期刊
CELL
卷 135, 期 6, 页码 1130-1142出版社
CELL PRESS
DOI: 10.1016/j.cell.2008.10.035
关键词
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资金
- NCI NIH HHS [R37 CA051105, R37 CA051105-21, R01 CA139032, R37 CA051105-19, R21 CA152497, R37 CA051105-20, R01 CA100504, R01 CA137060, R01 CA100504-06, R37 CA051105-18, R01 CA139032-01] Funding Source: Medline
- NIGMS NIH HHS [R01 GM043236-14, R01 GM056984, R01 GM043236, R01 GM056984-07] Funding Source: Medline
We have assembled, annotated, and analyzed a database of over 1700 breakpoints from the most common chromosomal rearrangements in human leukemias and lymphomas. Using this database, we show that although the CpG dinucleotide constitutes only 1% of the human genome, it accounts for 40%-70% of breakpoints at pro-B/pre-B stage translocation regions-specifically, those near the bcl-2, bcl-1, and E2A genes. We do not observe CpG hotspots in rearrangements involving lymphoid-myeloid progenitors, mature B cells, or T cells. The stage specificity, lineage specificity, CpG targeting, and unique breakpoint distributions at these cluster regions may be explained by a lesion-specific double-strand breakage mechanism involving the RAG complex acting at AID-deaminated methyl-CpGs.
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