期刊
CELL REPORTS
卷 6, 期 1, 页码 130-140出版社
CELL PRESS
DOI: 10.1016/j.celrep.2013.12.027
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资金
- NIH [RO1-CA37295, RO1-CA172492-01, RO1-CA136537]
- Specialized Center of Research grant from the Leukemia & Lymphoma Society
- Northeast Biodefense Center [U54-AI057158]
- National Library of Medicine [1R01LM010140-01]
- AIRC [10007]
- Cariplo Foundation
- Novara AIL
- NATIONAL CANCER INSTITUTE [R01CA164152, R01CA172492, R01CA136537, R01CA037295, R01CA171972] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [U54AI057158] Funding Source: NIH RePORTER
- NATIONAL LIBRARY OF MEDICINE [R01LM010140] Funding Source: NIH RePORTER
Follicular lymphoma (FL) is an indolent disease, but 30%-40% of cases undergo histologic transformation to an aggressive malignancy, typically represented by diffuse large B cell lymphoma (DLBCL). The pathogenesis of this process remains largely unknown. Using whole-exome sequencing and copy-number analysis, we show here that the dominant clone of FL and transformed FL (tFL) arise by divergent evolution from a common mutated precursor through the acquisition of distinct genetic events. Mutations in epigenetic modifiers and antiapoptotic genes are introduced early in the common precursor, whereas tFL is specifically associated with alterations deregulating cell-cycle progression and DNA damage responses (CDKN2A/B, MYC, and TP53) as well as aberrant somatic hypermutation. The genomic profile of tFL shares similarities with that of germinal center B cell-type de novo DLBCL but also displays unique combinations of altered genes with diagnostic and therapeutic implications.
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