Evidence map›Paper›PMID 41950373›Full record

ArticleThe Prostate2026

Castration Resistance Accelerates Prostate Cancer Kinetics.

Sheila Jonnatan, Luka Cavka, Angelo M De Marzo, Samuel R Denmeade, Mark C Markowski, Emmanuel S Antonarakis, Bruce J Trock, Catherine H Marshall, Ravi A Madan, David J Einstein and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Prostate, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

Sheila JonnatanSidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD, USA.ORCID https://orcid.org/0000-0003-0278-2475
Luka CavkaSidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD, USA.
Angelo M De MarzoSidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD, USA.
Samuel R DenmeadeSidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD, USA.ORCID https://orcid.org/0000-0001-5442-515X
Mark C MarkowskiSidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD, USA.
Emmanuel S AntonarakisMasonic Cancer Center, University of Minnesota, Minneapolis, MN, USA.
Bruce J TrockSidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD, USA.ORCID https://orcid.org/0000-0003-3529-9295
Catherine H MarshallSidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD, USA.ORCID https://orcid.org/0000-0002-2653-4110
Ravi A MadanGenitourinary Malignancies Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
David J EinsteinDivision of Medical Oncology, Beth Israel Deaconess Medical Center, Boston, MA, USA.
Laura A SenaSidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD, USA.

Funding

Synthetic lethal metabolic drug combinations for castration-resistant prostate cancerK08CA273167 · NCI · JOHNS HOPKINS UNIVERSITY · PI Laura A. Sena · 2023 to 2026
$877k
NCI NIH HHS K08 CA273167NIH HHS K08CA273167Prostate Cancer Foundation
6 · The paper itself

Abstract

backgroundProstate cancer can be an indolent disease with which patients can live for many years. Thus, an understanding of how therapy and its ensuing resistance affect prostate cancer kinetics may guide efforts to determine optimal timing of therapy initiation. Despite the fact that castration has been used as therapy for prostate cancer for more than 70 years, no prior study has systematically quantified the effect of castration resistance on the rate of progression. The prostate-specific antigen doubling time (PSADT) estimates prostate cancer kinetics and predicts overall survival, but whether PSADT changes as a result of castration resistance is not known.

methodsHere, we studied the longitudinal change in the PSADT before castration and following the development of castration resistance in a cohort of 40 patients with prostate cancer.

resultsThe PSADT of castration-resistant prostate cancer (CR-PSADT) was markedly shorter than the matched PSADT of castration-naïve prostate cancer (CN-PSADT) (median 2.6 months vs. 5.8 months, p < 0.001). The CR-PSADT positively correlated with the CN-PSADT and with overall survival. Sensitivity analysis suggested that the PSADT did not change as a function of time during progression when treatment was unchanged. Using a separate cohort of 36 patients with metastatic CRPC, we confirmed a positive correlation of CR-PSADT with overall survival and identified a negative correlation with the Ki-67 proliferation index of metastatic tumor biopsies.

conclusionsCastration-resistant prostate cancer is associated with markedly accelerated disease kinetics compared with castration-naïve prostate cancer. This acceleration of disease progression has the potential to shorten the survival of some patients with indolent disease who are treated prematurely with ADT.

Indexed as

Prostate-Specific AntigenProstatic NeoplasmsProstatic Neoplasms, Castration-ResistantAgedAged, 80 and overDisease ProgressionHumansKineticsMaleMiddle AgedProstate-Specific Antigencancer kineticscastration resistanceProstate cancerprostate‐specific antigen doubling time

Identifiers

PMID41950373
PMCPMC13172930

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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 OpenQuestion graph.