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Table representation of search results timeline featuring number of search results per year.

Year Number of Results
1995 1
1996 1
1997 19
1998 37
1999 54
2000 67
2001 55
2002 40
2003 39
2004 50
2005 40
2006 51
2007 45
2008 54
2009 69
2010 89
2011 132
2012 130
2013 189
2014 188
2015 246
2016 202
2017 193
2018 159
2019 72
2020 3
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1,969 results
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Page 1
Pathogenic Germline Variants in 10,389 Adult Cancers
Huang KL, et al. Cell 2018. PMID 29625052 Free PMC article.
We also discovered 33 such variants in oncogenes, including missenses in MET, RET, and PTPN11 associated with high gene expression. ...
We also discovered 33 such variants in oncogenes, including missenses in MET, RET, and PTPN11 associated with high gene expression. . …
ABBV-399, a c-Met Antibody-Drug Conjugate that Targets Both MET-Amplified and c-Met-Overexpressing Tumors, Irrespective of MET Pathway Dependence.
Wang J, et al. Clin Cancer Res 2017. PMID 27573171 Free article.
Purpose: Despite the importance of the MET oncogene in many malignancies, clinical strategies targeting c-Met have benefitted only small subsets of patients with tumors driven by signaling through the c-Met pathway, thereby necessitating selection of patients with MET amplification and/or c-Met activation most likely to respond. ...Antitumor activity was evaluated in cancer cells with overexpressed c-Met or amplified MET and in xenografts including patient-derived xenograft (PDX) models and those refractory to other c-Met inhibitors. ...
Purpose: Despite the importance of the MET oncogene in many malignancies, clinical strategies targeting c-Met ha …
Known and novel roles of the MET oncogene in cancer: a coherent approach to targeted therapy.
Comoglio PM, et al. Nat Rev Cancer 2018 - Review. PMID 29674709 Free article.
The MET oncogene encodes an unconventional receptor tyrosine kinase with pleiotropic functions: it initiates and sustains neoplastic transformation when genetically altered ('oncogene addiction') and fosters cancer cell survival and tumour dissemination when transcriptionally activated in the context of an adaptive response to adverse microenvironmental conditions ('oncogene expedience'). Moreover, MET is an intrinsic modulator of the self-renewal and clonogenic ability of cancer stem cells ('oncogene inherence'). ...
The MET oncogene encodes an unconventional receptor tyrosine kinase with pleiotropic functions: it initiates and sustains neop …
HGF/c-MET: A Promising Therapeutic Target in the Digestive System Cancers.
Zhang H, et al. Int J Mol Sci 2018 - Review. PMID 30360560 Free PMC article.
The HGF/c-MET pathway is active in the development of digestive system cancers, indicating that inhibition of HGF/c-MET signaling may have therapeutic potential. Various HGF/c-MET signaling inhibitors, mainly c-MET inhibitors, have been tested in clinical trials. The observed efficacy and adverse events of some c-MET inhibitors were not very suitable for treating digestive system cancers. ...
The HGF/c-MET pathway is active in the development of digestive system cancers, indicating that inhibition of HGF/c- …
MET in Lung Cancer: Biomarker Selection Based on Scientific Rationale.
Salgia R. Mol Cancer Ther 2017 - Review. PMID 28373408 Free article.
These include MET or HGF protein overexpression, MET gene amplification, MET gene mutation or fusion/rearrangement, or aberrations in downstream signaling or regulatory components. Responses to MET tyrosine kinase inhibitors have been documented in clinical trials in patients with MET-amplified or MET-overexpressing NSCLC, and case studies or case series have shown that MET mutation/deletion is a biomarker that is also predictive of response to these agents. ...
These include MET or HGF protein overexpression, MET gene amplification, MET gene mutation or fusion/rearrangement, or …
Fishing wild-type sparing inhibitors of proto-oncogene c-met variants in renal cell carcinoma from a curated tyrosine kinase inhibitor pool using analog-sensitive kinase technology.
Wang Z, et al. Biochimie 2018. PMID 30017898
A variety of missense mutations in proto-oncogene protein tyrosine kinase c-Met have been clinically observed in the patients and families of papillary renal cell carcinoma (pRCC), imparting that the kinase mutations can be exploited as a new and potential therapeutic target for pRCC. ...The type II inhibitor Nintedanib possesses a high selectivity (7.2-fold) for c-Met(Y1248H) variant over wild type. Structural and energetic analysis revealed that the Y1248H mutation is located in kinase's activation loop which can directly contact the extended moiety of type II inhibitor. ...
A variety of missense mutations in proto-oncogene protein tyrosine kinase c-Met have been clinically observed in …
Activation of MET via diverse exon 14 splicing alterations occurs in multiple tumor types and confers clinical sensitivity to MET inhibitors.
Frampton GM, et al. Cancer Discov 2015. PMID 25971938 Free article.
Focal amplification and activating point mutation of the MET gene are well-characterized oncogenic drivers that confer susceptibility to targeted MET inhibitors. Recurrent somatic splice site alterations at MET exon 14 (METex14) that result in exon skipping and MET activation have been characterized, but their full diversity and prevalence across tumor types are unknown. ...
Focal amplification and activating point mutation of the MET gene are well-characterized oncogenic drivers that confer susceptibility …
MET in glioma: signaling pathways and targeted therapies.
Cheng F and Guo D. J Exp Clin Cancer Res 2019 - Review. PMID 31221203 Free PMC article.
Mutations in MET, as well as the dysregulation of other regulators of cross-talk with MET signaling pathways, have also been identified. ...In this review, we highlight progress made in the understanding of MET signaling in glioma and advances in therapies targeting HGF/MET molecules for glioma patients in recent years, in addition to studies on the expression and mutation status of MET....
Mutations in MET, as well as the dysregulation of other regulators of cross-talk with MET signaling pathways, have also been i …
Regulation of the c-met proto-oncogene promoter by p53.
Seol DW, et al. J Biol Chem 1999. PMID 9920903 Free article.
Cotransfection of various c-met promoter reporter vectors with p53 expression plasmids demonstrated that only wild-type p53 but not tumor-derived mutant forms of p53 resulted in a significant enhancement of c-met promoter activity. ...These results suggest that the c-met gene is also a target of p53 gene regulation....
Cotransfection of various c-met promoter reporter vectors with p53 expression plasmids demonstrated that only wild-type p53 bu …
MET Exon 14 Skipping in Non-Small Cell Lung Cancer.
Heist RS, et al. Oncologist 2016. PMID 27022036 Free PMC article.
A clinical case of a patient with MET exon 14 skipping treated with the MET inhibitor crizotinib is also described. CONCLUSION: MET exon 14 skipping is a targetable gene alteration found in NSCLC. ...Patients whose cancers have MET exon 14 skipping can respond well to MET inhibitors. Molecular testing for MET exon 14 skipping should be performed on all lung cancers because this is a targetable alteration....
A clinical case of a patient with MET exon 14 skipping treated with the MET inhibitor crizotinib is also described. CONCLUSION …
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