Research Radartracking 1,762 published studies · 471 human · 11 safety signals · 58 clinical trials · 44 cancer pages · updated Sep 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 Sep 2026 · OncoForge editorial · How we review →

AI extractedhuman reviewedsources checkedretractions suppressed· last updated Sep 2026

Evidence at a glanceHuman · observationalMixed results⚠ Studies disagree
54 published studies that name Prostate Adenocarcinoma17 human studies approved & graded (trial, observational, or meta-analysis)40 human clinical studies in the Prostate Adenocarcinoma corpus694 source documents in the Prostate Adenocarcinoma corpus

last checked September 8, 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
  • open retropubic radical prostatectomy (RRP)
  • laparoscopic radical prostatectomy (LRP)
  • robot-assisted laparoscopic radical prostatectomy (RALRP)
  • radiotherapy
  • active surveillance
  • vitamin K antagonists (VKAs)
  • abiraterone
  • pelvic ultra-hypofractionated radiotherapy (UHF) + HDR brachytherapy
  • conventionally fractionated pelvic radiotherapy (CF) + HDR brachytherapy
  • two-fraction stereotactic ablative radiotherapy (SABR)
  • docetaxel
  • zoledronic acid
  • AURKA inhibitors (e.g. + alisertib
  • combination therapy (AURKA inhibitor plus targeted/ADC/immune therapy)
  • 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.

19
Interventions
0
Standard of care
12
Tested in people
4
Lab / animal
3
Named in lit.
8
Classes
Standard of care (0) Guideline option (0) Tested in people (12) Lab / animal only (4) Named in the literature (3)

Tested in people, by trial phase: Phase III ×5 · Phase I ×1 · phase not reported ×6

Clinical evidence
Preclinical evidence
Standard of care
Guideline option
Tested in people
Lab / animal only
Named in the literature
Surgery & procedures
—
—
3
—
—
Radiotherapy
—
—
4
—
—
Chemotherapy
—
—
1
3
—
Targeted therapy
—
—
—
—
1
Immunotherapy
—
—
—
1
—
Hormonal therapy
—
—
1
—
1
Repurposed drugs
—
—
1
—
—
Other
—
—
2
—
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 (19)
Phase III trial (5)
abirateroneconventionally fractionated pelvic radiotherapy (CF) + HDR brachytherapydocetaxelpelvic ultra-hypofractionated radiotherapy (UHF) + HDR brachytherapyzoledronic acid
Phase I trial (1)
two-fraction stereotactic ablative radiotherapy (SABR)
Meta-analysis (6)
active surveillancelaparoscopic radical prostatectomy (LRP)open retropubic radical prostatectomy (RRP)radiotherapyrobot-assisted laparoscopic radical prostatectomy (RALRP)vitamin K antagonists (VKAs)
Named in the literature
enzalutamideAURKA inhibitors (e.g. + alisertibcombination therapy (AURKA inhibitor plus targeted/ADC/immune therapy)· biomarker-selected

"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

Get cited updates on Prostate Adenocarcinoma
A monthly email when the research changes — $10/mo. Manage follows
Follow Prostate Adenocarcinoma

Snapshot

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

What it is
Prostate adenocarcinoma is the most common cancer in men in many Western countries and the second leading cause of cancer-related death; advanced disease commonly involves bone metastases (>80% of patients) and can give rise to treatment-emergent neuroendocrine prostate cancer after androgen-receptor-pathway inhibitor therapy. [1][2][3]
Survival
Median survival after development of bone metastases is approximately three years; in the United States an estimated 299,010 new cases and 35,250 deaths were anticipated in 2024. [2][4]
Standard treatment
Localized tumors are managed with active surveillance or local therapy (radical prostatectomy or radiation); systemic standard‑of‑care in trials has included androgen deprivation therapy (ADT) alone or ADT plus docetaxel. [1][5]
Key test
A molecular transcriptomic classifier (a set of 36 biomarkers) can identify a subtype of localized prostate cancer associated with non-evolutive disease and may help select patients (estimated ~22% of localized cases) for active surveillance rather than immediate surgery. [6]
Biggest challenge
The main clinical challenges are diagnosis and advanced-stage disease with treatment resistance—onset of castration-resistant prostate cancer substantially impairs prognosis—and an aggressive treatment-emergent neuroendocrine variant can arise after AR-pathway inhibitor therapy. [4][3]

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 riskHER-2/neu overexpression — Associated with a higher risk of death and recurrence. [7]
  • ▲ increases riskHistory of skeletal fracture — Median overall survival was 39 months longer in men without a history of skeletal fracture. [2]
  • ▲ increases riskFocal neuroendocrine differentiation — Pooled HR 1.39 (95% CI 1.07–1.81) for biochemical recurrence after radical prostatectomy. [1]
  • ▲ increases riskHigher lymphatic vessel density — Lymphatic vessel density was higher in tumoral compartments, rose with tumor grade, and correlated with main prognostic factors. [8]

Biomarkers

  • 36-transcriptomic biomarker setActionableIdentify a localized subtype associated with non-evolutive disease to select patients for active surveillance [6]
  • APOE, SPC25, TSPAN1, VGF (four-gene signature) · Associated with shorter biochemical recurrence-free survival [9]
  • Chromogranin A (CgA) · Tissue marker for neuroendocrine differentiation [1]
  • PSA · Not expressed by neuroendocrine cells (so neuroendocrine differentiation may be PSA-negative) [1]
  • PSMA · Diagnostic cytology marker with higher sensitivity and specificity than PSA and PSAP for metastatic prostate adenocarcinoma [10]
  • NKX3.1 · Diagnostic cytology marker with higher sensitivity and specificity than PSA and PSAP for metastatic prostate adenocarcinoma [10]
  • TMBIM6 · Overexpressed in tumors and associated with poorer overall survival; proposed as part of a predictive ceRNA axis [4]
  • HER-2/neu · Overexpression associated with higher risk of death and recurrence [7]
  • GATA3 · Nuclear expression observed in a minority of primary tumors (6.9%), seen in higher-grade components [11]
  • Lymphatic vessel density (D2-40) · Higher in tumoral compartments and correlated with prognostic factors and tumor grade [8]

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

Overview7 points
  • Prostate cancer is the most common cancer in men in many Western countries (and the most common solid cancer) and is the second leading cause of cancer-related death in men. [1][2]
  • Treatment-emergent neuroendocrine prostate cancer (t-NEPC) can arise after androgen receptor pathway inhibitor therapy and is described as an aggressive variant. [3]
  • Prostate adenocarcinoma has a marked propensity for bone metastases which occur in more than >80% of patients with advanced disease, typically involving the spine, pelvis and rib cage. [2]
  • Antihormonal therapy used to inhibit disease progression or prevent recurrence can lead to changes in bone metabolism resulting in loss of bone mineral density, a phenomenon described as cancer treatment-induced bone loss (CTIBL). [2]
  • A new prostate cancer grading system was proposed in 2013 and endorsed by major journals and societies in 2014, but there is still wide variation in how Gleason scores are grouped worldwide and only a minority of published articles group Gleason scores accurately. [12]
  • Prostate adenocarcinoma has challenges in diagnosis and advanced-stage management; the onset of castration-resistant prostate cancer (CRPC) substantially impairs prognosis. [4]
Show 1 lab & early-research finding
  • Small metastatic biopsies have limitations and a prostate rebiopsy confirmed the diagnosis in the reported case. [3]
Biology & pathways5 points
  • Proteomic profiling in TCEP-exposed prostate cancer models revealed dysregulation of pathways involved in cholesterol metabolism, lysosome function, and PPAR signaling. [9]
  • Neuroendocrine cells may regulate prostate epithelial growth by secreting neuropeptides, growth factors, and factors that degrade the extracellular matrix. [1]
  • ESPL1 expression was markedly elevated in prostate adenocarcinoma tissues compared with normal prostate samples and correlated with advanced disease features such as higher T and N stages and residual tumor presence; survival analysis linked high ESPL1 levels to reduced overall survival and progression-free interval; gene set enrichment analysis (GSEA) identified ESPL1-related enrichment in pathways tied to cell division and DNA repair; and suppressing ESPL1 in prostate adenocarcinoma cell lines reduced cell growth and induced apoptosis in vitro. [13]
  • TMBIM6 has been related to activation of mTORC2 and AKT, which have been implicated in tumor development. [4]
  • AURKA can phosphorylate and inhibit p53 activity and induce epithelial-mesenchymal transition by activating pathways such as PI3K/AKT and Wnt/β-catenin. [14]
Key biomarkers9 points

Key figures

Prognostic factors
FactorEffectHR (95% CI)p
RR recurrence with HER-2/neu over expression▲ worse1.87 (1.59–2.21)<0.0001
RR death with HER-2/neu over expression▲ worse1.63 (1.47–1.82)<0.0001
Source quotes
  • “In the presence of over expression the recurrence RR was 1.87 (95% CI 1.59-2.21, p <0.0001).”
  • “The overall RR of death in those with HER-2/neu over expression in the primary tumor was 1.63 (95% CI 1.47-1.82, p <0.0001).”
  • PSMA and NKX3.1 showed higher sensitivity and specificity than PSA and PSAP in cytology specimens for diagnosing metastatic prostate adenocarcinoma; PSMA showed a strong membranous staining pattern and NKX3.1 showed a moderate nuclear staining pattern in these cytology specimens. [10]
  • GATA3 nuclear expression was observed in 6.9% (4/58) of primary prostate adenocarcinoma cases and was present in higher-grade (Gleason 4 or 5) components while Gleason 3 components were negative. [11]
  • 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. [9]
  • Chromogranin A (CgA) was assessed as a tissue marker for neuroendocrine differentiation in all 16 studies included in a systematic review. [1]
  • Neuroendocrine cells do not express prostate specific antigen (PSA) and androgen receptors. [1]
  • A molecular classification study provided a set of 36 transcriptomic biomarkers to identify a subtype of localized prostate cancer associated with non-evolutive disease. [6]
  • Lymphatic vessel area and density were evaluated using the D2-40 monoclonal antibody; lymphatic vessel density was higher in tumoral than non-tumoral compartments (mainly in periglandular stroma), increased in parallel with tumor grade progression, and positively correlated with main prognostic factors of prostate adenocarcinoma. [8]
  • TMBIM6 was identified as overexpressed in prostate cancer tissue in multiple datasets, and higher TMBIM6 expression was associated with significantly poorer overall survival in TCGA-PRAD data; the study proposes the DHRS4-AS1/hsa-miR-222-3p/TMBIM6 ceRNA axis as a possible prediction biomarker, and in primary PRAD lower expression of hsa-miR-222-3p was detected in tumors while higher hsa-miR-222-3p expression was associated with better survival. [4]
Show 1 lab & early-research finding
  • HER-2/neu overexpression in primary prostate tumors is associated with a higher risk of death and recurrence. [7]
Prognosis9 points
  • A molecular classification identified a subtype strongly associated with absence of biochemical recurrence and estimated its prevalence at 22% of localized prostate cancers. [6]
  • A history of skeletal fracture was associated with shorter overall survival: median overall survival was 39 months longer in men without a history of skeletal fracture. [2]
  • High ESPL1 expression was associated with reduced overall survival and shorter progression-free interval in prostate adenocarcinoma. [13]
  • Evaluation of lymphatic vessel density on radical prostatectomy with positive nodes may help to discriminate patients at higher risk of developing aggressive disease who may be candidates for early androgen deprivation therapy to delay clinical worsening. [8]
  • In the TMBIM6 study, co-expression and survival analyses suggested that higher TMBIM6 expression correlated with poorer outcomes. [4]
  • Focal neuroendocrine differentiation (NED) in radical prostatectomy specimens was significantly associated with biochemical recurrence after radical prostatectomy (pooled HR 1.39, 95% CI 1.07–1.81) in a meta-analysis of five studies including 944 patients. [1]
Show 3 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. [9]
  • In this study, high AURKA expression characterized proliferative PRAD epithelial subpopulations, and AURKA-overexpressing patients with low Gleason scores or high PSA had a poor prognosis. [14]
  • Treatment-emergent neuroendocrine prostate cancer (t-NEPC) was described as an aggressive variant in the reported case. [3]
Safety & interactions3 points

Key figures

Prognostic factors
FactorEffectHR (95% CI)p
crude OR for prostate cancer associated with ≥3 years VKA use (case-control) vs no long-term VKA use—1.01 (0.95–1.08)—
Source quotes
  • “Among 38,832 prostate cancer cases, 1,089 (2.8%) had used VKAs for 3 or more years compared to 10,803 (2.8%) controls yielding a crude OR of 1.01 (95% CI, 0.95-1.08).”
  • 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. [9]
  • In a nationwide case-control study and meta-analysis, long-term use of vitamin K antagonists (VKAs) was not associated with a reduced risk of prostate cancer; the authors concluded a major protective effect seems unlikely. [15]
  • This meta-analysis found that ADT in prostate cancer reduces bone mineral density and increases fracture risk; longer ADT duration correlated negatively with lumbar spine and total hip BMD. [2]
Treatments & compounds studied18 treatments

Chemotherapy

  • carboplatin: The patient was treated with carboplatin as part of a combination regimen after diagnosis of treatment-emergent neuroendocrine prostate cancer. [3]
  • etoposide: The patient was treated with etoposide as part of a combination regimen after diagnosis of treatment-emergent neuroendocrine prostate cancer. [3]
  • docetaxel: Docetaxel was used in combination with ADT as part of standard-of-care or experimental groups in the STAMPEDE platform. [5]

Targeted therapy

  • AURKA inhibitors (e.g., alisertib): AURKA small-molecule inhibitors (for example, alisertib) have entered clinical trials in prostate cancer, and reported data suggest AURKA inhibitor monotherapy has not improved patient prognosis, possibly due to compensatory survival pathways. [14]

Immunotherapy

  • durvalumab: The patient was treated with carboplatin, etoposide, and durvalumab. [3]

Hormonal therapy

  • enzalutamide: The reported patient had been treated with enzalutamide prior to the development of lung lesions. [3]
  • abiraterone acetate · abiraterone: Abiraterone acetate (given with ADT) was associated with the longest survival among trial groups in the STAMPEDE platform. [5]

Radiotherapy

  • radiation therapy · radiotherapy: Radiation therapy is mentioned as a local therapy option alongside radical prostatectomy and active surveillance for localized prostate tumors. [1]
  • pelvic ultra-hypofractionated radiotherapy (UHF) + HDR brachytherapy: Pelvic ultra-hypofractionated whole-pelvis radiotherapy (UHF) given as 25 Gy in 5 fractions combined with a single-fraction 15 Gy HDR brachytherapy boost to the prostate and concomitant ADT was well tolerated and had low and comparable grade 2-3 genitourinary and gastrointestinal toxicity versus conventionally fractionated pelvic radiotherapy in an interim analysis. [16]
  • conventionally fractionated pelvic radiotherapy (CF) + HDR brachytherapy: Conventionally fractionated whole-pelvis radiotherapy (CF) delivered with a single-fraction 15 Gy HDR brachytherapy boost to the prostate and concomitant ADT had low and comparable short-term grade 2-3 genitourinary and gastrointestinal toxicity versus pelvic UHF in the interim analysis. [16]
  • two-fraction stereotactic ablative radiotherapy (SABR): Two-fraction prostate stereotactic ablative radiotherapy (SABR) with rectal spacing (27 Gy in two fractions, optional boost to 30 Gy) appeared safe with acceptable two-year toxicity and produced marked PSA declines in an initial cohort. [17]
    median PSA at baseline 5.35 vs 1-year and 2-year follow-upmedian PSA at 2 years 0.31 vs baseline
    Source quotes
    • “Mean and median PSA decreased from 5.66 and 5.35ng/mL at baseline to 1.22 and 0.88ng/mL and 0.42 and 0.31ng/mL at 1- and 2-year follow-up, respectively, representing a decrease of 81.3% and 94.8%.”
    • “Mean and median PSA decreased from 5.66 and 5.35ng/mL at baseline to 1.22 and 0.88ng/mL and 0.42 and 0.31ng/mL at 1- and 2-year follow-up, respectively, representing a decrease of 81.3% and 94.8%.”

Repurposed drugs

  • vitamin K antagonists (VKAs): Use of vitamin K antagonists (VKAs) has been studied for association with prostate cancer risk; a pooled estimate from a meta-analysis was 0.86 (95% CI, 0.70-1.05), and the authors concluded a major protective effect of VKAs seems unlikely. [15]
    pooled odds ratio for prostate cancer associated with VKA use 0.86 (95% CI 0.7–1.05) vs no VKA use
    Source quote
    • “Using random effect methods, a pooled effect estimate of 0.86 (95% CI, 0.70-1.05) was obtained; however, there was considerable across-study heterogeneity (I2 : 93.9%).”

Procedures & devices

  • open retropubic radical prostatectomy (RRP): Open retropubic radical prostatectomy (RRP) is one of the surgical approaches compared with laparoscopic and robot-assisted approaches for localized prostate cancer. [18]
  • laparoscopic radical prostatectomy (LRP): Laparoscopic radical prostatectomy (LRP) was compared with RRP and RALRP and was reported not to differ significantly from RRP for overall positive surgical margins, complication rate, continence, potency, total blood loss, and hospital stay. [18]
  • robot-assisted laparoscopic radical prostatectomy (RALRP): Robot-assisted laparoscopic radical prostatectomy (RALRP) was compared with LRP and RRP and was reported not to differ significantly from RRP for many perioperative and functional outcomes, while having shorter catheterization and reductions in blood transfusion and biochemical recurrence compared with RRP. [18]

Other

  • active surveillance: Active surveillance is named as an option instead of immediate surgery for selected localized prostate tumors. [1]
  • zoledronic acid: Zoledronic acid was included as an added agent to ADT plus docetaxel in some experimental groups within the STAMPEDE platform. [5]
  • combination therapy (AURKA inhibitor plus targeted/ADC/immune therapy): biomarker-selectedAuthors propose that an AURKA high-expressing population may be suitable for combination therapy pairing AURKA inhibitors with targeted agents, antibody-drug conjugates (ADCs), or immune therapies. [14]
What we don't know yet7 points
  • Molecular docking simulations suggested potential structural compatibility between TCEP and the four protein targets, supporting possible molecular interactions that require further experimental validation. [9]
  • Well-designed prospective studies are needed to confirm the prognostic findings of focal neuroendocrine differentiation in prostate cancer. [1]
  • Further clinical trials have been recommended to test whether HER-2/neu is a marker of worse outcome in prostate cancer and a potential therapeutic target. [7]
  • Further studies are needed to determine the clinical significance of GATA3 expression in prostate adenocarcinoma and its potential impact on tumor behavior and prognosis. [11]
  • Authors recommended more widespread adoption of the five-grade-group prostate cancer grading system to minimize incorrect Gleason score grouping in future studies. [12]
  • The role of TMBIM6 in the progression of prostate cancer cells has not been thoroughly explored and requires further study. [4]
  • Continued investigation into new biomarkers and therapeutic approaches is required to improve diagnostic precision and therapeutic success in prostate cancer. [4]
Epidemiology6 points

Key figures

Survival & outcomes
OutcomeValue95% CI
estimated deaths (2024, US)35250—
Source quotes
  • “An estimated 299,010 new cases and 35,250 deaths from prostate adenocarcinoma (PRAD) are anticipated in 2024 alone, making it the most common cancer in males and the second largest cause of cancer-related mortality in the US [1].”
  • The reported rate of incidental prostate adenocarcinoma detection in radical cystoprostatectomy specimens varies widely, ranging from 15% to 54%; in the studied series, seventy-two out of 158 radical cystoprostatectomy cases showed incidental prostate adenocarcinoma. [19]
  • Complete sampling of the prostate in radical cystoprostatectomy specimens was suggested to allow greater detection of clinically significant incidental prostate adenocarcinoma; in the incidental prostate adenocarcinoma cases, extraprostatic extension was detected in 13/72 (18.1%) cases, with 11/13 (84.6%) of these in the complete sampling group, and overall 4/72 (5.6%) of incidental prostate adenocarcinoma cases had a Gleason score >7 and all of these were found in the complete-sampling group. [19]
  • Incidental prostate adenocarcinoma was detected in 67 of 919 bladder cancer patients (7.3%) in a single-center series. [20]
  • An estimated 299,010 new cases and 35,250 deaths from prostate adenocarcinoma were anticipated in 2024 in the United States. [4]
  • The median survival time of patients with prostate cancer is approximately three years after the development of bone metastases. [2]
  • A meta-analysis found a lower prevalence of incidental prostate adenocarcinoma in Asian than in non-Asian countries (19% versus 32%). [20]
Standard management4 points
  • For localized prostate tumors, standard management is either active surveillance or local therapy with radical prostatectomy (RP) or radiation therapy. [1]
  • One molecular study concluded that at least 20% of patients with localized prostate cancer can be predicted to have non-evolutive disease and "should not undergo immediate surgery and rather be placed under active surveillance." [6]
  • In the STAMPEDE platform, standard of care included androgen deprivation therapy (ADT) alone or ADT plus docetaxel. [5]
  • Clinical trials have evaluated whole-pelvis ultra-hypofractionated radiotherapy versus conventionally fractionated radiotherapy delivered with a single-fraction 15 Gy HDR brachytherapy boost to the prostate together with concomitant ADT. [16]
Staging & risk4 points
  • The authors called for more widespread adoption of the new prostate cancer grading system composed of five grade groups to minimize incorrect grouping in future studies. [12]
  • In a review of 2016–2017 articles, pathology journals were more likely than non-pathology journals to grade Gleason score 7 separately (56.9% vs 40.0%, p<0.05). [12]
  • Differentiating atrophy, atypical adenomatous hyperplasia (AAH), atypical small acinar proliferation (ASAP), and adenocarcinoma is essential because malignant lesions require more restrictive treatment. [21]
  • A diagnosis of atypical small acinar proliferation (ASAP) on biopsy is an indication for repeat biopsy because the chance of finding prostate adenocarcinoma is greater than after a diagnosis of high-grade prostatic intraepithelial neoplasia. [21]

Sources

Every statement above is drawn from these reviewed sources. This page reports what they describe. Sources last checked September 8, 2026.

  1. Meta-analysisFocal Neuroendocrine Differentiation of Conventional Prostate Adenocarcinoma as a Prognostic Factor after Radical Prostatectomy: A Systematic Review and Meta-Analysis · 2019
  2. Meta-analysisA systematic review and meta-analysis of bone metabolism in prostate adenocarcinoma · 2010
  3. Review articleDiagnostic Challenge in Treatment-Emergent Neuroendocrine Prostate Cancer: A Case Requiring Prostate Rebiopsy After an Inconclusive Metastatic Lung Biopsy · 2026
  4. StudyIdentification of a Prognostic ceRNA Network Regulating TMBIM6 in Prostate Adenocarcinoma via Integrated Bioinformatic Analysis · 2025
  5. Randomized trialOn-treatment serum prostate-specific antigen and overall survival in prostate cancer (STAMPEDE platform protocol): a post-hoc analysis of data from five phase 3 trials · 2026
  6. Meta-analysisComprehensive molecular classification of localized prostate adenocarcinoma reveals a tumour subtype predictive of non-aggressive disease · 2018
  7. Meta-analysisHer-2/neu expression in prostate adenocarcinoma: a systematic review and meta-analysis · 2010
  8. Clinical trialLymphatic Vascularization in Prostate Adenocarcinoma: Correlation with Tumor Grade, Androgen Withdrawal and Prognosis · 2015
  9. Review articleTCEP flame retardant linked to prostate cancer progression: Integrative analysis and novel biomarker discovery · 2026
  10. Clinical trialPerformance of different prostate specific antibodies in the cytological diagnosis of metastatic prostate adenocarcinoma · 2017
  11. StudyImmunohistochemical GATA3 expression in prostate adenocarcinoma: pitfalls · 2025
  12. Clinical trialHow Are Gleason Scores Categorized in the Current Literature: An Analysis and Comparison of Articles Published in 2016-2017 · 2019
  13. StudyExploring the tumor-promoting function and prognostic value of ESPL1 in prostate adenocarcinoma · 2026
  14. StudyAurora kinase-a expression heterogeneity and potential benefit of combination therapy in prostate adenocarcinoma · 2025
  15. Meta-analysisUse of vitamin K antagonists and risk of prostate cancer: Meta-analysis and nationwide case-control study · 2019
  16. Randomized trialPelvic nodes ultra-hypo fractionated versus conventionally fractionated IMRT with HDR brachytherapy in prostate cancer: interim analysis of a collaborative multi-institutional non-inferiority phase 3 trial (PCS-XI, NCT05820633) · 2026
  17. Clinical trialTwo-year toxicity and PSA dynamics in the initial cohort of the SABR-Dual trial - two-fraction stereotactic radiotherapy for localized prostate cancer using rectal spacing · 2026
  18. Meta-analysisProstatectomies for localized prostate cancer: a mixed comparison network and cumulative meta-analysis · 2018
  19. Clinical trialIncidental Prostate Adenocarcinoma in Cystoprostatectomy Specimens: Partial Versus Complete Prostate Sampling · 2017
  20. Meta-analysisPrevalence and clonality of synchronous primary carcinomas in the bladder and prostate · 2018
  21. Systematic reviewDiagnostic Difficulties With Atrophy, Atypical Adenomatous Hyperplasia, and Atypical Small Acinar Proliferation: A Systematic Review of Current Literature · 2016

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
14
Observational
3
Case report
179
Review
433
Preclinical
0
Other
30

Living document — last change September 8, 2026: Cancer page updated. 3 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 9/1/2026.

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 evidenceMixed results

No primary experimental studies yet.

Largest credible effect: patient_age 63, n=1 PMID 33413292 · effect sizes 2–63 across 2 studies

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

No human studies yet · Findings conflict across studies · Effect sizes reported in only 1 of 3 studies · All studies are small (n < 30).
ChemotherapyFDA off-label3 studiesFull profile →
CisplatinInsufficient evidenceMixed results

No primary experimental studies yet.

Largest credible effect: patient_age 63, n=1 PMID 33413292 · effect sizes 2–63 across 2 studies

Most authoritative study: Dermatomyositis associated with prostate adenocarcinoma with neuroendocrine differentiation

No human studies yet · Findings conflict across studies · Effect sizes reported in only 1 of 2 studies · 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 →
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.

54 studies17 human5 animal3 lab⚠ Conflicting evidenceMechanism (33)Supportive care (2)Absorption (PK) (1)Trial (1)

Tracking 54 published studies of Prostate Adenocarcinoma: 17 in humans, 5 in animals, 3 in the lab, 29 reviews/other.

Reported direction across studies: 36 positive, 3 mixed, 3 negative, 12 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 (3)Cisplatin (2)Carboplatin (1)Durvalumab (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

Lab · in vitroMechanismReported positivePreclinical onlyTier 1 · lab

Identify GDPD3 as a key regulator of epithelial-mesenchymal transition and prostate adenocarcinoma progression via the LPA/LPAR1/AKT axis: transcriptomic and experimental study

Frontiers in immunology · Jan 2026 · Integrated single-cell and bulk transcriptomic analysis with in vitro knockdown experiments in DU145 prostate cancer cells

prostate adenocarcinoma

The authors combined single-cell and bulk RNA sequencing analyses with laboratory experiments in DU145 prostate cancer cells. They found GDPD3 was upregulated in malignant prostate tissues and that knocking down GDPD3 reduced cell proliferation, invasion, migration and EMT. Mechanistically, GDPD3 influenced lysophosphatidic acid (LPA) levels; LPA induced EMT via LPAR1 and activation of AKT, and blocking LPAR1 or AKT reversed EMT. The study proposes GDPD3 as a potential therapeutic target and biomarker in prostate adenocarcinoma.

Key findings
  • A 21-gene prognostic model was established from integrated single-cell and bulk RNA-seq analyses.
  • QPCR and immunohistochemistry showed GDPD3 expression was significantly elevated in malignant prostate tissues.
  • Knockdown of GDPD3 in DU145 cells inhibited tumor cell proliferation, invasion, and migration.
  • GDPD3 regulated levels of lysophosphatidic acid (LPA).
  • Inhibition or knockdown of the LPA receptor LPAR1 suppressed EMT.
  • LPA promoted EMT through activation of the AKT signaling pathway, and inhibition of AKT reversed LPA-induced EMT.
Limitations: Functional validation was performed only in vitro (DU145 cell line); no in vivo (animal) experiments reported.; Prognostic model details, validation cohort performance metrics, and sample sizes are not provided in the abstract.; No clinical intervention or patient-level functional validation was reported.; Causality in patients is not established; transcriptomic associations may not translate to clinical benefit..

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

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

Case reportInconclusiveLimited evidenceTier 3 · early humann = 1

Laryngeal Metastasis of Prostate Adenocarcinoma-A Case Report

Turkish archives of otorhinolaryngology · Dec 2025

prostate adenocarcinomalarynx

This is a case report of an 80-year-old man who presented with productive cough and hoarseness. Laryngoscopy showed submucosal fullness in the right hemilarynx with airway narrowing, and biopsy with histopathology and immunohistochemistry diagnosed the lesion as laryngeal metastasis from prostate adenocarcinoma. The authors present the case because laryngeal metastases from prostate adenocarcinoma are rare.

Key findings
  • Patient: 80-year-old male presented with productive cough and hoarseness.
  • Videolaryngoscopy showed submucosal fullness in the right hemilarynx, pushing the right band ventricle mucosa medially and causing evident narrowing of the airway.
  • Histopathological evaluation and immunohistochemical staining of an endolaryngeal submucosal biopsy specimen from the right ventricular fold diagnosed laryngeal metastasis of prostate adenocarcinoma.
  • The case is presented because laryngeal metastases from prostate adenocarcinoma are scarce in the literature.
Limitations: Single-patient case report limits generalizability.; No information provided on treatment, follow-up, or patient outcome.; No quantitative data or comparative analysis.; Imaging and staging details beyond the described laryngoscopic findings are not provided..

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

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

Case reportSupportive careReported negativeLimited evidenceTier 3 · early humann = 1

An 85-Year-Old Man With Dyspnea and a History of Hormone Therapy for Prostate Adenocarcinoma

Chest · Sep 2025 · case report

Supportive careprostate adenocarcinoma

This case report describes an 85-year-old man with prostate adenocarcinoma who had received bicalutamide and leuprorelin for about 3 years. He presented with dyspnea, respiratory failure, and loss of appetite and was found on chest radiography to have a left pleural effusion. He had a history of COPD and a 20-pack-year smoking history and was admitted for further evaluation of the pleural effusion.

Key findings
  • Patient had undergone hormone therapy with bicalutamide and leuprorelin for approximately 3 years for prostate adenocarcinoma with a Gleason score of 4 + 5.
  • The patient presented to the emergency department with dyspnea, respiratory failure, and loss of appetite.
  • He had a history of COPD with a 20-pack-year smoking history.
  • Chest radiography showed a left pleural effusion and he was admitted for further examination of the pleural effusion.
Limitations: Single-patient case report limits generalizability.; No control or comparator; cannot establish causality between therapies and respiratory findings.; Abstract provides limited clinical detail and no follow-up or final diagnostic outcome for the pleural effusion.; Potential confounders (COPD, smoking) are present and not fully explored in the abstract..

Reports a prostate cancer patient on androgen-deprivation therapy who presented with respiratory failure and a left pleural effusion.

AI summary of the abstract, human-reviewed · Sep 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

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————
Cisplatin————
Carboplatin————
Durvalumab————

Study mix

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

17 Human5 Animal3 Lab29 Review/other
Reported directionReported positive36Mixed results3Reported negative3Inconclusive12

Compounds with reported-positive results in Prostate Adenocarcinoma

Where at least one study reported a positive result, shown with the full picture, not just the wins. Positive results are more likely to be published, and most of these are early lab or animal studies that may not translate to people. This reports what studies found, not what works.

Preclinical only: lab / animal (2)
Etoposide1 positive1 negative/mixed
Limitations: Single-patient case report; findings may not generalize.; No control or comparator group.; No doses, objective outcome scales, or detailed timelines provided in the abstract.; Causality between cancer treatment changes and dermatomyositis course cannot be established from this report.; Duration and long-term follow-up are not specified in the abstract..
Cited positive studies (1)
Cisplatin1 positive1 negative/mixed
Limitations: Single-patient case report; findings may not generalize.; No control or comparator group.; No doses, objective outcome scales, or detailed timelines provided in the abstract.; Causality between cancer treatment changes and dermatomyositis course cannot be established from this report.; Duration and long-term follow-up are not specified in the abstract..
Cited positive studies (1)

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 evidenceMixed results

No primary experimental studies yet.

Largest credible effect: patient_age 63, n=1 PMID 33413292 · effect sizes 2–63 across 2 studies

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

No human studies yet · Findings conflict across studies · Effect sizes reported in only 1 of 3 studies · All studies are small (n < 30).
CisplatinInsufficient evidenceMixed results

No primary experimental studies yet.

Largest credible effect: patient_age 63, n=1 PMID 33413292 · effect sizes 2–63 across 2 studies

Most authoritative study: Dermatomyositis associated with prostate adenocarcinoma with neuroendocrine differentiation

No human studies yet · Findings conflict across studies · Effect sizes reported in only 1 of 2 studies · 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.
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

48 ongoing · 89 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
33 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

We list only non-profit and government resources — never product sellers — and take no affiliate fees. If a link is broken or a resource doesn't meet that bar, tell us.

Heading to an appointment? Get a printable one-page summary — studied compounds, open trials, interactions, and questions to ask.
Bring this to your appointment →