2026-04-14T02:32:31Zhttps://recercat.cat/oai/request

oai:recercat.cat:2445/1535582025-12-05T09:21:26Zcom_2072_1057col_2072_478799col_2072_478917

00925njm 22002777a 4500 dc Yamamoto, Hidemi S. author Gil Santano, Juan author Schwartz Navarro, Simó author Perucho, Manuel author 2020-03-24T10:00:20Z 2020-03-24T10:00:20Z 2000-02-01 2020-03-24T10:00:20Z Dear Editor, in a letter to the editor in a recent issue of Cell Death and Differentiation, Abdel-Rahman et al1. reported the absence of mutations in the death pathways gene Fas (Apo-1/CD95) in colorectal carcinomas. From the absence of mutations in 24 colon cancers, 12 of which were classified as replication error positive (RER+), Abdel-Rahman et al1. concluded that such mutations confer no substantial growth advantage in colorectal carcinogenesis. In agreement with this report, we identified Fas mutations in only 10% of colon and gastric cancers of the microsatellite mutator phenotype (MMP), also denominated as RER or microsatellite instability (MSI). Mutations were also found in Apaf-1 and Bcl-10, two other genes involved in the cell death pathways. The mutations were detected in mononucleotide tracts within these three genes (Figure 1). The frequency of these frameshift mutations was low (Table 1) and they appeared to be heterozygous (Figure 2). However, considering the peculiar features of these tumors, we suggest that these frameshift mutations contribute to cancer progression by providing survival advantage. Proteïnes Transducció de senyal cel·lular Càncer gastrointestinal Genètica Proteins Cellular signal transduction Gastrointestinal cancer Genetics Frameshift mutations in Fas, Apaf-1, and Bcl-10 in gastro-intestinal cancer of the microsatellite mutator phenotype