Role of genetic and epigenetic changes in Burkitt lymphoma

被引：78

作者：

Lindström, MS ^{[1
]}

Wiman, KG ^{[1
]}

机构：

[1] Karolinska Hosp, Karolinska Inst, Canc Ctr Karolinska, Dept Oncol Pathol,CCK, SE-17176 Stockholm, Sweden

来源：

SEMINARS IN CANCER BIOLOGY | 2002年 / 12卷 / 05期

关键词：

Burkitt lymphoma; c-myc; p53; p16; methylation; Epstein-Barr virus;

D O I：

10.1016/S1044-579X(02)00058-5

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

All Burkitt lymphomas (BLs) carry reciprocal chromosomal translocations that activate the c-myc oncogene through juxtaposition to one of the immunoglobulin (Ig) loci. Many BL carry point mutation in the p53 tumor suppressor gene or other defects in the p14ARF-MDM2-p53 pathway, and inactivation of the p16INK4a gene by promoter methylation or homozygous deletion. This indicates that disruption of both the pRb and p53 tumor suppressor pathways is critical for BL development. Alterations of other genes, including Bax, p73, and BCL-6, may provide further growth stimulation and apoptosis protection. Thus, BL development involves multiple genetic and epigenetic changes that drive cell cycle Progression and avert cell death by apoptosis.

引用

页码：381 / 387

页数：7

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