chemistry, 271, 22211–22217.PubMedCrossRef
31.
O’brien, L. E., Tang, K., Kats, E. S., Schutz-Geschwender, A., Lipschutz, J. H., & Mostov, K. E. (2004). ERK and MMPs sequentially regulate distinct stages of epithelial tubule development. Developments in Cell, 7, 21–32.CrossRef
32.
Marshall, C. J. (1995). Specificity of receptor tyrosine kinase signaling: Transient versus sustained extracellular signal-regulated kinase activation. Cell, 80, 179–185.PubMedCrossRef
33.
Graziani, A., Gramaglia, D., Cantley, L. C., & Comoglio, P. M. (1991). The tyrosine-phosphorylated hepatocyte growth factor/scatter factor receptor associates with phosphatidylinositol 3-kinase. Journal of Biological Chemistry, 266, 22087–22090.PubMed
34.
Ponzetto, C., Bardelli, A., Maina, F., Longati, P., Panayotou, G., Dhand, R., et al. (1993). A novel recognition motif for phosphatidylinositol 3-kinase binding mediates its association with the hepatocyte growth factor/scatter factor receptor. Molecular Cell Biology, 13, 4600–4608.
35.
Royal, I., & Park, M. (1995). Hepatocyte growth factor-induced scatter of Madin–Darby canine kidney cells requires phosphatidylinositol 3-kinase. Journal of Biological Chemistry, 270, 27780–27787.PubMedCrossRef
36.
Trusolino, L., Cavassa, S., Angelini, P., Ando, M., Bertotti, A., Comoglio, P. M., et al. (2000). HGF/scatter factor selectively promotes cell invasion by increasing integrin avidity. FASEB Jounal, 14, 1629–1640.CrossRef
37.
Xiao, G. H., Jeffers, M., Bellacosa, A., Mitsuuchi, Y., Vande Woude, G. F., & Testa, J. R. (2001). Anti-apoptotic signaling by hepatocyte growth factor/Met via the phosphatidylinositol 3-kinase/Akt and mitogen-activated protein kinase pathways. Proceedings of the National Academy of Sciences of the United States of America, 98, 247–252.PubMedCrossRef
38.
Wells, C. M., Abo, A., & Ridley, A. J. (2002). PAK4 is activated via PI3K in HGF-stimulated epithelial cells. Journal of Cell Science, 115, 3947–3956.PubMedCrossRef
39.
Boccaccio, C., Ando, M., Tamagnone, L., Bardelli, A., Michieli, P., Battistini, C., et al. (1998). Induction of epithelial tubules by growth factor HGF depends on the STAT pathway. Nature, 391, 285–288.PubMedCrossRef
40.
Corso, S., Comoglio, P. M., & Giordano, S. (2005). Cancer therapy: Can the challenge be MET. Trends in Molecular Medicine, 11, 284–292.PubMedCrossRef
41.
Palka, H. L., Park, M., & Tonks, N. K. (2003). Hepatocyte growth factor receptor tyrosine kinase met is a substrate of the receptor protein-tyrosine phosphatase DEP-1. Journal of Biological Chemistry, 278, 5728–5735.PubMedCrossRef
42.
Sangwan, V., Paliouras, G. N., Cheng, A., Dube, N., Tremblay, M. L., & Park, M. (2006). Protein-tyrosine phosphatase 1B deficiency protects against Fas-induced hepatic failure. Journal of Biological Chemistry, 281, 221–228.PubMedCrossRef
43.
Machide, M., Hashigasako, A., Matsumoto, K., & Nakamura, T. (2006). Contact inhibition of hepatocyte growth regulated by functional association of the c-Met/hepatocyte growth factor receptor and LAR protein-tyrosine phosphatase. Journal of Biological Chemistry, 281, 8765–8772.PubMedCrossRef
44.
Birchmeier, C., & Gherardi, E. (1998). Developmental roles of HGF/SF and its receptor, the c-Met tyrosine kinase. Trends in Cell Biology, 8, 404–410.PubMedCrossRef
45.
Uehara, Y., Minowa, O., Mori, C., Shiota, K., Kuno, J., Noda, T., et al. (1995). Placental defect and embryonic lethality in mice lacking hepatocyte growth factor/scatter factor. Nature, 373, 702–705.PubMedCrossRef
46.
Bladt, F., Riethmacher, D., Isenmann, S., Aguzzi, A., & Birchmeier, C. (1995). Essential role for the c-Met receptor in the migration of myogenic precursor cells into the limb bud. Nature, 376, 768–771.PubMedCrossRef
47.
Schmidt, C., Bladt, F., Goedecke, S., Brinkmann, V., Zschiesche, W., Sharpe, M., et al. (1995). Scatter factor/hepatocyte growth factor is essential for liver development. Nature, 373, 699–702.PubMedCrossRef
48.
Maina, F., Pante, G., Helmbacher, F., Andres, R., Porthin, A., Davies, A. M., et al. (2001). Coupling Met to specific pathways results in distinct developmental outcomes. Molecular Cell, 7, 1293–1306.PubMedCrossRef
49.
Huh, C. G., Factor, V. M., Sanchez, A., Uchida, K., Conner, E. A., & Thorgeirsson, S. S. (2004). Hepatocyte growth factor/c-met signaling pathway is required for efficient liver regeneration and repair. Proceedings of the National Academy of Sciences of the United States of America, 101, 4477–4482.PubMedCrossRef
50.
Chmielowiec, J., Borowiak, M., Morkel, M., Stradal, T., Munz, B., Werner, S., et al. (2007). c-Met is essential for wound healing in the skin. Journal of Cell Biology, 177, 151–162.PubMedCrossRef
51.
Bussolino, F., Di Renzo, M. F., Ziche, M., Bocchietto, E., Olivero, M., Naldini, L., et al. (1992). Hepatocyte growth factor is a potent angiogenic factor which stimulates endothelial cell motility and growth. Journal of Cell Biology, 119, 629–641.PubMedCrossRef
52.
Boccaccio, C., Sabatino, G., Medico, E., Girolami, F., Follenzi, A., Reato, G., et al. (2005). The MET oncogene drives a genetic programme linking cancer to haemostasis. Nature, 434, 396–400.PubMedCrossRef
53.
Boccaccio, C., & Medico, E. (2006). Cancer and blood coagulation. Cellular and Molecular Life Sciences, 63, 1024–1027.PubMedCrossRef
54.
Rickles, F. R., & Levine, M. N. (2001). Epidemiology of thrombosis in cancer. Acta Haematologica, 106, 6–12.PubMedCrossRef
55.
Rong, S., Segal, S., Anver, M., Resau, J. H., & Vande Woude, G. F. (1994). Invasiveness and metastasis of NIH 3T3 cells induced by Met-hepatocyte growth factor/scatter factor autocrine stimulation. Proceedings of the National Academy of Sciences of the United States of America, 91, 4731–4735.PubMedCrossRef
56.
Taulli, R., Scuoppo, C., Bersani, F., Accornero, P., Forni, P. E., Miretti, S., et al. (2006). Validation of Met as a therapeutic target in alveolar and embryonal rhabdomyosarcoma. Cancer Research, 66, 4742–4749.PubMedCrossRef
57.
Lutterbach, B., Zeng, Q., Davis, L. J., Hatch, H., Hang, G., Kohl, N. E., et al. (2007). Lung cancer cell lines harboring MET gene amplification are dependent on Met for growth and survival. Cancer Research, 67, 2081–2088.PubMedCrossRef
58.
Takayama, H., LaRochelle, W. J., Sharp, R., Otsuka, T., Kriebel, P., Anver, M., et al. (1997). Diverse tumorigenesis associated with aberrant development in mice overexpressing hepatocyte growth factor/scatter factor. Proceedings of the National Academy of Sciences of the United States of America, 94, 701–706.PubMedCrossRef
59.
Wang, R., Ferrell, L. D., Faouzi, S., Maher, J. J., & Bishop, J. M. (2001). Activation of the Met receptor by cell attachment induces and sustains hepatocellular carcinomas in transgenic mice. Journal of Cell Biology, 153, 1023–1034.PubMedCrossRef
60.
Schmidt, L., Junker, K., Nakaigawa, N., Kinjerski, T., Weirich, G., Miller, M., et al. (1999). Novel mutations of the MET proto-oncogene in papillary renal carcinomas. Oncogene, 18, 2343–2350.PubMedCrossRef
61.
Ferracini, R., Di Renzo, M. F., Scotlandi, K., Baldini, N., Olivero, M., Lollini, P., et al. (1995). The Met/HGF receptor is over-expressed in human osteosarcomas and is activated by either a paracrine or an autocrine circuit. Oncogene, 10, 739–749.PubMed
62.
Ferracini, R., Olivero, M., Di Renzo, M. F., Martano, M., De, G. C., Nanni, P., et al. (1996). Retrogenic expression of the MET proto-oncogene correlates with the invasive phenotype of human rhabdomyosarcomas. Oncogene, 12, 1697–1705.PubMed
63.
Tuck, A. B., Park, M., Sterns, E. E., Boag, A., & Elliott, B. E. (1996). Coexpression of hepatocyte growth factor and receptor (Met) in human breast carcinoma. American Journal of Pathology, 148, 225–232.PubMed
64.
Koochekpour, S., Jeffers, M., Rulong, S., Taylor, G., Klineberg, E., Hudson, E. A., et al. (1997). Met and hepatocyte growth factor/scatter factor expression in human gliomas. Cancer Research, 57, 5391–5398.PubMed
65.
Kijima, Y., Hokita, S., Yoshinaka, H., Itoh, T., Koriyama, C., Eizuru, Y., et al. (2002). Amplification and overexpression of c-met gene in Epstein–Barr virus-associated gastric carcinomas. Oncology, 62, 60–65.PubMedCrossRef
66.
Nakazawa, K., Dobashi, Y., Suzuki, S., Fujii, H., Takeda, Y., & Ooi, A. (2005). Amplification and overexpression of c-erbB-2, epidermal growth factor receptor, and c-Met in biliary tract cancers. Journal of Pathology, 206, 356–365.PubMedCrossRef
67.
Engelman, J. A., Zejnullahu, K., Mitsudomi, T., Song, Y., Hyland, C., Park, J. O., et al. (2007). MET amplification leads to gefitinib resistance in lung cancer by activating ERBB3 signaling. Science, 316, 1039–1043.PubMedCrossRef
68.
Christensen, J. G., Burrows, J., & Salgia, R. (2005). c-Met as a target for human cancer and characterization of inhibitors for therapeutic intervention. Cancer Letters, 225, 1–26.PubMedCrossRef
69.
Di Renzo, M. F., Olivero, M., Martone, T., Maffe, A., Maggiora, P., Stefani, A. D., et al. (2000). Somatic mutations of the MET oncogene are selected during metastatic spread of human HNSC carcinomas. Oncogene, 19, 1547–1555.PubMedCrossRef
70.
Ivan, M., Bond, J. A., Prat, M., Comoglio, P. M., & Wynford-Thomas, D. (1997). Activated Ras and Ret oncogenes induce over-expression of c-Met (hepatocyte growth factor receptor) in human thyroid epithelial cells. Oncogene, 14, 2417–2423.PubMedCrossRef
71.
Shirasaki, F., Makhluf, H. A., LeRoy, C., Watson, D. K., & Trojanowska, M. (1999). Ets transcription factors cooperate with Sp1 to activate the human tenascin-C promoter. Oncogene, 18, 7755–7764.PubMedCrossRef
72.
Gambarotta, G., Boccaccio, C., Giordano, S., Ando, M., Stella, M. C., & Comoglio, P. M. (1996). Ets up-regulates MET transcription. Oncogene, 13, 1911–1917.PubMed
73.
Pennacchietti, S., Michieli, P., Galluzzo, M., Mazzone, M., Giordano, S., & Comoglio, P. M. (2003). Hypoxia promotes invasive growth by transcriptional activation of the Met protooncogene. Cancer Cell, 3, 347–361.PubMedCrossRef
74.
Morotti, A., Mila, S., Accornero, P., Tagliabue, E., & Ponzetto, C. (2002). K252a inhibits the oncogenic properties of Met, the HGF receptor. Oncogene, 21, 4885–4893.PubMedCrossRef
75.
Berthou, S., Aebersold, D. M., Schmidt, L. S., Stroka, D., Heigl, C., Streit, B., et al. (2004). The Met kinase inhibitor SU11274 exhibits a selective inhibition pattern toward different receptor mutated variants. Oncogene, 23, 5387–5393.PubMedCrossRef
76.
Christensen, J. G., Schreck, R., Burrows, J., Kuruganti, P., Chan, E., Le, P., et al. (2003). A selective small molecule inhibitor of c-Met kinase inhibits c-Met-dependent phenotypes in vitro and exhibits cytoreductive antitumor activity in vivo. Cancer Research, 63, 7345–7355.PubMed
77.
Smolen, G. A., Sordella, R., Muir, B., Mohapatra, G., Barmettler, A., Archibald, H., et al. (2006). Amplification of MET may identify a subset of cancers with extreme sensitivity to the selective tyrosine kinase inhibitor PHA-665752. Proceedings of the National Academy of Sciences of the United States of America, 103, 2316–2321.PubMedCrossRef
78.
Date, K., Matsumoto, K., Kuba, K., Shimura, H., Tanaka, M., & Nakamura, T. (1998). Inhibition of tumor growth and invasion by a four-kringle antagonist (HGF/NK4) for hepatocyte growth factor. Oncogene, 17, 3045–3054.PubMedCrossRef
79.
Matsumoto, K., & Nakamura, T. (2003). NK4 (HGF-antagonist/angiogenesis inhibitor) in cancer biology and therapeutics. Cancer Science, 94, 321–327.PubMedCrossRef
80.
Cao, B., Su, Y., Oskarsson, M., Zhao, P., Kort, E. J., Fisher, R. J., et al. (2001). Neutralizing monoclonal antibodies to hepatocyte growth factor/scatter factor (HGF/SF) display antitumor activity in animal models. Proceedings of the National Academy of Sciences of the United States of America, 98, 7443–7448.PubMedCrossRef
81.
Burgess, T., Coxon, A., Meyer, S., Sun, J., Rex, K., Tsuruda, T., et al. (2006). Fully human monoclonal antibodies to hepatocyte growth factor with therapeutic potential against hepatocyte growth factor/c-Met-dependent human tumors. Cancer Research, 66, 1721–1729.PubMedCrossRef
82.
Mazzone, M., Basilico, C., Cavassa, S., Pennacchietti, S., Risio, M., Naldini, L., et al. (2004). An uncleavable form of pro-scatter factor suppresses tumor growth and dissemination in mice. Journal of Clinical Investigation, 114, 1418–1432.PubMedCrossRef
83.
Michieli, P., Mazzone, M., Basilico, C., Cavassa, S., Sottile, A., Naldini, L., et al. (2004). Targeting the tumor and its microenvironment by a dual-function decoy Met receptor. Cancer Cell, 6, 61–73.PubMedCrossRef
84.
Kong-Beltran, M., Stamos, J., & Wickramasinghe, D. (2004). The Sema domain of Met is necessary for receptor dimerization and activation. Cancer Cell, 6, 75–84.PubMedCrossRef
85.
Petrelli, A., Circosta, P., Granziero, L., Mazzone, M., Pisacane, A., Fenoglio, S., et al. (2006). Ab-induced ectodomain shedding mediates hepatocyte growth factor receptor down-regulation and hampers biological activity. Proceedings of the National Academy of Sciences of the United States of America, 103, 5090–5095.PubMedCrossRef
86.
Corso, S., Migliore, C., Ghiso, E., De Rosa, G., Comoglio, P. M., & Giordano, S. (2007). Silencing the MET oncogene leads to regression of experimental tumors and metastases. Oncogene (in press). DOI 10.​1038/​sj.​onc.​1210697.
Metadaten
Titel
The Met tyrosine kinase receptor in development and cancer
verfasst von
Alessandra Gentile
Livio Trusolino
Paolo M. Comoglio
Publikationsdatum
01.03.2008
Verlag
Springer US
Erschienen in
Cancer and Metastasis Reviews / Ausgabe 1/2008
Print ISSN: 0167-7659
Elektronische ISSN: 1573-7233
DOI
https://doi.org/10.1007/s10555-007-9107-6

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