Targeting MET in Lung Cancer: Will Expectations Finally Be MET?
نویسندگان
چکیده
منابع مشابه
Targeting MET in Lung Cancer: Will Expectations Finally Be MET?
The hepatocyte growth factor receptor (MET) is a potential therapeutic target in a number of cancers, including NSCLC. In NSCLC, MET pathway activation is thought to occur through a diverse set of mechanisms that influence properties affecting cancer cell survival, growth, and invasiveness. Preclinical and clinical evidence suggests a role for MET activation as both a primary oncogenic driver i...
متن کاملMet in lung cancer
Receptor tyrosine kinases play important roles in the biology of many tumor cell types. In approximately 10% of non-small cell lung cancer (NSCLC) patients mutational activation of the epidermal growth factor receptor (EGFR) results in tumor cells that are exquisitely addicted to signaling by this receptor. (1) Thus expression of mutant active EGFR but in general not wild-type EGFR predisposes ...
متن کاملBreast Cancer Prevention: Can Women’s Expectations Be Met?
The recent publication of a landmark paper on cancer etiology byCristianTomasetti andBert Vogelstein in the journal Science instantly generated a great amount of media interest in how and why cancer arises and fueled similar discussions in the scientific community [1]. The key message of the paper, that most types of cancer are due to bad luck rather than lifestyle or genes, is likely responsib...
متن کاملTargeting MET in cancer therapy
MET encodes a receptor tyrosine kinase c-MET for hepatocyte growth factor (HGF). The specific combination of c-MET and HGF activates downstream signaling pathways to trigger cell migration, proliferation, and angiogenesis. MET exon 14 alterations and MET gene amplification play a critical role in the origin of cancer. Several monoclonal antibodies and small-molecule inhibitors of c-MET have bee...
متن کاملTargeting MET in Cancer: Obstacles and Potentials
MET is a tyrosine kinase receptor involved in cell proliferation, survival, and migration. MET pathway is activated in cancer by gene amplification and overexpression, ligand overexpression and autocrine/paracrine activation, and activating MET mutations. MET dysregulation is also found to be responsible for resistance to treatment and targeted therapy including EGFR TKIs for NSCLC. Preclinical...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
ژورنال
عنوان ژورنال: Journal of Thoracic Oncology
سال: 2017
ISSN: 1556-0864
DOI: 10.1016/j.jtho.2016.10.014