Cancer susceptibility variants and the risk of adult glioma in a US case-control study.
Cancer susceptibility variants and the risk of adult glioma in a US case-control study.
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DOI：
10.1007/s11060-010-0506-0
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发表时间：
2011-09
影响因子：
3.9
通讯作者：
Chen, Y. Ann
中科院分区：
文献类型：
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作者：
Egan, Kathleen M.;Thompson, Reid C.;Nabors, L. B.;Olson, Jeffrey J.;Brat, Daniel J.;LaRocca, Renato V.;Brem, Steven;Moots, Paul L.;Madden, Melissa H.;Browning, James E.;Chen, Y. Ann
恶性神经胶质瘤是最常见和致命的脑肿瘤。尽管其病因仍然难以捉摸，但最近的研究缩小了对影响风险的遗传位点的搜索范围。我们在美国的一项病例对照研究中检查了最近癌症全基因组关联研究 (GWAS) 中涉及的变异与神经胶质瘤风险的关联。病例是从美国东南部主要学术中心的神经外科和神经肿瘤诊所发现的。对照是从社区中确定的，或者是病例的朋友或其他同事。我们检查了已发表的包括神经胶质瘤在内的癌症 GWAS 中鉴定出的基因中总共 191 个易感性变异。总共 639 例神经胶质瘤病例和 649 例对照者（均为白种人）被纳入分析。病例入组时间中位为诊断后 1 个月。在神经胶质瘤 GWAS 识别的变异中，我们检测到 CDKN2B、RTEL1、TERT 和 PHLDB1 的关联，而我们没有发现 CCDC26 的总体关联。结果显示，根据神经胶质瘤的组织学亚型，存在明显的异质性，TERT 和 RTEL 变异是星形细胞肿瘤和胶质母细胞瘤 (GBM) 的特征，CCDC26 和 PHLDB1 变异是星形细胞肿瘤和少突胶质细胞肿瘤的特征，CDKN2B 变异在 GBM 中最为突出。经过多重比较调整后，未发现其他癌症 GWAS 中检查的变异与风险相关。这些结果表明，GWAS 鉴定的神经胶质瘤中的 SNP 标志着神经胶质瘤中不同的分子病因。按广泛的组织学亚组进行分层可能有助于揭示分子机制，并有助于在未来的神经胶质瘤遗传易感性变异研究中发现新的位点。
Malignant gliomas are the most common and deadly brain tumors. Although their etiology remains elusive, recent studies have narrowed the search for genetic loci that influence risk. We examined variants implicated in recent cancer genome-wide association studies (GWAS) for associations with glioma risk in a US case–control study. Cases were identified from neurosurgical and neuro-oncology clinics at major academic centers in the Southeastern US. Controls were identified from the community or were friends or other associates of cases. We examined a total of 191 susceptibility variants in genes identified in published cancer GWAS including glioma. A total of 639 glioma cases and 649 controls, all Caucasian, were included in analysis. Cases were enrolled a median of 1 month following diagnosis. Among glioma GWAS-identified variants, we detected associations in CDKN2B, RTEL1, TERT and PHLDB1, whereas we did not find overall associations for CCDC26. Results showed clear heterogeneity according to histologic subtypes of glioma, with TERT and RTEL variants a feature of astrocytic tumors and glioblastoma (GBM), CCDC26 and PHLDB1 variants a feature of astrocytic and oligodendroglial tumors, and CDKN2B variants most prominent in GBM. No examined variant in other cancer GWAS was found to be related to risk after adjustment for multiple comparisons. These results suggest that GWAS-identified SNPs in glioma mark different molecular etiologies in glioma. Stratification by broad histological subgroups may shed light on molecular mechanisms and assist in the discovery of novel loci in future studies of genetic susceptibility variants in glioma.
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影响因子：
30.8
作者：
McKay, James D.;Hung, Rayjean J.;Gaborieau, Valerie;Boffetta, Paolo;Chabrier, Amelie;Byrnes, Graham;Zaridze, David;Mukeria, Anush;Szeszenia-Dabrowska, Neonilia;Lissowska, Jolanta;Rudnai, Peter;Fabianova, Eleonora;Mates, Dana;Bencko, Vladimir;Foretova, Lenka;Janout, Vladimir;McLaughlin, John;Shepherd, Frances;Montpetit, Alexandre;Narod, Steven;Krokan, Hans E.;Skorpen, Frank;Elvestad, Maiken Bratt;Vatten, Lars;Njolstad, Inger;Axelsson, Tomas;Chen, Chu;Goodman, Gary;Barnett, Matt;Loomis, Melissa M.;Lubinski, Jan;Matyjasik, Joanna;Lener, Marcin;Oszutowska, Dorota;Field, John;Liloglou, Triantafillos;Xinarianos, George;Cassidy, Adrian;Zelenika, Diana;Boland, Anne;Delepine, Marc;Foglio, Mario;Lechner, Doris;Matsuda, Fumihiko;Blanche, Helene;Gut, Ivo;Heath, Simon;Lathrop, Mark;Brennan, Paul
通讯作者：
Brennan, Paul
影响因子：
30.8
作者：
Shete S;Hosking FJ;Robertson LB;Dobbins SE;Sanson M;Malmer B;Simon M;Marie Y;Boisselier B;Delattre JY;Hoang-Xuan K;El Hallani S;Idbaih A;Zelenika D;Andersson U;Henriksson R;Bergenheim AT;Feychting M;Lönn S;Ahlbom A;Schramm J;Linnebank M;Hemminki K;Kumar R;Hepworth SJ;Price A;Armstrong G;Liu Y;Gu X;Yu R;Lau C;Schoemaker M;Muir K;Swerdlow A;Lathrop M;Bondy M;Houlston RS
通讯作者：
Houlston RS
影响因子：
15.9
作者：
Fang, ZX;Kulldorff, M;Gregorio, DI
通讯作者：
Gregorio, DI
DOI：
10.1111/j.2517-6161.1995.tb02031.x
发表时间：
1995-01-01
影响因子：
5.8
作者：
BENJAMINI, Y;HOCHBERG, Y
通讯作者：
HOCHBERG, Y
影响因子：
30.8
作者：
通讯作者：
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