Skip to content
PaperFren

Concept

Prostate cancer

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.

Studies

3

Findings

3

3 supporting · 0 challenging · 4 qualifying citations

Open tensions

1

Currently

What we know

  1. A 22-marker genomic classifier predicts early metastasis after prostatectomy better than clinical variables alone.
  2. HDAC2 immunohistochemistry independently tracks shorter PSA relapse.
  3. Five integrative CNA+expression subgroups predict biochemical relapse across cohorts.

Largest unresolved question

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.

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.

Related