EMTome
EMTome enables pan-cancer analysis of epithelial-mesenchymal transition (EMT) genes and signatures to investigate molecular drivers of metastatic progression and prognostic markers such as FGFR1, β3 integrin, and FAK.
Key Features:
- Pan-Cancer Analysis: Performs comparative analysis of EMT-related genes and pathways across multiple cancer types.
- EMT Signature Identification: Detects and catalogs molecular signatures associated with epithelial-mesenchymal transition.
- Predictive Molecular Signatures: Identifies prognostic markers including FGFR1, β3 integrin, and FAK correlated with patient survival in subtypes such as basal-like breast cancer.
- Mechanistic Data Integration: Integrates mechanistic findings on β3 integrin, FGFR1, FGF2 signaling, and FAK activity into analyses.
- Clinical Correlation Analyses: Supports correlation of molecular signatures with clinical outcomes and prognostic assessment.
- Preclinical Inhibitor Evaluation: Incorporates data relevant to evaluation of inhibitors such as FIIN-4 in preclinical contexts.
Scientific Applications:
- Metastatic Research: Investigates how EMT-associated genes contribute to acquisition of metastatic capabilities.
- Therapeutic Targeting: Supports identification of EMT program components, such as FGFR1 and β3 integrin, as potential therapeutic targets.
- Drug Development: Facilitates evaluation of candidate therapeutics, exemplified by FIIN-4, that disrupt EMT-related signaling pathways.
- Mechanistic Studies: Enables exploration of interactions among β3 integrin, FGFR1, E-cadherin, and downstream signaling in cancer cell behavior.
- Clinical Correlation: Allows association of EMT signatures with clinical outcomes to inform prognostic marker development.
- Preclinical Testing: Assists assessment of inhibitor efficacy and mechanistic impact in preclinical models.
Methodology:
Leverages and integrates published study data, incorporating mechanistic findings that β3 integrin alters FGFR1 subcellular localization to enhance FGF2 signaling and 3D outgrowth, and integrates findings on FAK enzymatic activity.
Topics
Details
- Added:
- 1/18/2021
- Last Updated:
- 11/24/2024
Operations
Publications
Brown WS, Tan L, Smith A, Gray NS, Wendt MK. Covalent Targeting of Fibroblast Growth Factor Receptor Inhibits Metastatic Breast Cancer. Molecular Cancer Therapeutics. 2016;15(9):2096-2106. doi:10.1158/1535-7163.mct-16-0136. PMID:27371729. PMCID:PMC5010989.