Cancer cells, namely squamous cell carcinomas of the head and neck, colorectal cancer (CRC), glioblastoma, and non-small cell lung cancer (NSCLC), express RTKs such as EGFR and c-Met. However, RTKs on tumor cells have altered functions due to mutations or overexpression, which can result in increased activation and tumorigenesis. Inhibition of these altered tyrosine kinases has become a therapeutic strategy for patients with tumors that overexpress these receptors or contain mutated forms of these RTKs. Inhibition methods and therapeutic options include molecules that inhibit tyrosine kinase activity, and monoclonal antibodies (MAbs) that interfere with ligand binding to RTKs. MAbs, such as cetuximab (EGFR inhibitor), and small molecule tyrosine kinase inhibitors (TKIs), such as gefitinib, erlotinib (EGFR inhibitors) and crizotinib (c-Met/ALK/ROS1 inhibitor), are currently used for NSCLC therapy and have shown great promise in improving prognosis of several other forms of cancer. Neelu Puri, EGFR and c-Met Inhibitors are Effective in Reducing Tumorigenicity in Cancer
Last date updated on April, 2024