Evidence map›Paper›PMID 35552660›Full record

ArticleClinical cancer research : an official journal of the American Association for Cancer Research2022

Therapeutic Implications for Intrinsic Phenotype Classification of Metastatic Castration-Resistant Prostate Cancer.

Ilsa M Coleman, Navonil DeSarkar, Colm Morrissey, Li Xin, Martine P Roudier, Erolcan Sayar, Dapei Li, Eva Corey, Michael C Haffner, Peter S Nelson

Open access · hybridAbstract read
In one paragraph

Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
5.5field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

43 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
  2. Article
  3. SPEN inactivation drives resistance to androgen receptor pathway inhibitors in metastatic prostate cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026
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  4. Review
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  12. Lack of synergy between AR-targeted therapies and PARP inhibitors in homologous recombination-proficient prostate cancer.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  13. Article
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  15. Circadian regulator REV-ERBα is a master regulator of tumor lineage plasticity and an effective therapeutic target.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  16. Article
  17. Review
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  20. PROX1 is an early driver of lineage plasticity in prostate cancer.The Journal of clinical investigation · 2025
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 1 country.

Ilsa M ColemanDivision of Human Biology, Fred Hutchinson Cancer Research Center, University of Washington, Seattle, Washington.
Navonil DeSarkarDivision of Human Biology, Fred Hutchinson Cancer Research Center, University of Washington, Seattle, Washington.ORCID 0000-0003-2139-7951
Colm MorrisseyDepartment of Urology, University of Washington, Seattle, Washington.
Li XinDepartment of Urology, University of Washington, Seattle, Washington.
Martine P RoudierDepartment of Urology, University of Washington, Seattle, Washington.
Dapei LiDivision of Human Biology, Fred Hutchinson Cancer Research Center, University of Washington, Seattle, Washington.
Eva CoreyDepartment of Urology, University of Washington, Seattle, Washington.ORCID 0000-0002-9244-3807
Michael C HaffnerDivision of Human Biology, Fred Hutchinson Cancer Research Center, University of Washington, Seattle, Washington.ORCID 0000-0003-0809-6425
Peter S NelsonDivision of Human Biology, Fred Hutchinson Cancer Research Center, University of Washington, Seattle, Washington.ORCID 0000-0002-5451-5726
University of Washington · USFred Hutch Cancer Center · US

Funding

Translational Bioimaging Core Shared ResourceP30CA015704 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI Marian Esvelt · 1985 to 2026
$296.4M
TRANSCRIPTOME AND PROTEOME STRATIFICATION OF PROSTATE ADENOCARCINOMA PHENOTYPESP50CA097186 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI John Kyung Lee · 2002 to 2026
$58.1M
Steroid Metabolism in Castration-Resistant Prostate CancerP01CA163227 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI Steven P. Balk · 2013 to 2026
$25.0M
The MSKCC-UW/Fred Hutch Prostate Cancer Drug Resistance and Sensitivity CenterU54CA224079 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI SAWYERS, CHARLES L. · 2017 to 2021
$6.8M
Defining and Targeting Lineage Transition Programs Operative in AR Pathway Independent Prostate CancerR01CA234715 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI NELSON, PETER S · 2020 to 2024
$2.0M
High-Performance Compute Cluster for Comprehensive Cancer and Infectious Diseases ResearchS10OD028685 · OD · FRED HUTCHINSON CANCER RESEARCH CENTER · PI BRADLEY, PHILIP · 2020 to 2020
$2.0M
Statistical modeling to support population and translational cancer researchR50CA221836 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI Roman Gulati · 2017 to 2026
$2.0M
NCI NIH HHS P01 CA163227NCI NIH HHS P30 CA015704NCI NIH HHS P50 CA097186NCI NIH HHS R01 CA234715NCI NIH HHS R50 CA221836NCI NIH HHS U54 CA224079NIH HHS S10 OD028685
6 · The paper itself

Abstract

purposeTo determine whether metastatic castration-resistant prostate cancers (mCRPC) partition into molecular phenotypes corresponding to intrinsic differentiation states and ascertain whether these subtypes exhibit specific druggable features and associate with treatment outcomes. EXPERIMENTAL

designWe used RNAseq, digital spatial profiling, and histological assessments from metastatic biopsies and patient-derived xenografts to segregate mCRPCs into subtypes defined by the PAM50 breast cancer classification algorithm. Subtype associations with treatment responses in preclinical models and patients were determined.

resultsUsing the PAM50 algorithm, we partitioned 270 mCRPC tumors into LumA (42%), LumB (24%), and Basal (34%) subtypes with classification largely driven by proliferation rates and androgen receptor (AR) activity. Most neuroendocrine tumors classified as Basal. Pathways enriched in the LumA subtype include TGFß and NOTCH signaling. LumB subtype tumors were notable for elevated MYC activity. Basal subtype tumors exhibited elevated IL6-STAT3 signaling and features of adult stem cell states. In patients where multiple tumors were evaluated, the majority had concordant PAM50 subtype determination, though a subset exhibited marked inter- and intratumor heterogeneity, including divergent classifications between primary and metastatic sites. In preclinical models, LumA subtype tumors were highly responsive to androgen deprivation and docetaxel chemotherapy whereas Basal tumors were largely resistant. In clinical cohorts patients with Basal subtype tumors demonstrated a shorter time on treatment with AR signaling inhibitors and docetaxel relative to patients with luminal subtypes.

conclusionsSubtyping of mCRPC based on cell differentiation states has potential clinical utility for identifying patients with divergent expression of treatment targets and responses to systemic therapy.

Indexed as

Breast NeoplasmsProstatic Neoplasms, Castration-ResistantAndrogen AntagonistsDocetaxelHumansMalePhenotypeAndrogen AntagonistsDocetaxel

Identifiers

PMID35552660
PMCPMC9365375
OpenAlexW4280587240

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.