MTAP [MD166R]

The S-methyl-5′-thioadenosine phosphorylase (MTAP) metabolizes methylthioadenosine (MTA), a byproduct of polyamine synthesis and regulator of protein methylation, to salvage adenine and methionine residues for reuse in many pathways affecting cell proliferation, signaling, and apoptosis. The MTAP gene, located at 9p12.3, is co-deleted with CDKN2A (encodes p16 tumor-suppressor) in several types of cancer and is abundant in all normal tissues but is deficient in various tumors. The gene encoding MTAP is linked to the tumor suppressor gene, p16INK4A. Deficient levels of MTAP can occur in cancers, primarily through co-deletion of the MTAP gene and the p16INK4A gene. Studies show that the frequency of MTAP deficiency was found to be relatively high in NSCLC abd MTAP represents a highly promising immunohistochemical marker for prognosis and interferon response of patients with malignant melanoma. Overexpression of MTAP is also associated with increased proliferation and epithelial-to-mesenchymal transition in Colorectal Carcinoma. A combination of MTAP antibody or BAP1 antibody loss may likely detect malignant pleural mesothelioma (MPM) with good sensitivity and 100% specificity, and help discriminate MPM from reactive mesothelial hyperplasia (RMH).