Whole-exome Sequencing of Nigerian Prostate Tumors from the Prostate Cancer Transatlantic Consortium (CaPTC) Reveals DNA Repair Genes Associated with African Ancestry.
Journal
Cancer research communications
ISSN: 2767-9764
Titre abrégé: Cancer Res Commun
Pays: United States
ID NLM: 9918281580506676
Informations de publication
Date de publication:
09 2022
09 2022
Historique:
received:
31
03
2022
revised:
23
06
2022
accepted:
08
08
2022
entrez:
16
3
2023
pubmed:
17
3
2023
medline:
17
3
2023
Statut:
epublish
Résumé
In this study, we used whole-exome sequencing of a cohort of 45 advanced-stage, treatment-naïve Nigerian (NG) primary prostate cancer tumors and 11 unmatched nontumor tissues to compare genomic mutations with African American (AA) and European American (EA) The Cancer Genome Atlas (TCGA) prostate cancer. NG samples were collected from six sites in central and southwest Nigeria. After whole-exome sequencing, samples were processed using GATK best practices. MAA have higher rates of prostate cancer incidence and mortality, however, are severely underrepresented in genomic studies. This is the first study utilizing whole-exome sequencing in NG men to identify West African ancestry-linked variant patterns that impact DNA damage repair pathways.
Identifiants
pubmed: 36922933
doi: 10.1158/2767-9764.CRC-22-0136
pii: CRC-22-0136
pmc: PMC10010347
doi:
Substances chimiques
Mismatch Repair Endonuclease PMS2
EC 3.6.1.3
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, U.S. Gov't, Non-P.H.S.
Research Support, Non-U.S. Gov't
Langues
eng
Pagination
1005-1016Subventions
Organisme : NCI NIH HHS
ID : U54 CA118623
Pays : United States
Informations de copyright
© 2022 The Authors; Published by the American Association for Cancer Research.
Déclaration de conflit d'intérêts
F. Mohammed reports other from BIO Ventures for Global Health outside the submitted work. M. Davis reports grants from Weill Cornell Prostate SPORE during the conduct of the study; grants from Genentech and grants and non-financial support from NIH outside the submitted work. P. Polak reports other from C2i Genomcis outside the submitted work. C. Yates reports other from Leidos contract YT16-010 (Project ID# 001.050.0010), NCI contracts HHSN261201600732P (University of Florida); grants from U54-MD007585-26, U54 CA118623 (NIH/NCI), and PC170315P1, W81XWH-18-1-0589) awarded to C. Yates during the conduct of the study; personal fees from Riptide Biosciences, QED Therapeutics, and Amgen and other from Riptide Biosciences outside the submitted work. No disclosures were reported by the other authors.
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