6q21 上的变异与霍奇金淋巴瘤治疗后诱导的第二恶性肿瘤的发病机制有关。
Variants at 6q21 implicate PRDM1 in the etiology of therapy-induced second malignancies after Hodgkin's lymphoma.
机构信息
Committee on Cancer Biology, University of Chicago, Chicago, Illinois, USA.
出版信息
Nat Med. 2011 Jul 24;17(8):941-3. doi: 10.1038/nm.2407.
Abstract
Survivors of pediatric Hodgkin's lymphoma are at risk for radiation therapy-induced second malignant neoplasms (SMNs). We identified two variants at chromosome 6q21 associated with SMNs in survivors of Hodgkin's lymphoma treated with radiation therapy as children but not as adults. The variants comprise a risk locus associated with decreased basal expression of PRDM1 (encoding PR domain containing 1, with ZNF domain) and impaired induction of the PRDM1 protein after radiation exposure. These data suggest a new gene-exposure interaction that may implicate PRDM1 in the etiology of radiation therapy-induced SMNs.
摘要
儿童霍奇金淋巴瘤幸存者有罹患放射治疗所致第二恶性肿瘤（SMN）的风险。我们在接受放射治疗的儿童霍奇金淋巴瘤幸存者中鉴定出与 SMN 相关的两个位于 6q21 染色体上的变异体，但在成年接受放射治疗的患者中未发现。这些变异体包括一个与 PRDM1（编码含有 ZNF 结构域的 PR 结构域蛋白 1）的基础表达降低以及放射暴露后 PRDM1 蛋白的诱导受损相关的风险位点。这些数据提示了一种新的基因-暴露相互作用，可能提示 PRDM1 参与放射治疗所致 SMN 的发病机制。
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