Research Radartracking 1,189 published studies · 293 human · 6 safety signals · 42 clinical trials · 44 cancer pages · updated Jul 2026Open the Research Map →

Prostate Adenocarcinoma

A plain-English summary of the published research on Prostate Adenocarcinoma, reviewed and approved by our editors — not a hand-curated clinical overview.

Research summary · reviewed
Educational only: This page is not medical advice. Coordinate decisions with your oncology team.

Reviewed Jun 2026 · OncoForge editorial · How we review →

AI extractedhuman reviewedsources checkedretractions suppressed· last updated Jun 2026

Evidence at a glanceHuman · observationalMixed results⚠ Studies disagree
45 published studies that name Prostate Adenocarcinoma16 human studies approved & graded (trial, observational, or meta-analysis)39 human clinical studies in the Prostate Adenocarcinoma corpus630 source documents in the Prostate Adenocarcinoma corpus

last checked June 19, 2026

Why this grade?

Human · observational — Human observational evidence only — no trials.

Computed deterministically from the studies’ types and reported outcomes — not written by AI, and not a claim that anything works.

What the guidelines say

NCI PDQESMONCCNASCO

We link the authoritative guidelines rather than reproduce them. Below, the treatments on this page are split into standard care, guideline or regulatory options, supportive care, and studied but not standard so established care is not mixed with experimental or supportive items.

Studied, not standard - investigational
  • enzalutamide
  • carboplatin
  • etoposide
  • durvalumab
  • Cisplatin

Read the guidelines

Cancer-specific deep links aren’t curated yet — these search the authoritative sources for Prostate Adenocarcinoma.

Treatment map: Prostate Adenocarcinoma

Open as a full page →

Standard care plus every compound studied in the literature (each cited) and graded by evidence, organized by clinical readiness. A category, not a verdict that anything works — confirm anything here with your oncology team.

5
Interventions
0
Standard of care
0
Tested in people
4
Lab / animal
1
Named in lit.
3
Classes
Standard of care (0) Guideline option (0) Tested in people (0) Lab / animal only (4) Named in the literature (1)
Clinical evidence
Preclinical evidence
Standard of care
Guideline option
Tested in people
Lab / animal only
Named in the literature
Chemotherapy
—
—
—
3
—
Immunotherapy
—
—
—
1
—
Hormonal therapy
—
—
—
—
1

Columns group into clinical evidence (used in, or tested on, people) and preclinical evidence (lab/animal, or only named in the literature). Cell = number of interventions; a dashed cell means none recorded there.

Investigational & adjunct compounds — detail (5)
Named in the literature
enzalutamide

"Tested in people" rows show the highest trial phase found in that compound's cited human studies (Phase I–IV; "phase not reported" = a human study with no phase tag). "Studied" = named in the cited literature for this cancer. "FDA ✓" = FDA-approved for this cancer; "off-label" = an FDA-approved drug used outside its approved indications (per openFDA). Not a claim that anything works.

Reported figures

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Snapshot

The essentials in ~60 seconds — every line is drawn from the cited sources below.

What it is
Prostate adenocarcinoma can evolve into treatment-emergent neuroendocrine prostate cancer (t-NEPC), an aggressive variant that can arise after androgen receptor pathway inhibitor therapy. [1]
Survival
t-NEPC is described as an aggressive variant; a four-gene signature (APOE, SPC25, TSPAN1, VGF) was associated with shorter biochemical recurrence-free survival. [1][2]
Biggest challenge
The main challenges are the emergence of aggressive t-NEPC after androgen-receptor pathway inhibitor therapy and diagnostic limitations of small metastatic biopsies that may require rebiopsy to confirm the diagnosis. [1][2]

Ask about Prostate Adenocarcinoma

Answers come only from the cited sources on this page — with the supporting evidence shown. If the sources here don't cover your question, it will say so. Educational information, not medical advice.

Key numbers & factors

Risk factors

  • ▲ increases riskAndrogen receptor pathway inhibitor therapy — Can lead to emergence of treatment-emergent neuroendocrine prostate cancer (t-NEPC). [1]
  • ▲ increases riskTris(2-chloroethyl) phosphate (TCEP) exposure — In experimental models increased cell migration, invasion, proliferation and accelerated tumor growth and metastasis; TCEP is a widely used organophosphate flame retardant listed as a chemical known to cause cancer. [2]

Biomarkers

  • APOE, SPC25, TSPAN1, VGF (four-gene signature) · Associated with shorter biochemical recurrence-free survival. [2]

7 sections — tap any heading to expand its cited detail. Key points are above.

OverviewTreatment-emergent neuroendocrine prostate cancer (t-NEPC) is an aggressive variant that can arise after androgen receptor pathway inhibitor therapy. Small metastatic biopsies have limitations, and prostate rebiopsy can confirm the diagnosis in reported cases.2 points
  • Treatment-emergent neuroendocrine prostate cancer (t-NEPC) can arise after androgen receptor pathway inhibitor therapy and is described as an aggressive variant. [1]
Show 1 lab & early-research finding
  • Small metastatic biopsies have limitations and a prostate rebiopsy confirmed the diagnosis in the reported case. [1]
Biology & pathways1 point
  • Proteomic profiling in TCEP-exposed prostate cancer models revealed dysregulation of pathways involved in cholesterol metabolism, lysosome function, and PPAR signaling. [2]
Key biomarkers1 point
  • Mapping TCEP-altered proteins to TCGA data identified a four-gene signature (APOE, SPC25, TSPAN1, VGF) that was associated with shorter biochemical recurrence-free survival. [2]
PrognosisIn experimental models, TCEP exposure increased prostate cancer cell migration, invasion, and proliferation in vitro and accelerated tumor growth and metastasis in vivo. A reported case described treatment-emergent neuroendocrine prostate cancer (t-NEPC) as an aggressive variant.2 points
Show 2 lab & early-research findings
  • In experimental models, TCEP exposure significantly increased prostate cancer cell migration, invasion, and proliferation in vitro and accelerated tumor growth and metastasis in vivo compared to controls. [2]
  • Treatment-emergent neuroendocrine prostate cancer (t-NEPC) was described as an aggressive variant in the reported case. [1]
Safety & interactionsTris(2-chloroethyl) phosphate (TCEP) is a widely used organophosphate flame retardant found in consumer products and human tissues and is listed by the source as a chemical known to cause cancer; its effects on prostate cancer progression were previously unexplored.1 point
  • Tris(2-chloroethyl) phosphate (TCEP) is a widely used organophosphate flame retardant found in consumer products and human tissues and is listed by the source as a chemical known to cause cancer; its effects on prostate cancer progression were previously unexplored. [2]
Treatments & compounds studiedFour therapeutics are reported across hormonal therapy, chemotherapy, and immunotherapy classes in the case report.4 treatments

Chemotherapy

  • carboplatin: The patient was treated with carboplatin as part of a combination regimen after diagnosis of treatment-emergent neuroendocrine prostate cancer. [1]
  • etoposide: The patient was treated with etoposide as part of a combination regimen after diagnosis of treatment-emergent neuroendocrine prostate cancer. [1]

Immunotherapy

  • durvalumab: The patient was treated with carboplatin, etoposide, and durvalumab. [1]

Hormonal therapy

  • enzalutamide: The reported patient had been treated with enzalutamide prior to the development of lung lesions. [1]
What we don't know yet1 point
  • Molecular docking simulations suggested potential structural compatibility between TCEP and the four protein targets, supporting possible molecular interactions that require further experimental validation. [2]

Common questions

What is Prostate Adenocarcinoma?

Treatment-emergent neuroendocrine prostate cancer (t-NEPC) is an aggressive variant that can arise after androgen receptor pathway inhibitor therapy. Small metastatic biopsies have limitations, and prostate rebiopsy can confirm the diagnosis in reported cases.

What treatments are studied for Prostate Adenocarcinoma?

Four therapeutics are reported across hormonal therapy, chemotherapy, and immunotherapy classes in the case report.

What is the prognosis for Prostate Adenocarcinoma?

In experimental models, TCEP exposure increased prostate cancer cell migration, invasion, and proliferation in vitro and accelerated tumor growth and metastasis in vivo. A reported case described treatment-emergent neuroendocrine prostate cancer (t-NEPC) as an aggressive variant.

What do studies report about safety & interactions in Prostate Adenocarcinoma?

Tris(2-chloroethyl) phosphate (TCEP) is a widely used organophosphate flame retardant found in consumer products and human tissues and is listed by the source as a chemical known to cause cancer; its effects on prostate cancer progression were previously unexplored.

Sources

Every statement above is drawn from these reviewed sources. This page reports what they describe. Sources last checked June 19, 2026.

  1. Review articleDiagnostic Challenge in Treatment-Emergent Neuroendocrine Prostate Cancer: A Case Requiring Prostate Rebiopsy After an Inconclusive Metastatic Lung Biopsy · 2026
  2. Review articleTCEP flame retardant linked to prostate cancer progression: Integrative analysis and novel biomarker discovery · 2026

What supports this page

The kinds of sources behind this page, strongest at the top. Faint rungs show what is not here yet.

Guideline
1
Meta-analysis
15
Systematic review
16
Randomized trial
3
Clinical trial
13
Observational
2
Case report
149
Review
401
Preclinical
0
Other
30

Living document — last change June 19, 2026: Cancer page updated. 2 recent updates logged.

Compounds compared by evidence

PubMed

How to read this: Ranked by the strength and volume of the evidence — NOT by how well a treatment works. A higher rank means a compound has been studied more, or in stronger study designs (e.g. randomized trials over lab studies), not that it produces better outcomes. The effect column shows the largest pooled figure reported, not a head-to-head comparison.

#CompoundEvidence strengthStudiesLargest pooled effect
1Etoposide ChemotherapyInsufficient evidence2—
2Carboplatin ChemotherapyInsufficient evidence1—
3Cisplatin ChemotherapyInsufficient evidence1—
4Durvalumab ImmunotherapyInsufficient evidence1—

Ranked across 4 compounds with published studies for this cancer. Updated 7/18/2026.

Medicines & supplements studied for Prostate Adenocarcinoma

PubMedFDAClinicalTrials.gov

Every drug, supplement, and other agent the published studies cover for Prostate Adenocarcinoma, ranked by how strong the evidence is — what studies report, not a recommendation. Tap any to see its full profile.

Medicines · 4

EtoposideInsufficient evidenceReported negative

No primary experimental studies yet.

Most authoritative study: Managing a Rare Case of Mixed Extrapulmonary Small Cell Carcinoma and Adenocarcinoma of the Prostate

No human studies yet · No numeric effect sizes reported · All studies are small (n < 30).
ChemotherapyFDA off-label2 studiesFull profile →
CarboplatinInsufficient evidenceInconclusive

No primary experimental studies yet.

Most authoritative study: Managing a Rare Case of Mixed Extrapulmonary Small Cell Carcinoma and Adenocarcinoma of the Prostate

No human studies yet · No numeric effect sizes reported · Based on a single study.
ChemotherapyFDA off-label1 studyFull profile →
CisplatinInsufficient evidenceReported negative

No primary experimental studies yet.

Most authoritative study: Prostate small cell carcinoma and skin metastases: a rare entity

No human studies yet · No numeric effect sizes reported · Based on a single study.
ChemotherapyFDA off-label1 studyFull profile →
DurvalumabInsufficient evidenceInconclusive

No primary experimental studies yet.

Most authoritative study: Managing a Rare Case of Mixed Extrapulmonary Small Cell Carcinoma and Adenocarcinoma of the Prostate

No human studies yet · No numeric effect sizes reported · Based on a single study.
ImmunotherapyFDA off-label1 studyFull profile →

What recent studies report in Prostate Adenocarcinoma

These are reviewed studies whose abstracts concern Prostate Adenocarcinoma. Each describes only what that study reported. This is not a claim by OncoForge that any compound helps or harms Prostate Adenocarcinoma. Most are early lab, animal, or small human studies, and findings often conflict.

45 studies16 human4 animal2 lab⚠ Conflicting evidenceMechanism (29)Absorption (PK) (1)Trial (1)

Tracking 45 published studies of Prostate Adenocarcinoma: 16 in humans, 4 in animals, 2 in the lab, 23 reviews/other.

Reported direction across studies: 32 positive, 2 mixed, 1 negative, 10 inconclusive.

Findings conflict — both supportive and negative/mixed results exist (see below). Human evidence is limited.

These counts summarize what the studies reported; they are not a measure of whether anything works for Prostate Adenocarcinoma.

Compounds with studies mentioning Prostate Adenocarcinoma

Etoposide (2)Carboplatin (1)Durvalumab (1)Cisplatin (1)
ReviewInconclusiveLimited evidenceTier 4 · clinical

Modern Radiotherapy for High-Risk and Very-High-Risk Prostate Adenocarcinoma

The Urologic clinics of North America · May 2026

prostate adenocarcinomaprostate cancer

This review summarizes modern radiotherapy approaches for patients with high-risk or very-high-risk prostate adenocarcinoma, noting shorter courses, selectively higher radiation doses, and elective pelvic nodal irradiation. It also discusses combining radiotherapy with intensification of androgen-deprivation therapy and active studies using genomic risk stratification to guide treatment intensification or deintensification.

Studied with: androgen-deprivation therapy.

Key findings
  • Modern radiotherapy strategies include fewer treatments (shorter courses).
  • Approaches permit selectively higher radiation doses.
  • Elective pelvic nodal treatment is used in some modern strategies.
  • There is potential to intensify androgen-deprivation therapy alongside radiotherapy.
  • Active studies are evaluating tailoring radiotherapy and androgen-deprivation based on genomic risk stratification tools.
Limitations: Narrative review without primary data reported in the abstract.; Abstract provides no quantitative outcomes, effect sizes, or specific trial results.; Very brief abstract; details on methods, evidence quality, or recommendations are not provided..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

ReviewReported positiveLimited evidenceTier 4 · clinical

Managing Clinical N1 Prostate Cancer

The Urologic clinics of North America · May 2026 · review

prostate adenocarcinomaclinical N1 prostate cancer (lymph node positive)

Clinical N1 prostate cancer means prostate adenocarcinoma with regional lymph node metastases identified before definitive therapy. The abstract emphasizes thorough diagnostic imaging to distinguish regional nodal disease from distant metastases. It states that multimodal therapy—typically combinations of surgery, radiation, and hormone (androgen deprivation) therapy—is the mainstay of management and that treatment should be individualized.

Studied with: surgery, radiation therapy, hormone therapy / androgen deprivation therapy.

Key findings
  • Clinical lymph node positive prostate cancer is prostate adenocarcinoma with metastasis to regional lymph nodes detected prior to definitive therapy.
  • This is an aggressive cancer with varying presentations and prognosis.
  • Thorough diagnostic imaging is key to establishing this stage and distinguishing it from distant metastatic disease.
  • The mainstay of therapy is multimodal treatment, typically surgery + radiation + hormone therapy or radiation therapy + hormone therapy.
  • Both surgery- and radiation-based strategies can be effective when appropriately combined with androgen deprivation therapy; treatment individualization is important.
Limitations: Review article without primary new patient-level data reported in the abstract.; No quantitative outcomes, effect sizes, or sample sizes are provided in the abstract.; No details on specific agents, doses, timing, or selection criteria for surgery versus radiation are provided.; Heterogeneity of presentations and prognosis is noted but not stratified or quantified in the abstract..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

Case reportMechanismReported positiveLimited evidenceTier 3 · early humann = 1

Elevated PSMA Activity in Kimura Disease

Clinical nuclear medicine · May 2026 · case report

prostate adenocarcinoma

The authors report a case in which 68Ga-PSMA PET/CT showed elevated PSMA activity in a left axillary lesion of Kimura disease in a patient with prostate adenocarcinoma. The case indicates that Kimura disease can produce false-positive findings on PSMA PET used for staging prostate cancer.

Key findings
  • In a patient with prostate adenocarcinoma, 68Ga-PSMA PET/CT demonstrated elevated PSMA activity in a left axillary Kimura disease lesion.
  • The finding suggests Kimura disease may cause false-positive PSMA PET results during staging of prostate cancer.
Limitations: Single case report (n=1), so findings may not generalize.; No systematic evaluation of how often Kimura disease causes PSMA uptake.; No quantitative or comparative data provided in the abstract..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

ReviewReported positiveLimited evidenceTier 3 · early human

Active surveillance for prostate cancer: current status and future directions

Current opinion in urology · Mar 2026 · review

prostate adenocarcinoma

This is a narrative review of active surveillance strategies for prostate adenocarcinoma, emphasizing patient selection and monitoring. The authors state that active surveillance is the recommended approach for very low-grade and low-grade prostate cancer and is being offered to some favorable intermediate-risk patients, relying on periodic PSA testing, digital rectal exam, imaging, and repeat needle biopsies. They report that with accurate selection and a comprehensive surveillance plan, active surveillance avoids overtreatment and reduces treatment-associated comorbidities.

Key findings
  • Active surveillance is considered the treatment of choice in very low-grade and low-grade prostate cancer.
  • New data show success in management of some intermediate-risk prostate cancer.
  • Active surveillance programs use periodic PSA assessments, digital rectal examination, imaging studies, and needle biopsies for monitoring.
  • Successful active surveillance depends on accurate patient selection, comprehensive surveillance planning, proper use of diagnostic tests, and continuous patient commitment.
  • Active surveillance can avoid overtreatment and reduce treatment-associated comorbidities when the patient population is accurately selected.
Limitations: Narrative review article with no original patient-level data reported in this abstract; Abstract does not describe systematic review methods or quantitative synthesis.

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed

Human · observationalMechanismReported positiveLimited evidenceTier 3 · early human

Exploring the tumor-promoting function and prognostic value of ESPL1 in prostate adenocarcinoma

Urologic oncology · Jan 2026 · Bioinformatic analysis of TCGA and GEO datasets, immunohistochemistry on tissues, Gene Set Enrichment Analysis, and in vitro functional assays (colony formation, CCK-8, EdU, TUNEL, flow cytometry, cell cycle) in prostate cancer cell lines

prostate adenocarcinoma

The study analyzed ESPL1 (encoding Separase) expression in prostate adenocarcinoma using public datasets and tissue IHC, performed pathway analysis, and tested ESPL1 function in prostate cancer cell lines. ESPL1 was higher in tumor versus normal tissue, associated with more advanced disease and worse survival, and GSEA linked it to cell division and DNA repair pathways. In vitro suppression of ESPL1 reduced cell growth and induced apoptosis. The authors propose ESPL1 as a prognostic marker and a potential target for further study.

Key findings
  • ESPL1 expression was markedly elevated in PRAD tissues compared to normal prostate samples.
  • High ESPL1 expression correlated with advanced disease features (higher T and N stages and residual tumor presence).
  • Survival analysis associated high ESPL1 levels with reduced overall survival (OS) and progression-free interval (PFI).
  • GSEA showed enrichment of pathways related to cell division and DNA repair in samples with high ESPL1.
  • Suppressing ESPL1 in prostate cancer cell lines reduced cell growth and induced apoptosis in vitro.
Limitations: Observational analysis of public datasets and IHC provides correlation but not proof of causation in patients.; Functional experiments were performed in vitro only; no in vivo (animal) or clinical validation was reported.; Sample sizes and cohort details are not provided in the abstract.; Prognostic utility was demonstrated retrospectively; prospective validation is needed..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

Human · observationalMechanismReported positiveLimited evidenceTier 3 · early human

Identification of a Prognostic ceRNA Network Regulating TMBIM6 in Prostate Adenocarcinoma via Integrated Bioinformatic Analysis

International journal of molecular sciences · Dec 2025 · integrated bioinformatic analysis of TCGA and GEO datasets

prostate adenocarcinoma

The authors performed integrated bioinformatic analyses of TCGA and GEO datasets to investigate TMBIM6 in prostate adenocarcinoma. They identified a putative DHRS4-AS1 / hsa-miR-222-3p / TMBIM6 ceRNA axis that was associated with prognosis and found correlations with co-expression pathways and immune infiltration (notably epithelial cell abundance). The study proposes this axis as a potential prognostic biomarker and calls for experimental validation.

Key findings
  • Identification of a proposed TMBIM6/hsa-miR-222-3p/DHRS4-AS1 ceRNA axis associated with prostate adenocarcinoma prognosis.
  • The network was supported by differential expression, correlation, and survival analyses in TCGA and GEO datasets.
  • Co-expression analysis identified pathways potentially involved in tumor progression linked to TMBIM6.
  • Immune infiltration analysis suggested a correlation between TMBIM6 expression and the abundance of epithelial cells.
  • Authors propose the DHRS4-AS1/hsa-miR-222-3p/TMBIM6 axis may act as a prognostic biomarker and recommend further experimental validation.
Limitations: Computational/bioinformatic analysis only — no experimental (in vitro or in vivo) validation reported in the abstract.; Associations reported are correlative and do not establish causation.; Abstract does not report sample sizes, independent validation cohorts, or adjustment for potential confounders.; Clinical utility and prognostic performance metrics are not provided; further experimental and clinical validation required..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Lab · in vitroMechanismReported positivePreclinical onlyTier 1 · lab

Aurora kinase-a expression heterogeneity and potential benefit of combination therapy in prostate adenocarcinoma

Frontiers in cell and developmental biology · Jul 2025 · Integrative analysis of TCGA/GEO multi-omics and single-cell RNA-seq with in vitro experiments on prostate cancer cells

prostate adenocarcinoma

This study used public multi-omics datasets and single-cell RNA sequencing, plus in vitro experiments, to examine heterogeneity of Aurora kinase A (AURKA) expression in prostate adenocarcinoma. High-AURKA epithelial subpopulations were associated with proliferation and DNA repair programs, while low-AURKA subpopulations activated TNF-alpha and androgen receptor pathways linked to drug resistance. The authors report that AURKA may compensate after androgen receptor inhibition and that computational drug-sensitivity analyses suggest AURKA inhibitors could have benefit in combination with targeted therapies, ADCs, or immunotherapy; TMB and CD274 were identified as potential biomarkers for AURKA-high patients.

Studied with: targeted therapy, antibody-drug conjugate (ADC) therapy, immunotherapy, androgen receptor (AR) inhibition.

Key findings
  • Pan-cancer analysis showed AURKA expression heterogeneity among urological tumors across multiple molecular levels.
  • AURKA alteration positively correlated with MYC and E2F pathways in pan-cancer analysis.
  • Single-cell analysis identified epithelial subpopulations with high AURKA expression (epi3/4/6) that promoted proliferation via cell cycle and DNA repair regulation.
  • Low AURKA expression subsets (epi1/2/7) activated TNF-alpha and androgen receptor pathways associated with drug resistance.
  • AURKA may act as a compensatory pathway supporting tumor activity after androgen receptor (AR) inhibition in prostate cancer.
  • Clinical analysis associated AURKA overexpression with poorer prognosis in patients with low Gleason scores or high PSA.
  • Drug-sensitivity co-analysis suggested AURKA inhibitors may have benefit when combined with targeted therapy, ADC therapy, and immunotherapy.
  • Tumor mutational burden (TMB) and CD274 (PD-L1) expression were identified as biomarkers in AURKA high-expression prostate adenocarcinoma patients for clinical outcome.
Limitations: Primary evidence is computational (TCGA/GEO integration and single-cell analysis) and in vitro; no in vivo (animal) or clinical trial validation reported in the abstract.; Abstract does not report sample sizes, cohorts, or statistical details for prognostic associations.; Drug-sensitivity co-analysis appears to be predictive/correlative and not validated experimentally in vivo or clinically.; Prognostic associations may be confounded and are not demonstrated to be independent of other clinical variables in the abstract..

This preclinical and computational study characterizes AURKA expression heterogeneity in prostate adenocarcinoma and proposes molecular subtyping to guide combination strategies involving AURKA inhibitors and other therapies.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Case reportMechanismReported positiveLimited evidenceTier 3 · early humann = 1

Plasma epigenomic profiling reveals treatment-emergent squamous transformation in prostate cancer

NPJ precision oncology · Jul 2025 · Serial plasma epigenomic (circulating chromatin) profiling from a single patient case report

prostate adenocarcinomametastatic prostate cancer

The authors performed serial plasma circulating chromatin (epigenomic) profiling in a single patient with metastatic prostate cancer who developed squamous transformation. They detected dynamic changes in gene regulation in circulating chromatin that reflected emergence of squamous differentiation, enabling non-invasive diagnosis and monitoring of this resistance phenotype. The abstract notes potential therapeutic implications but provides no validation data.

Key findings
  • Circulating chromatin (plasma epigenome) showed dynamic changes corresponding to squamous differentiation in a patient with metastatic prostate cancer.
  • These plasma epigenomic changes enabled non-invasive detection and monitoring of treatment-emergent squamous transformation.
  • Authors state the findings have potential therapeutic implications.
Limitations: Single-patient case report (n=1), limiting generalizability.; No validation cohort or independent replication reported in the abstract.; No quantitative results or performance metrics provided in the abstract.; Observational profiling; cannot establish clinical utility or impact on outcomes from the data presented..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Human · observationalMechanismReported positiveModerate evidenceTier 3 · early human

Construction of a prostate adenocarcinoma molecular classification: integrating spatial transcriptomics with retrospective cohort validation

Journal of translational medicine · Jul 2025 · Spatial transcriptome analysis; Monocle 2 trajectory analysis; TCGA-PRAD cohort prognostic analysis (Kaplan-Meier and univariate Cox); Consensus clustering to define subtypes; retrospective cohort validation with immunohistochemistry and follow-up

prostate adenocarcinoma

The authors integrated spatial transcriptomics, TCGA-PRAD prognostic analyses, and a retrospective clinical cohort to define malignant cell differentiation-related prognostic genes and build a three-subtype molecular classification (MDPC) for prostate adenocarcinoma. They identified three malignant spot types and 33 MDPGs, produced three MDPC subtypes (DPP4+MSMB+, NHP2+NVL+, COL1A1+MYLK+), and validated that the COL1A1+MYLK+ subtype was associated with markedly worse overall survival and progression-free survival in their cohort. The COL1A1+MYLK+ subtype was also linked to higher Gleason/WHO grades, prior bone metastasis, and treatment history.

Reported effects: OS hazard ratio 20.72, p=0.0018 · PFS hazard ratio 117, p=0.0036 · +3 more

Key findings
  • Three malignant spot types were identified through spatial transcriptome analysis.
  • Thirty-three malignant cell differentiation-related prognostic genes (MDPGs) were defined.
  • A malignant cell differentiation-based PRAD classification (MDPC) with three subtypes was constructed: DPP4+MSMB+, NHP2+NVL+, and COL1A1+MYLK+.
  • MDPC correlated with tumor genomics and immunomics and had prognostic predictive value.
  • In the retrospective cohort, the COL1A1+MYLK+ MDPC subtype was an independent risk factor for overall survival (HR = 20.720, P = 0.0018) and progression-free survival (HR = 117.00, P = 0.0036).
  • The COL1A1+MYLK+ subtype was closely correlated with Gleason grade, WHO/ISUP grade, radiotherapy, chemotherapy, endocrinotherapy, bone metastasis before treatment, and progression after treatment.
Limitations: Retrospective cohort design for validation (potential for selection and confounding biases).; Abstract does not report sample sizes for spatial transcriptomics, TCGA-PRAD subanalyses, or the retrospective cohort.; No prospective or external prospective validation reported in the abstract.; Abstract-level report lacks detail on cohort composition, methods for controlling confounders, and reproducibility metrics..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Human · observationalMechanismReported positiveLimited evidenceTier 3 · early human

EPHB1 Protein Promoted the Progression of Prostate Adenocarcinoma Through Phosphorylating GSK3B and Activating EPHB1-GSK3B-SMAD3 Pathway

Human mutation · Jun 2025 · RNA-seq cohort analysis (GSVA, WGCNA, LASSO) and somatic mutation analysis combined with in vitro cell line functional experiments (CCK-8, EdU, Transwell, western blot, coculture, immunofluorescence)

prostate adenocarcinoma

The study combined RNA-seq analysis of prostate adenocarcinoma patients with cell-line experiments to investigate apoptosis-related features and identify drivers of high-risk disease. EPHB1 was identified as overexpressed in tumor cells and associated with poorer prognosis; in cell lines, EPHB1 interacted with GSK3B to increase p-SMAD3 and raise antiapoptotic and invasion markers, while knockdown of EPHB1 or GSK3B reduced p-SMAD3, promoted proapoptotic features, and decreased macrophage M2 polarization.

Key findings
  • Prostate adenocarcinoma samples had significantly lower apoptosis scores (by GSVA) and a RiskScore derived from WGCNA/LASSO stratified patient risk.
  • Somatic mutation analysis identified EPHB1 and KIF13A among top mutant genes and EPHB1 was overexpressed in 22RV1 and PC-3 tumor cell lines.
  • Low levels of EPHB1 indicated a better prognosis in Kaplan-Meier survival analysis.
  • Overexpression of EPHB1 increased cell viability, proliferation, and invasion in cell-line assays; knockdown reduced these phenotypes.
  • EPHB1 physically interacted with GSK3B and high EPHB1 expression promoted p-SMAD3 expression along with higher levels of antiapoptotic and invasion markers (BCL2, Snail, N-CAD) in 22RV1 cells.
  • Knockdown of GSK3B and EPHB1 inhibited p-SMAD3 activation, promoted proapoptotic features, and reduced macrophage M2 polarization in coculture assays.
Limitations: No sample size or cohort size for the RNA-seq/patient analyses reported in the abstract.; Mechanistic validation was performed in cell lines (22RV1, PC-3) without in vivo (animal) experiments.; The RiskScore and bioinformatic findings are observational and require external clinical validation.; No clinical intervention or patient-level experimental manipulation was performed..

This study implicates EPHB1 in promoting prostate adenocarcinoma progression via the EPHB1-GSK3B-SMAD3 signaling axis and links it to tumor cell invasion, apoptosis regulation, and macrophage M2 polarization.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewMechanismInconclusiveLimited evidenceTier 4 · clinical

Concurrent occurrence of adenocarcinoma and urothelial carcinoma of the prostate: Coexistence mechanisms from multiple perspectives

World journal of clinical cases · Apr 2025

prostate adenocarcinomaprostate urothelial carcinoma

This editorial/review examines the concurrent occurrence of prostate adenocarcinoma and prostate urothelial carcinoma by synthesizing existing literature. It summarizes proposed mechanisms for their coexistence and for a possible transformation between histologies — including androgen receptor involvement, gene mutations, altered cell signaling, tumor multipotent stem cell differentiation, epithelial-mesenchymal transition, and mesenchymal-epithelial transition. The authors aim to improve diagnostic accuracy and support more personalized clinical approaches, but the article discusses hypotheses and literature rather than reporting new experimental trial data.

Key findings
  • The article explores potential mechanisms underlying coexistence of prostate adenocarcinoma and prostate urothelial carcinoma, including androgen receptor roles, gene mutations, and complex interactions in cell signaling pathways.
  • The authors discuss hypotheses that prostate adenocarcinoma may transform into urothelial carcinoma via processes such as tumor multipotent stem cell differentiation, epithelial-mesenchymal transition, and mesenchymal-epithelial transition.
  • The stated goal is to inform more accurate diagnoses and more personalized clinical treatments and to lay groundwork for improving patient prognoses.
Limitations: Editorial/narrative review rather than original experimental study.; Mechanisms and transformation hypotheses are speculative and based on literature synthesis, not on new experimental validation within this article.; No methods, sample sizes, or systematic review/meta-analysis methodology are reported in the abstract..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewMechanismInconclusiveLimited evidenceTier 3 · early human

Metabolic dysfunction-associated steatotic liver disease and urinary system cancers: Mere coincidence or reason for concern?

Metabolism: clinical and experimental · Jan 2025 · narrative review

renal cell carcinomaurothelial carcinomaprostate adenocarcinoma

This narrative review summarizes and interprets conflicting evidence about whether metabolic dysfunction-associated steatotic liver disease (MASLD) is associated with urinary system cancers (renal cell carcinoma, urothelial carcinoma, and prostate adenocarcinoma). It discusses possible linking mechanisms such as insulin resistance and lipotoxicity but does not present new primary data.

Key findings
  • MASLD is described as a systemic disease characterized by insulin resistance and lipotoxicity.
  • Associations between MASLD and type 2 diabetes, cardiovascular disease, liver cirrhosis, and hepatocellular carcinoma are well described.
  • The association between MASLD and extra-hepatic cancers, specifically urinary system cancers, has received significantly less attention and the existing evidence is conflicting.
  • The review explores potential mechanisms (including insulin resistance and lipotoxicity) that could explain a higher risk of urinary system cancers in patients with MASLD.
  • The article is a narrative synthesis intended to help readers interpret the available literature rather than reporting new experimental or clinical data.
Limitations: Narrative review design (not a systematic review or meta-analysis) which may be prone to selection bias in included evidence.; No new primary data are presented in this article.; Abstract indicates the underlying evidence is conflicting, limiting firm conclusions.; Does not provide quantitative pooled estimates of association between MASLD and urinary system cancers..

Review examines potential links and mechanisms between MASLD and urinary system cancers.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

Browse all studies mentioning Prostate Adenocarcinoma →

Where the evidence is

What has been studied, and how strong it is, by topic. A dashed cell means no studies were found for that combination — a gap, not evidence of no effect. Open a row to see its studies.

CompoundHuman evidenceMechanismSafetyTrial
Etoposide————
Carboplatin————
Cisplatin————
Durvalumab————

Study mix

45 published studies by what they were done in. Lab and animal findings often do not carry over to people.

16 Human4 Animal2 Lab23 Review/other
Reported directionReported positive32Mixed results2Reported negative1Inconclusive10

Evidence at a glance: compounds studied in Prostate Adenocarcinoma

A deterministic grade of what published studies report for each: strength of evidence, the reported direction, and the largest credible effect, strongest-evidence first. This summarizes findings; it is not a claim that anything works.

EtoposideInsufficient evidenceReported negative

No primary experimental studies yet.

Most authoritative study: Managing a Rare Case of Mixed Extrapulmonary Small Cell Carcinoma and Adenocarcinoma of the Prostate

No human studies yet · No numeric effect sizes reported · All studies are small (n < 30).
CarboplatinInsufficient evidenceInconclusive

No primary experimental studies yet.

Most authoritative study: Managing a Rare Case of Mixed Extrapulmonary Small Cell Carcinoma and Adenocarcinoma of the Prostate

No human studies yet · No numeric effect sizes reported · Based on a single study.
CisplatinInsufficient evidenceReported negative

No primary experimental studies yet.

Most authoritative study: Prostate small cell carcinoma and skin metastases: a rare entity

No human studies yet · No numeric effect sizes reported · Based on a single study.
DurvalumabInsufficient evidenceInconclusive

No primary experimental studies yet.

Most authoritative study: Managing a Rare Case of Mixed Extrapulmonary Small Cell Carcinoma and Adenocarcinoma of the Prostate

No human studies yet · No numeric effect sizes reported · Based on a single study.

What the research shows for Prostate Adenocarcinoma

A plain-language summary of the reviewed studies OncoForge tracks for Prostate Adenocarcinoma. It reports what those studies described, not a claim that any compound or therapy helps or harms Prostate Adenocarcinoma. Most of this evidence is early, and findings often conflict.

  • These studies report an observational case report describing two male patients (ages 72 and 58) who presented with gross hematuria and bladder lesions on MRI.
  • These studies report that pathology after radical cystectomy and prostatectomy showed concurrent primary small cell carcinoma of the bladder and prostate adenocarcinoma in these patients.
  • These studies report mixed clinical outcomes: the abstract indicates one patient died, while details on the other patient's course are limited in the available summary.
  • These studies report only a very small, descriptive human series (n = 2) without systematic follow-up, control groups, or statistical analysis.

Supportive & alternative options discussed

  • Exercise / prehabilitation: Also discussed as a supportive option to help maintain function, reduce fatigue, and improve quality of life for people with prostate cancer; exercise was not evaluated in these studies.
  • Mind–body (MBSR / CBT): Also discussed as a supportive approach (stress reduction, coping) in prostate cancer care; mind–body therapies were not evaluated in these studies.
  • Acupuncture: Also discussed as a supportive option for symptom relief (for example, pain or treatment-related side effects) in prostate cancer care; acupuncture was not evaluated in these studies.
  • Ketogenic / metabolic therapy: Also discussed by some as a dietary approach of interest in prostate cancer, but not evaluated or supported by the data in these studies.

What we don’t know yet

  • How common is the concurrent occurrence of small cell carcinoma of the bladder with prostate adenocarcinoma in broader patient populations?
  • What are the optimal diagnostic, staging, and treatment strategies when both tumor types are present?
  • How does the co-occurrence of these two tumors affect prognosis, treatment response, and survivorship?
  • Are there shared risk factors or biological mechanisms that explain concurrent primary tumors in bladder and prostate?
  • Do larger observational studies or clinical trials replicate these findings or provide guidance for management?
The evidence consists of a single, very small descriptive case report and is too limited to draw conclusions about frequency, prognosis, or management.

Clinical trials in Prostate Adenocarcinoma

23 ongoing · 46 completed · tracked from ClinicalTrials.gov. Recruiting is not the same as proven, and completed is not the same as positive — read the results. Not a recommendation.

Completed
22 stopped (terminated / withdrawn / suspended)

Search all trials on ClinicalTrials.gov →

Getting care & support

Nonprofit / Gov

Practical, vetted help for Prostate Adenocarcinoma — advocacy, paying for treatment, second opinions, and caregivers.

If you’re struggling emotionally, you don’t have to wait.

Advocacy & community

No dedicated organization for this specific cancer is curated yet — these general organizations can help in the meantime.

Financial help

  • PAN Foundation ↗ — Copay assistance funds by diagnosis (funds open and close as money allows). · status changes often — check the fund’s site
  • HealthWell Foundation ↗ — Copay and premium assistance funds by disease. · status changes often — check the fund’s site
  • CancerCare — financial assistance ↗ — Limited grants plus free financial counseling. · status changes often — check the fund’s site
  • Family Reach ↗ — Help with everyday living costs (rent, transport, food) during treatment. · status changes often — check the fund’s site
  • NeedyMeds ↗ — Searchable directory of drug patient-assistance and discount programs. · status changes often — check the fund’s site
What you’ll typically need to apply
  • Your diagnosis and, if you have it, the specific drug/treatment name (from your care team).
  • Insurance details — your member ID card, or a note that you're uninsured (some funds require active insurance, some don't).
  • Proof of income and household size (recent pay stubs, a tax return, or a benefits letter) — most funds are income-based.
  • Your prescriber's contact information; some programs need the clinic to submit part of the application.
  • Apply early and re-check: funds open and close as money is available, so a closed fund may reopen.

General guidance — each program sets its own eligibility. Confirm requirements on the program’s site.

Help paying for the medicines on this page

Second opinions

Caregiver support

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