癌症肿瘤,抑制基因TP53 z-bo 2020-10-21 328

　　The internationally renowned Nature Publishing Group published on the Internet the latest discovery of the tumor suppressor gene TP53 by researcher Scott W.owe of the Memorial Sloan Kettering Cancer Center (Memorial Sloan Kettering Cancer Center), which revealed The removal of fragments related to the loss of TP53 has nothing to do with p53, and the sexual mechanism causes cancer.

　　"Mutations that cause loss of function of the tumor suppressor gene TP53 are the most common events in human cancer. This is usually caused by a "double-hit" mechanism involving missense mutations containing one and the other allele. The chromosomes appear in segments called "loss of heterozygosity" (loss of heterozygosity). TP53 missense mutations can trigger the gain of function activity and affect tumor progression, but in addition to TP53 deletion, whether deletion events that usually involve many genes also affect tumor development is still unknown. In this article, the researchers found that the somatic heterozygous deletion in the linear region of the 11B3 chromosome of human 17p13.1-4Mb mice has a greater impact on the formation of lymphoma and leukemia than the deletion of Trp53. I confirmed. Mechanism studies have confirmed that the effect of 11B3 deletion on tumorigenesis is related to the simultaneous deletion of Eif5a and Alox15b (also known as Alox8) genes. The synergistic effect of suppressing these genes and deletion of Trp53 can lead to more aggressive cancers. This study provides convincing evidence that the removal of 17p has other phenotypes besides losing the effects of TP53. Taking into account the established function gain characteristics of some Trp53 missense mutations, the results of the study indicate that the most common somatic event in cancer has nothing to do with Trp53 inactivation, thereby promoting tumorigenesis.

　　It shows that it contributes to various activities and thus functions. Therefore, based on the nature of the TP53 mutation and the extent of the 17p deletion, tumors containing TP53 damage may have different phenotypes. For this reason, the model described in this article also helps to accurately analyze the mechanisms by which various 17p structures affect disease development and ultimately affect treatment response. In a broader sense, the new research provides direct in vivo evidence that the occurrence of fragment deletion events may be caused by multiple gene disruptions and the selective benefits of these common cancer-promoting lesions. Provide a method of research and analysis.