Variants at 6q21 implicate PRDM1 in the etiology of therapy-induced second malignancies after Hodgkin's lymphoma.

Variants at 6q21 implicate PRDM1 in the etiology of therapy-induced second malignancies after Hodgkin's lymphoma.
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6q21的变体暗示PRDM1在霍奇金淋巴瘤后治疗引起的第二次恶性肿瘤的病因中。

DOI:
10.1038/nm.2407
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发表时间:
2011-07-24
期刊:
影响因子:
82.9
通讯作者:
--
中科院分区:
医学1区
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--
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儿童霍奇金淋巴瘤(HL)的存活者存在放射治疗(RT)诱导的继发性恶性肿瘤(SMN)的显著风险。我们在儿童接受RT治疗的HL幸存者中发现了两个与SMNs相关的染色体6q21变异体,但在成人中未发现。所述变体包含与降低的基础PRDM1表达和通过辐射暴露受损的PRDM1诱导相关的风险基因座。这些数据表明,一种新的基因暴露相互作用,可能涉及PRDM1的RT诱导的SMNs的病因。
Survivors of pediatric Hodgkin lymphoma (HL) are at significant risk for radiation therapy (RT)-induced second malignant neoplasms (SMNs). We identified two variants at chromosome 6q21 associated with SMNs in HL survivors treated with RT as children but not as adults. The variants comprise a risk locus associated with decreased basal PRDM1 expression and impaired induction of PRDM1 by radiation exposure. These data suggest a novel gene-exposure interaction that may implicate PRDM1 in the etiology of RT-induced SMNs.
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