Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
2 · The registry
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Rajendra KumarProstate Cancer/Genitourologic Program, Oncology, The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.ORCID https://orcid.org/0000-0002-2845-8115
Janet MendoncaProstate Cancer/Genitourologic Program, Oncology, The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.ORCID https://orcid.org/0009-0004-2736-6229
Abhishek ShettyProstate Cancer/Genitourologic Program, Oncology, The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.ORCID https://orcid.org/0000-0002-9892-1267
Yuhan YangProstate Cancer/Genitourologic Program, Oncology, The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.ORCID https://orcid.org/0009-0008-0722-7407
Olutosin OwoyemiProstate Cancer/Genitourologic Program, Oncology, The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.ORCID https://orcid.org/0000-0002-7527-5768
Lillian WilsonProstate Cancer/Genitourologic Program, Oncology, The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.ORCID https://orcid.org/0009-0006-2929-1368
Kavya BoyapatiProstate Cancer/Genitourologic Program, Oncology, The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.ORCID https://orcid.org/0000-0002-1731-7480
Deven TopiwalaProstate Cancer/Genitourologic Program, Oncology, The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.ORCID https://orcid.org/0009-0009-1224-5965
Naiju ThomasProstate Cancer/Genitourologic Program, Oncology, The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.ORCID https://orcid.org/0000-0002-3892-5389
Huong NguyenProstate Cancer/Genitourologic Program, Oncology, The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.ORCID https://orcid.org/0009-0005-6716-0169
Jun LuoProstate Cancer/Genitourologic Program, Oncology, The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.ORCID https://orcid.org/0000-0002-1414-473X
Channing J PallerProstate Cancer/Genitourologic Program, Oncology, The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.ORCID https://orcid.org/0000-0003-3658-1858
Samuel R DenmeadeProstate Cancer/Genitourologic Program, Oncology, The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.ORCID https://orcid.org/0000-0001-5442-515X
Michael A CarducciProstate Cancer/Genitourologic Program, Oncology, The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.ORCID https://orcid.org/0000-0002-7908-1215
Sushant K KachhapProstate Cancer/Genitourologic Program, Oncology, The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.ORCID https://orcid.org/0000-0002-6892-0140
Funding
SPORE in Prostate CancerP50CA272391 · NCI · JOHNS HOPKINS UNIVERSITY · PI Samuel R Denmeade, SHAWN LUPOLD · 2024 to 2026
$9.0M
Androgen Activation of Innate Immune Signaling to Enhance Prostate Cancer Immune ResponseR01CA243184 · NCI · JOHNS HOPKINS UNIVERSITY · PI Samuel R Denmeade, Sushant Krishna Kachhap · 2022 to 2026
$2.0M
DOD | USA | MEDCOM | CDMRP | DOD Prostate Cancer Research Program (PCRP) HT94252310029DOD | USA | MEDCOM | CDMRP | DOD Prostate Cancer Research Program (PCRP) W81XWH1910724DOD | USA | MEDCOM | CDMRP | DOD Prostate Cancer Research Program (PCRP) W81XWH2210118NCI NIH HHS P50 CA272391NCI NIH HHS R01 CA243184NIH NCI 1R01CA243184Patrick C. Walsh Prostate Cancer Research Fund (Patrick C Walsh Prostate Cancer Research Fund)Prostate Cancer Foundation (PCF) 21YOUN22
6 · The paper itself
Abstract
Among the known nuclear exportins, CRM1 is the most studied prototype. Dysregulation of CRM1 occurs in many cancers, hence, understanding the role of CRM1 in cancer can help in developing synergistic therapeutics. The study investigates how CRM1 affects prostate cancer growth and survival. It examines the role of CRM1 in regulating androgen receptor (AR) and DNA repair in prostate cancer. Our findings reveal that CRM1 influences AR mRNA and protein stability, leading to a loss of AR protein upon CRM1 inhibition. Furthermore, it highlights the involvement of HSP90 alpha, a known AR chaperone, in the CRM1-dependent regulation of AR protein stability. The combination of CRM1 inhibition with an HSP90 inhibitor demonstrates potent effects on decreasing prostate cancer cell growth and survival. The study further explores the influence of CRM1 on DNA repair proteins and proposes a strategy of combining CRM1 inhibitors with DNA repair pathway inhibitors to decrease prostate cancer growth. Overall, the findings suggest that CRM1 plays a crucial role in prostate cancer growth, and a combination of inhibitors targeting CRM1 and DNA repair pathways could be a promising therapeutic strategy.
Indexed as
DNA RepairKaryopherinsProstatic NeoplasmsReceptors, AndrogenReceptors, Cytoplasmic and NuclearCell Line, TumorCell ProliferationExportin 1 ProteinGene Expression Regulation, NeoplasticHSP90 Heat-Shock ProteinsHumansMaleProtein StabilityAR protein, humanExportin 1 ProteinHSP90 Heat-Shock ProteinsKaryopherinsReceptors, AndrogenReceptors, Cytoplasmic and Nuclearandrogen receptorCRM1DNA repairprostate cancer
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.
CRM1 regulates androgen receptor stability and impacts DNA repair pathways in prostate cancer, independent of the androgen receptor. · full record | Socratic