ArticleBMC cancer2025
Androgenic effects of 11-oxyandrogens in castration-resistant prostate cancer.
Article in BMC cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors.
Funding
Abstract
backgroundAdrenal-derived 11-oxygenated androgens (11-oxyandrogens) emerged as potential key contributors to prostate cancer (PCa) progression by activating the androgen receptor (AR). This study investigates their clinical and mechanistic role in metastatic castration-resistant prostate cancer (mCRPC) patients initiating AR pathway inhibitors (ARPI).
methodsIn a pilot study of 35 mCRPC patients initiating ARPI, serum steroids were quantified via mass spectrometry and correlated with survival. Functional assays assessed the proliferative effects of 11-oxyandrogens on CRPC cells and their inhibition by enzalutamide, supported by transcriptomic and proteomic profiling.
results11-ketotestosterone (11KT) and its hydroxylated derivative, 11-hydroxytestosterone (11OHT) are the predominant potent androgens, accounting for 81% of circulating androgens. Higher baseline levels of 11KT, 11OHT, the abundant precursor 11β-hydroxyandrostenedione (11OHA4), and the downstream metabolite 11-hydroxyandrosterone (11OHAST) are linked to prolonged progression-free survival (PFS) (HR: 0.56–0.69; P < 0.05), suggesting an enhanced treatment response. 11KT and 11OHT promoted AR-driven proliferation of CRPC cells and gene expression, which was reversed by AR antagonism, suggesting they are primarily AR-mediated. Additionally, 11-oxyandrogens display distinct effects, including the activation of AR-independent pathways.
conclusions11-oxyandrogens are potent AR activators in mCRPC, with evidence suggesting they may exert distinct biological effects compared to canonical androgens. Their association with longer PFS and improved response to ARPI may reflect a more hormonally active tumor environment, potentially indicative of tumors with higher AR dependency and responsiveness to therapy. Their profiling may help predict ARPI response, warranting further investigation.
Indexed as
Identifiers
What Socratic holds
Registered trials
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.