Selected Articles from This Issue

Abstract

Highlights| December 02 2022 Selected Articles from This Issue Author & Article Information Online Issn: 1557-3125 Print Issn: 1541-7786 ©2022 American Association for Cancer Research2022American Association for Cancer Research Mol Cancer Res (2022) 20 (12): 1709. https://doi.org/10.1158/1541-7786.MCR-20-12-HI Related Content A commentary has been published: The C-terminus of Gain-of-Function Mutant p53 R273H Is Required for Association with PARP1 and Poly-ADP-Ribose A commentary has been published: A Recurrent ADPRHL1 Germline Mutation Activates PARP1 and Confers Prostate Cancer Risk in African American Families A commentary has been published: Regulation of Cyclin D1 Degradation by Ubiquitin-Specific Protease 27X Is Critical for Cancer Cell Proliferation and Tumor Growth View more A commentary has been published: Raptinal Induces Gasdermin E–Dependent Pyroptosis in Naïve and Therapy-Resistant Melanoma View less Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn MailTo Tools Icon Tools Get Permissions Cite Icon Cite Search Site Article Versions Icon Versions Version of Record December 2 2022 Citation Selected Articles from This Issue. Mol Cancer Res 1 December 2022; 20 (12): 1709. https://doi.org/10.1158/1541-7786.MCR-20-12-HI Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest Search Advanced Search African American men are particularly susceptible to prostate cancer incidence, but genetic factors mediating prostate cancer risk in African American men remain poorly defined. To search for genetic contributors to prostate cancer occurrence in African American men, Zhang and colleagues performed whole exome sequencing using blood samples from men from 20 families affected by hereditary prostate cancer. Sequencing revealed a rare non-synonymous ADPRHL1 variant, c.A233T, encoding a p.D78V amino acid conversion, that was present in men affected by prostate cancer in four of the families but not present in 170 unrelated healthy African American men. Functional studies demonstrated that the A233T variant increases prostate cancer cell growth and induces PARP activation. A233T variant-mediated PARP activation renders prostate cancer cells resistant to DNA damaging agents but susceptible to PARP inhibitor olaparib. The authors also found that ADPRHL1 abundance decreases during prostate cancer progression, suggesting A233T is a loss-of-function variant. Altogether, this... You do not currently have access to this content.