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所有伯基特淋巴瘤(BLs)携带交互染色体异位,通过与一个免疫球蛋白位点并排从而激活c-myc原癌基因。一些BL携带肿瘤抑制基因p53的点突变或p14ARF-MDM2-p53途径的其他缺陷,使p16INK4a基因通过增强子甲基化或纯合子缺失而失活。这说明pRb和p53肿瘤抑制途径的破坏对于BL的发展是重要的。其他基因的改变,包括Bax、p73和BCL-6,可以提供进一步的生长刺激和凋亡保护。因此,BL发展包括多种遗传学和渐成学的改变,驱动细胞周期进展,通过凋亡避免细胞死亡。
All Burkitt’s lymphoma (BLs) carry an interactive chromosomal ectopic activation of the c-myc oncogene by side-by-side with an immunoglobulin site. Some BLs carry point mutations in the tumor suppressor p53 or other defects in the p14ARF-MDM2-p53 pathway, rendering the p16INK4a gene inactivated by enhancer methylation or homozygous deletion. This suggests that the destruction of pRb and p53 tumor suppressor pathways is important for the development of BL. Other genetic alterations, including Bax, p73 and BCL-6, can provide further growth stimulation and apoptosis protection. Thus, BL development involves a variety of genetics and progressive changes that drive the progression of the cell cycle and prevent cell death by apoptosis.