Abstract

Highlights| May 04 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 (5): 671. https://doi.org/10.1158/1541-7786.MCR-20-5-HI Related Content A commentary has been published: Modeling Androgen Deprivation Therapy–Induced Prostate Cancer Dormancy and Its Clinical Implications A commentary has been published: Targeted Rejuvenation of Exhausted Chimeric Antigen Receptor T Cells Regresses Refractory Solid Tumors A commentary has been published: Inactivation of p21-Activated Kinase 2 (Pak2) Inhibits the Development of Nf2-Deficient Tumors by Restricting Downstream Hedgehog and Wnt Signaling View more A commentary has been published: MOB3A Bypasses BRAF and RAS Oncogene-Induced Senescence by Engaging the Hippo Pathway 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 May 4 2022 Citation Selected Articles from This Issue. Mol Cancer Res 1 May 2022; 20 (5): 671. https://doi.org/10.1158/1541-7786.MCR-20-5-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 Androgen-deprivation therapy (ADT) is a frontline therapy for prostate cancer patients. However, many patients experience post-ADT disease recurrence owing to ADT-induced tumor cell dormancy and subsequent dormant tumor cell outgrowth. Elucidating mechanisms underlying ADT-induced tumor cell dormancy could facilitate improved prognostic and therapeutic options for prostate cancer patients, but dormant tumor cells are difficult to study given they are rare and difficult to isolate. To address these challenges, Dong and colleagues used prostate cancer patient-derived xenograft models to derive and study ADT-induced tumor cell dormancy. Immunohistochemical analysis revealed two subtypes of tumor dormancy: tumor mass dormancy and cellular dormancy. Transcriptomic analysis of samples from each subtype defined a corresponding signature of differentially expressed genes—termed the pre-disposed gene signature (PGS)—between the subtypes. Training and validation of the PGS using clinical samples demonstrated the ability of the PGS to predict ADT responsiveness, suggesting molecular characteristics underlying tumor dormancy subtypes discovered in this... You do not currently have access to this content.

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