Concept · medicine
Prostate cancer
Follow Prostate cancer — see important new research and changes in evidence.Change log
What changed
Dated edits to this page's evidence: studies added or removed from a claim, claims added or withdrawn, and new explanations tagged here. Rewordings are not listed.
- Concept page published
Prostate cancer risk after local therapy is tracked with overlapping tools—expression classifiers for early metastasis, isoform-specific HDAC IHC for PSA relapse, and integrative CNA/transcriptome subgroups for biochemical relapse. This page keeps those claims separate.
Students hear “genomic risk” as one test. A 22-marker metastasis classifier, HDAC2 IHC, and five-group integrative subtypes answer different endpoints and molecular layers. Mixing them invents false agreement.
Evidence
What the evidence shows
Drawn from 3 studies in this library. Each finding starts with a plain-language takeaway, then the denser detail. Supports means evidence for a finding; Challenges means evidence against a stated position; Qualifies marks scope with a short note on each study’s contribution. Challenged positions are labeled — they are not findings.
A 22-marker genomic classifier predicts early metastasis after prostatectomy better than clinical variables alone.
In Mayo radical-prostatectomy men enriched for PSA rise, a 22-marker expression classifier achieved validation AUC 0.75 for early clinical metastasis and was the only significant factor in multivariable models.
- HDAC2 IHC tracks shorter PSA relapse in prostate cancer— different layer — single-isoform IHC prognosis for PSA relapse, not a multi-gene metastasis classifier
- Five integrated genomic subgroups track prostate-cancer relapse risk— related risk theme, but five integrative subgroups for biochemical relapse, not the 22-marker GC
Study Role Design N Population Outcome A 22-gene classifier flags early metastasis after prostatectomy Supports Case-controlNested case-control of Mayo Clinic radical-prostatectomy patients; genomic classifier for early metastasis N=545 · 545 unique expression profiles from a 639-patient nested case-control sample; median follow-up 16.9 years Men after radical prostatectomy with biochemical recurrence risk for metastasis Genomic classifier discrimination for early clinical metastasis (validation AUC) HDAC2 IHC tracks shorter PSA relapse in prostate cancer Qualifiesdifferent layer — single-isoform IHC prognosis for PSA relapse, not a multi-gene metastasis classifier CohortIHC scoring of HDAC1/2/3 with PSA-relapse follow-up N=192 · Prostate carcinomas scored by immunohistochemistry Patients with prostate carcinoma assessed for HDAC expression HDAC expression associations with clinicopathology, proliferation, and PSA relapse Five integrated genomic subgroups track prostate-cancer relapse risk Qualifiesrelated risk theme, but five integrative subgroups for biochemical relapse, not the 22-marker GC CohortDiscovery/validation integrating CNA and array transcriptomics for risk subgroups N=259 · 259 men / 482 samples; discovery 125, validation 103 Men with primary prostate cancer with tumour/benign/germline samples Integrative molecular subgroups predicting biochemical relapse HDAC2 immunohistochemistry independently tracks shorter PSA relapse.
Across 192 prostate carcinomas, class I HDACs were frequently strongly expressed; HDAC2 was an independent prognostic marker associated with shorter PSA relapse and with dedifferentiation/proliferation patterns.
- A 22-gene classifier flags early metastasis after prostatectomy— different endpoint — early metastasis after BCR vs PSA-relapse timing by HDAC2 IHC
Study Role Design N Population Outcome HDAC2 IHC tracks shorter PSA relapse in prostate cancer Supports CohortIHC scoring of HDAC1/2/3 with PSA-relapse follow-up N=192 · Prostate carcinomas scored by immunohistochemistry Patients with prostate carcinoma assessed for HDAC expression HDAC expression associations with clinicopathology, proliferation, and PSA relapse A 22-gene classifier flags early metastasis after prostatectomy Qualifiesdifferent endpoint — early metastasis after BCR vs PSA-relapse timing by HDAC2 IHC Case-controlNested case-control of Mayo Clinic radical-prostatectomy patients; genomic classifier for early metastasis N=545 · 545 unique expression profiles from a 639-patient nested case-control sample; median follow-up 16.9 years Men after radical prostatectomy with biochemical recurrence risk for metastasis Genomic classifier discrimination for early clinical metastasis (validation AUC) Five integrative CNA+expression subgroups predict biochemical relapse across cohorts.
In 259 men, five subgroups from 100 discriminating genes predicted biochemical relapse in discovery and validation and again in a third long-follow-up cohort, with integrative analysis outperforming single data types.
- A 22-gene classifier flags early metastasis after prostatectomy— both are expression-era risk tools, but GC targets early metastasis after BCR; this paper’s subgroups target biochemical relapse
Study Role Design N Population Outcome Five integrated genomic subgroups track prostate-cancer relapse risk Supports CohortDiscovery/validation integrating CNA and array transcriptomics for risk subgroups N=259 · 259 men / 482 samples; discovery 125, validation 103 Men with primary prostate cancer with tumour/benign/germline samples Integrative molecular subgroups predicting biochemical relapse A 22-gene classifier flags early metastasis after prostatectomy Qualifiesboth are expression-era risk tools, but GC targets early metastasis after BCR; this paper’s subgroups target biochemical relapse Case-controlNested case-control of Mayo Clinic radical-prostatectomy patients; genomic classifier for early metastasis N=545 · 545 unique expression profiles from a 639-patient nested case-control sample; median follow-up 16.9 years Men after radical prostatectomy with biochemical recurrence risk for metastasis Genomic classifier discrimination for early clinical metastasis (validation AUC)
Open questions
Tensions and limits
Some items are genuine disagreements on the same question. Others mark different assays, populations, or outcomes — limits on how far one study travels — not a forced fight between papers.
GC discriminates early metastasis after PSA rise; HDAC2 IHC tracks PSA-relapse timing; integrative subgroups stratify biochemical relapse. Shared “aggressive prostate cancer” language does not make the assays interchangeable.
- A 22-gene classifier flags early metastasis after prostatectomy
- HDAC2 IHC tracks shorter PSA relapse in prostate cancer
- Five integrated genomic subgroups track prostate-cancer relapse risk
Study Role Design N Population Outcome A 22-gene classifier flags early metastasis after prostatectomy Supports Case-controlNested case-control of Mayo Clinic radical-prostatectomy patients; genomic classifier for early metastasis N=545 · 545 unique expression profiles from a 639-patient nested case-control sample; median follow-up 16.9 years Men after radical prostatectomy with biochemical recurrence risk for metastasis Genomic classifier discrimination for early clinical metastasis (validation AUC) HDAC2 IHC tracks shorter PSA relapse in prostate cancer Supports CohortIHC scoring of HDAC1/2/3 with PSA-relapse follow-up N=192 · Prostate carcinomas scored by immunohistochemistry Patients with prostate carcinoma assessed for HDAC expression HDAC expression associations with clinicopathology, proliferation, and PSA relapse Five integrated genomic subgroups track prostate-cancer relapse risk Supports CohortDiscovery/validation integrating CNA and array transcriptomics for risk subgroups N=259 · 259 men / 482 samples; discovery 125, validation 103 Men with primary prostate cancer with tumour/benign/germline samples Integrative molecular subgroups predicting biochemical relapse
Common misconceptions
One genomic risk score covers metastasis, PSA relapse, and subgroup biology the same way.
These papers use different endpoints and molecular readouts. A metastasis classifier, HDAC2 IHC, and five-group integrative subtypes are not one test.
Prognostic HDAC2 staining proves HDAC inhibitors will help this cohort.
IHC prognosis supports biology and risk; treatment benefit requires dedicated inhibitor trials.
Exam-style questions
Short-answer questions that ask you to explain or compare, not recall.
Why can GC’s metastasis AUC and HDAC2’s PSA-relapse link both be true without being one biomarker?
They measure different outcomes (early clinical metastasis after BCR vs PSA-relapse timing) with different assays (22-gene classifier vs isoform IHC).
A student treats five integrative subgroups as identical to the 22-marker GC. What difference matters?
Subgroups come from joint CNA+expression clustering tied mainly to biochemical relapse across cohorts; GC is a fixed 22-marker score trained for early metastasis after PSA rise.
The studies
3 studies in this library bear on Prostate cancer, ordered by citations.
- A 22-gene classifier flags early metastasis after prostatectomy
In Mayo radical-prostatectomy men, a 22-marker genomic classifier from primary-tumour expression predicted early clinical metastasis after PSA rise better than clinical variables (validation AUC 0.75).
- HDAC2 IHC tracks shorter PSA relapse in prostate cancer
In 192 prostate carcinomas, class I HDACs were often strongly expressed; HDAC2 independently predicted shorter PSA relapse and linked to dedifferentiation/proliferation.
- Five integrated genomic subgroups track prostate-cancer relapse risk
Across 259 men (482 samples), integrating copy-number and expression data defined five subgroups on 100 genes that predicted biochemical relapse in discovery, validation, and a third long-follow-up cohort.
Learn alongside