Role of genetic and epigenetic changes in Burkitt lymphoma.
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.
Department of Oncology-Pathology, Cancer Center Karolinska, Karolinska Institutet, R8:04 Karolinska Hospital, SE-17176 Stockholm, Sweden.
Mikael S
MS
Lindström
Klas G
KG
Wiman
D000818:Animals; D002051:Burkitt Lymphoma / Q000235:genetics* / Q000821:virology; D002471:Cell Transformation, Neoplastic; D019941:Cyclin-Dependent Kinase Inhibitor p16 / Q000235:genetics; D019175:DNA Methylation; D020031:Epstein-Barr Virus Infections / Q000235:genetics; D015972:Gene Expression Regulation, Neoplastic; D016259:Genes, myc; D019942:Genes, p16; D016158:Genes, p53; D006801:Humans; D051379:Mice; D009154:Mutation; D025803:Tumor Suppressor Protein p14ARF / Q000235:genetics
D019941:Cyclin-Dependent Kinase Inhibitor p16; D025803:Tumor Suppressor Protein p14ARF