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- Biological Pathways
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- Cancer Biomarkers
- Breast Cancer
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- HER1/EGFR in pancreatic cancer
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- Receptor activation
- Dimerization
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- HER1/EGFR and prognosis
- HER1/EGFR as a therapeutic target
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- HER1/EGFR in lung cancer
- HER1/EGFR in pancreatic cancer
- HER2 dysregulation
- HER2:HER3 dimer
- HER2 and prognosis
- HER2 detection methods
- HER2 as a therapeutic target
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- HER2 in ovarian cancer
- HER3 dysregulation
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- HER3 evaluation
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What is Met?
Met is a cell surface receptor tyrosine kinase (RTK) first discovered as a translocation product in a cancer cell line treated with a mutagen.1-3 Hepatocyte growth factor/scatter factor (HGF/SF) is the only known high affinity Met ligand; HGF/SF promotes hepatocyte proliferation and epithelial cell motility.1,3-5
HGF/SF binding to Met stimulates receptor dimerization and activates Met signaling.1-3 Once activated, the Met kinase domain mediates signaling through adaptor proteins and other signaling proteins.1,4,5
Met signaling promotes activation of cellular signaling pathways that may lead to cell proliferation, modification of cell-cell adhesion, cell survival in response to environmental or therapeutic stress and induction of motility and invasion.1,4,6
Met and its ligand HGF/SF are frequently overexpressed in a variety of human cancers.1,6
References:
- 1.
- Gherardi E, et al. Nature Rev Cancer. 2008;14:6171-6180. PMID: 22270953
- 2.
- Cooper C, et al. Nature. 1984;311(5981):29-33. PMID: 6590967
- 3.
- Peschard P, Park M. Oncogene.2007;26:1276-1285. PMID: 17322912
- 4.
- Trusolino L, et al. Nature Rev Mol Cell Biol. 2010;11:834-848. PMID: 21102609
- 5.
- Liu X, et al. Trends in Mol Med. 2010;16(1):37-45. PMID: 20031486
- 6.
- Birchmeier C, et al. Nature Rev Mol Cell Biol. 2003;4:915-925. PMID: 14685170