Liu Baodong
Department of Thoracic Surgery, Xuanwu Hospital, Capital Medical University, Beijing 100053, China.
Zhongguo Fei Ai Za Zhi. 2024 Jan 2;26(12):943-949. doi: 10.3779/j.issn.1009-3419.2023.101.34.
So far, the monoclonal hypothesis of tumor occurrence and development cannot be justified. The genetic diversity selection hypothesis for the occurrence and development of lung cancer links Mendelian genetics with Darwin's theory of evolution, suggesting that the genetic diversity of tumor cell populations with polyclonal origins-monoclonal selection-subclonal expansion is the result of selection pressure. Normal cells acquire mutations in oncogenic driver genes and have a selective advantage over other cells, becoming tumor initiating cells; In the interaction with the tumor microenvironment (TME), the vast majority of initiating cells are recognized and killed by the human immune system. If immune escape occurs, the incidence of malignant tumors will greatly increase, and subclonal expansion, intratumour heterogeneity, etc. will occur. This article proposed the hypothesis of genetic diversity selection and analyzed its clinical significance. .
到目前为止,肿瘤发生发展的单克隆假说尚无法得到证实。肺癌发生发展的遗传多样性选择假说将孟德尔遗传学与达尔文进化论联系起来,表明具有多克隆起源的肿瘤细胞群体的遗传多样性——单克隆选择——亚克隆扩增是选择压力的结果。正常细胞在致癌驱动基因中获得突变,并比其他细胞具有选择性优势,成为肿瘤起始细胞;在与肿瘤微环境(TME)的相互作用中,绝大多数起始细胞被人体免疫系统识别并杀死。如果发生免疫逃逸,恶性肿瘤的发病率将大大增加,并会出现亚克隆扩增、肿瘤内异质性等情况。本文提出了遗传多样性选择假说并分析了其临床意义。