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Pubmed ID: 35079693
Publication Date: 2021/12/27

DNA Repair Pathways and Their Association With Lethal Prostate Cancer in African American and European American Men.


Altered DNA damage response (DDR) has emerged as an important mechanism for the development of aggressive prostate cancer among men of European ancestry but not other ancestry groups. Because common mechanisms for aggressive disease are expected, we explored a large panel of DDR genes and pathways to demonstrate that DDR alterations contribute to development of aggressive prostate cancer in both African American and European American men.

We performed a case-case study of 764 African American and European American men with lethal or indolent prostate cancer treated at 4 US hospitals. We calculated carrier frequencies of germline pathogenic or likely pathogenic sequence variants within 306 DDR genes, summarized by DDR pathway, and compared lethal cases against indolent cases using 2-sided Fisher's exact tests. Secondary analysis examined if carrier frequencies differed by ancestry.

Lethal cases were more likely to carry a pathogenic sequence variant in a DDR gene compared with indolent cases (18.5% vs 9.6%,  = 4.30 × 10), even after excluding (14.6% vs 9.6%,  = .04). The carrier frequency was similar among lethal cases of African (16.7% including and 15.8% excluding ) and lethal cases of European (19.3% including and 14.2% excluding ) ancestry. Three DDR pathways were statistically significantly associated with lethal disease: homologous recombination ( = .003), Fanconi anemia ( = .002), and checkpoint factor ( = .02).

Our findings suggest that altered DDR is an important mechanism for aggressive prostate cancer not only in men of European but also of African ancestry. Therefore, interrogation of entire DDR pathways is needed to fully characterize and better define genetic risk of lethal disease.
Authors: Plym Anna , Dióssy Miklós , Szallasi Zoltan , Sartor Oliver , Silberstein Jonathan , Powell Isaac J , Rebbeck Timothy R , Penney Kathryn L , Mucci Lorelei A , Pomerantz Mark M , Kibel Adam S ,

Reference:

  1. ncbi.nlm.nih.gov. [Last access 2021/12/27].

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