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Type I MET inhibitors cooperate with PD-1 blockade to promote rejection of hepatocellular carcinoma.
J Immunother Cancer
October 2024
Department of Immunology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA
Blockade of the immune checkpoints programmed death-1 (PD-1) and cytotoxic lymphocyte antigen 4 has improved outcomes for patients with hepatocellular carcinoma (HCC), yet most still fail to achieve objective clinical benefit. MET plays key roles in both HCC tumorigenesis and immunosuppressive conditioning; however, inhibition of MET causes upregulation of PD-ligand 1 (PD-L1) suggesting the use of these inhibitors in the context of PD-1 blockade. We sought to investigate across the Hepa1-6, HCA-1 and diethylnitrosamine (DEN) models of HCC whether the combination of more specific type I versus more pleiotropic type II MET inhibitors would confer superior outcomes in combination with PD-1 blockade.
View Article and Find Full Text PDFTargeted and cytotoxic inhibitors used in the treatment of lung cancers.
Pharmacol Res
November 2024
Blue Ridge Institute for Medical Research, 221 Haywood Knolls Drive, Hendersonville, NC 28791, United States. Electronic address:
Article Synopsis
- * Stage I/II NSCLC is typically treated with surgery, while other treatments like chemoradiotherapy, immune checkpoint inhibitors, and specific targeted therapies are available for various mutations present in NSCLC cases.
- * SCLC, representing about 15% of lung cancer, has a poor prognosis; treatment for extensive-stage SCLC involves a combination of platinum-based chemotherapy and anti-PDL1 inhibitors.
Functional interaction between receptor tyrosine kinase MET and ETS transcription factors promotes prostate cancer progression.
Mol Oncol
October 2024
UMR9020 - UMR1277 - Canther - Cancer Heterogeneity, Plasticity and Resistance to Therapies, Institut Pasteur de Lille, Univ. Lille, CNRS, Inserm, CHU Lille, France.
Prostate cancer, the most common malignancy in men, has a relatively favourable prognosis. However, when it spreads to the bone, the survival rate drops dramatically. The development of bone metastases leaves patients with aggressive prostate cancer, the leading cause of death in men.
View Article and Find Full Text PDFArticle Synopsis
- Cancer-associated fibroblasts (CAFs) promote tumor growth and alter cancer cells' response to drugs, especially in non-small cell lung cancer (NSCLC) treated with ALK tyrosine kinase inhibitors (TKIs).
- Research identified HGF-MET signaling and the fibronectin-integrin pathway as key mechanisms in CAF-mediated drug resistance, with integrin β1 activation in cancer cells found through flow cytometry.
- Combining MET and integrin inhibitors with ALK TKIs showed greater anti-tumor effects in mouse models, highlighting the need for targeting multiple signaling pathways to improve cancer treatment outcomes.
Current Trial Report: A Multicenter Phase I/Ib study of Capmatinib Plus Trametinib in Patients With Metastatic Nonsmall Cell Lung Center Harboring MET Exon 14 Skipping Mutations and Other MET-Alterations.
Clin Lung Cancer
December 2024
University of California San Francisco Helen Diller Comprehensive Cancer Center, San Francisco, CA, USA. Electronic address:
Introduction: MET tyrosine kinase inhibitor (TKI) therapy is associated with improved outcomes in patients with nonsmall cell lung cancer (NSCLC) harboring a MET alteration, including MET exon 14 (METex14) skipping mutation, MET amplification, or MET fusion. However, primary or acquired resistance to TKI therapy ultimately develops. In preclinical models, hyperactivation of MAPK signaling was shown to promote resistance to MET TKI; resistance was overcome by co-treatment with a MET inhibitor and a MEK inhibitor.
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