MET deregulation in breast cancer.

Area of Science:

• Oncology
• Molecular Biology
• Cancer Research

Background:

• Mesenchymal-epithelial transition (MET) is a receptor tyrosine kinase crucial for development and tissue homeostasis.
• Deregulation of the HGF/MET pathway, through amplification, mutation, or overexpression, drives cancer progression, invasion, and metastasis.
• In breast cancer (BC), HGF/MET signaling is implicated in carcinogenesis, progression, and resistance to therapies.

Purpose of the Study:

• To review and analyze published data on the role of HGF/MET signaling in breast cancer.
• To evaluate MET as a potential therapeutic target in various breast cancer subtypes.
• To assess the involvement of MET in resistance mechanisms to targeted therapies.

Main Methods:

• A comprehensive literature search and analysis of all published data concerning HGF/MET in breast cancer.
• Evaluation of prognostic significance of MET in early-stage BC.
• Review of preclinical and clinical evidence supporting MET as a therapeutic target.

Main Results:

• MET overexpression in early BC is an independent negative prognostic indicator across BC subtypes.
• MET is identified as a relevant therapeutic target, particularly in basal-like (BL) and triple-negative BC.
• MET deregulation is critically involved in the development of resistance to targeted agents, including anti-HER2 therapies.

Conclusions:

• MET represents a promising therapeutic target for breast cancer treatment.
• Several anti-MET agents are currently under investigation.
• Ongoing clinical trials are expected to define the clinical relevance of MET inhibition in BC management.