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Matthew L. Kosel

Researcher at Mayo Clinic

Publications -  48
Citations -  3903

Matthew L. Kosel is an academic researcher from Mayo Clinic. The author has contributed to research in topics: Genome-wide association study & Population. The author has an hindex of 23, co-authored 40 publications receiving 3306 citations. Previous affiliations of Matthew L. Kosel include Erasmus University Rotterdam.

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Associations of Breast Cancer Risk Factors With Tumor Subtypes: A Pooled Analysis From the Breast Cancer Association Consortium Studies

Xiaohong R. Yang, +173 more
TL;DR: It is shown that reproductive factors and BMI are most clearly associated with hormone receptor-positive tumors and suggest that triple-negative or CBP tumors may have distinct etiology.
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Genome-wide association study in BRCA1 mutation carriers identifies novel loci associated with breast and ovarian cancer risk

Fergus J. Couch, +261 more
- 27 Mar 2013 - 
TL;DR: It is estimated that the breast cancer lifetime risks for the5% of BRCA1 carriers at lowest risk are 28%–50% compared to 81%–100% for the 5% at highest risk, and the ovarian cancer lifetime risk is 63% or higher, based on the known cancer risk-modifying loci.
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A germline variant in the TP53 polyadenylation signal confers cancer susceptibility

Simon N. Stacey, +108 more
- 01 Nov 2011 - 
TL;DR: A genome-wide association study of 16 million SNPs identified through whole-genome sequencing of 457 Icelanders found that rs78378222 is in the 3′ untranslated region of TP53 and changes the AATAAA polyadenylation signal to AATACA, resulting in impaired 3′-end processing of TP 53 mRNA.
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Association of Maximal Extent of Resection of Contrast-Enhanced and Non-Contrast-Enhanced Tumor With Survival Within Molecular Subgroups of Patients With Newly Diagnosed Glioblastoma.

TL;DR: An association between maximal resection of CE tumor and OS in patients with glioblastoma is confirmed across all subgroups and was associated with longer OS in younger patients, regardless of IDH status, and among patients with IDH-wild-type gliOBlastoma regardless of the methylation status of the promoter region of the DNA repair enzyme O6-methylguanine-DNA methyltransferase.