The met oncogene is the normal counterpart of a chemically-induced transforming gene. The chromosomal localization of met is 7q21-31. In a patient with myelofibrosis and an interstitial deletion on 7q, we demonstrate that a Taq I polymorphism for the met oncogene is lost in the neoplastic cells, thus indicating that the deletion occuring in the long arm of chromosome 7 involves the met locus.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1007/BF00351120 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
MET Activation in Lung Cancer and Response to Targeted Therapies.
Cancers (Basel)
January 2025
Integrative Oncology, BC Cancer Research Institute, Vancouver, BC V5Z 1L3, Canada.
The hepatocyte growth factor receptor (MET) is a receptor tyrosine kinase (RTK) that mediates the activity of a variety of downstream pathways upon its activation. These pathways regulate various physiological processes within the cell, including growth, survival, proliferation, and motility. Under normal physiological conditions, this allows MET to regulate various development and regenerative processes; however, mutations resulting in aberrant MET activity and the consequent dysregulation of downstream signaling can contribute to cellular pathophysiology.
View Article and Find Full Text PDFExploring practical experience with different treatments in NSCLC patients with MET-deregulated: a retrospective analysis from the real world.
BMC Pulm Med
January 2025
Department of Medical Oncology, The Affiliated Cancer Hospital of Zhengzhou University & Henan Cancer Hospital, 127 Dong Ming Road, Zhengzhou, 450008, China.
Background: Mesenchymal to epithelial transition factor (MET) dysregulation in non-small-cell-lung-cancer (NSCLC) is understudied, with scant data on treatment outcomes.
Methods: We retrospectively examined 160 NSCLC patients: 125 with primary MET mutations (further classified into MET exon 14 (METex14) skipping mutations and primary MET amplifications) and 35 with secondary MET amplifications. Patients underwent varied treatments: Chemotherapy, Immune monotherapy, Crizotinib, or Savolitinib.
Targeting HGF/c-MET signaling to regulate the tumor microenvironment: Implications for counteracting tumor immune evasion.
Cell Commun Signal
January 2025
Department of Oncology, The First Affiliated Hospital of Nanchang University, 17 Yongwaizheng Street, Nanchang, Jiangxi Province, 330006, China.
The hepatocyte growth factor (HGF) along with its receptor (c-MET) are crucial in preserving standard cellular physiological activities, and imbalances in the c-MET signaling pathway can lead to the development and advancement of tumors. It has been extensively demonstrated that immune checkpoint inhibitors (ICIs) can result in prolonged remission in certain patients. Nevertheless, numerous preclinical studies have shown that MET imbalance hinders the effectiveness of anti-PD-1/PD-L1 treatments through various mechanisms.
View Article and Find Full Text PDFCD36 enrichment in HER2-positive mesenchymal stem cells drives therapy refractoriness in breast cancer.
J Exp Clin Cancer Res
January 2025
Microenvironment and Biomarkers of Solid Tumors Unit, Department of Experimental Oncology, Amadeolab Fondazione IRCCS Istituto Nazionale Dei Tumori Di Milano, Milan, Italy.
Background: Growing evidence shows that the reprogramming of fatty acid (FA) metabolism plays a key role in HER2-positive (HER2 +) breast cancer (BC) aggressiveness, therapy resistance and cancer stemness. In particular, HER2 + BC has been defined as a "lipogenic disease" due to the functional and bi-directional crosstalk occurring between HER2-mediated oncogenic signaling and FA biosynthesis via FA synthase activity. In this context, the functional role exerted by the reprogramming of CD36-mediated FA uptake in HER2 + BC poor prognosis and therapy resistance remains unclear.
View Article and Find Full Text PDFThe endonuclease activity of MCPIP1 controls the neoplastic transformation of epithelial cells via the c-Met/CD44 axis.
Cell Commun Signal
January 2025
Department of General Biochemistry, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University, Krakow, Poland.
The RNase activity of MCPIP1 is essential for regulating cellular homeostasis, proliferation, and tumorigenesis. Our study elucidates the effects of downregulation of MCPIP1 expression and an RNase-inactivating mutation (D141N) on normal epithelial kidney cells, indicating that MCPIP1 expression is a key factor that suppresses neoplastic transformation. We observed that either expression downregulation or mutation of MCPIP1 significantly increased its clonogenicity and altered the expression of cancer stem cell (CSC) markers and factors involved in epithelial-to-mesenchymal transition (EMT).
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!