Mutations in the VAV1 gene cause mice to develop T cell tumors

  T-cell tumors include a mature subtype called peripheral T-cell lymphoma. Studies have shown that the VAV1 gene involved in the signal transduction of several T-cell receptors has been altered in several peripheral T-cell lymphoma variants. Therefore, in this new study, these researchers tried to reveal the VAV1 mutation in vivo. The role of T cells in malignant transformation. The tumor suppressor gene p53 is called a genome protector because it prevents mutations in the genome. These researchers replicated the VAV1 mutation found in human T cell tumors in normal ("wild") mice and mice lacking p53. Kota Fukumoto, the lead author of the paper, described their findings. "During the observation year, wild-type mice with VAV1 mutations did not develop tumors, while mice lacking p53 developed immature tumors. Mice lacking p53 and VAV1 mutations also developed. It is worthwhile. Note that it is a mature tumor similar to human peripheral T-cell lymphoma, and its prognosis is worse than that of mice lacking only p53.

  These researchers also found that mice lack functional thymus. Transplant tumor cells. The results indicate that the development of tumors may be due to the internal mechanisms of these cells. Professor Shigeru Chiba, the corresponding author of the paper, explained: “I noticed that T-cell tumors with VAV1 mutations exhibit enrichment of the Myc pathway and changes in the somatic replication count (SCNA).” It is worth noting that Both Myc and SCNA are tumorigenesis. Among them, Myc is a family of regulatory genes and proto-oncogenes, while SCNA causes changes in DNA copy number.

  Professor Chiba added: “Interestingly, the use of drugs that block the Myc pathway can increase the overall viability of mice with VAV1 mutant tumors. Therefore, our methods and results show that this new study expresses VAV1 This indicates that it has been developed. Mutant alkane mice may be a research tool for evaluating specific T-cell tumor therapeutics.