ReviewThe oncologist2026
Non-conventional histologies of prostate cancer: from morphology to biology-driven precision oncology.
Review in The oncologist, 2026. 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
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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.
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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.
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0 citing papers in PubMed.
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non-conventional prostate cancer histologies represent a small but clinically significant subset characterized by aggressive behavior, atypical biomarker profiles, and reduced dependence on androgen receptor signaling. Evidence indicates these histologies reflect dynamic biological states driven by genomic instability, lineage plasticity, and therapeutic selection rather than static morphologic entities, with several morphologies acting as accessible, if imperfect, surrogates for actionable alterations. We performed a translational narrative review integrating anatomic pathology, genomic and epigenomic biology, and biomarker-selected therapy, searching PubMed/MEDLINE, Embase, Cochrane CENTRAL, the ASCO Meeting Library, ESMO publications, and APCCC through May 2026, spanning neuroendocrine, ductal, intraductal, cribriform, adenosquamous, sarcomatoid, adenoid cystic, signet ring cell, and mucinous subtypes. These histologies are individually uncommon but are consistently associated with advanced stage and inferior survival. Neuroendocrine prostate cancer is the most aggressive phenotype and a major mechanism of resistance to AR-directed therapy, driven by combined RB1 and TP53 loss, epigenetic reprogramming, and lineage plasticity, and marked by DLL3 expression. Cribriform and intraductal carcinoma are often enriched for BRCA2 and DNA-repair deficiency, whereas ductal differentiation is associated with mismatch-repair deficiency in a subset, with implications for PARP inhibition and checkpoint blockade. Emerging strategies include platinum-based chemoimmunotherapy and investigational lineage-directed agents targeting DLL3, STEAP1, KLK2, and TROP-2, alongside radioligands. These histologies are best viewed as biologically distinct, evolving disease states. By integrating pathology, molecular biology, and biomarker-selected therapy into one translational pathway, this review reframes non-conventional histology as a prompt for early molecular characterization and adaptive, biology-driven treatment.
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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 OpenQuestion graph.