Evidence mapPaperPMID 40169837Full record

ReviewNature reviews. Urology2025

Targeting the tumour cell surface in advanced prostate cancer.

Cristina Boixareu, Tarek Taha, Varadha Balaji Venkadakrishnan, Johann de Bono, Himisha Beltran

Abstract readReview
In one paragraph

Review in Nature reviews. Urology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
field-weighted citation impact
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

21 citing papers in PubMed.

  1. Trial
  2. B7-H3 Gene Expression Shapes Prognosis and Therapeutic Opportunities across Patient Groups with Prostate Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026
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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

5 authors.

Cristina Boixareu *The Institute of Cancer Research, The Royal Marsden Hospital, London, UK.ORCID 0000-0002-7630-3556
Tarek Taha *The Institute of Cancer Research, The Royal Marsden Hospital, London, UK.ORCID 0000-0001-7936-5245
Varadha Balaji Venkadakrishnan *Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.ORCID 0000-0001-7071-4584
Johann de BonoThe Institute of Cancer Research, The Royal Marsden Hospital, London, UK. johann.debono@icr.ac.uk.ORCID 0000-0002-2034-595X
Himisha BeltranDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA. himisha_beltran@dfci.harvard.edu.ORCID 0000-0003-3259-2226

Funding

Molecular Determinants of Response and Resistance to EZH2 and PARP inhibition in Prostate CancerP50CA272390 · DANA-FARBER CANCER INST · 2025 to 2025
$2.1M
Molecular mechanisms underlying lineage plasticity in prostate cancerR37CA241486 · DANA-FARBER CANCER INST · 2025 to 2025
$601k
NCI NIH HHS P50 CA272390NCI NIH HHS R37 CA241486
6 · The paper itself

Abstract

Prostate cancer remains a substantial health challenge, with >375,000 annual deaths amongst men worldwide. Most prostate cancer-related deaths are attributable to the development of resistance to standard-of-care treatments. Characterization of the diverse and complex surfaceome of treatment-resistant prostate cancer, combined with advances in drug development that leverage cell-surface proteins to enhance drug delivery or activate the immune system, have provided novel therapeutic opportunities to target advanced prostate cancer. The prostate cancer surfaceome, including proteins such as prostate-specific membrane antigen (PSMA), B7-H3, six transmembrane epithelial antigen of the prostate 1 (STEAP1), delta-like ligand 3 (DLL3), trophoblastic cell-surface antigen 2 (TROP2), prostate stem cell antigen (PSCA), HER3, CD46 and CD36, can be exploited as therapeutic targets, as regulatory mechanisms might contribute to the heterogeneity of expression of these proteins and subsequently affect treatment response and resistance. Specific treatment strategies targeting the surfaceome are in clinical development, including radionuclides, antibody-drug conjugates, T cell engagers and chimeric antigen receptor (CAR) T cells. Ultimately, biomarker development and clinical implementation of these agents will be informed and refined by further understanding of the biology of various targets; the target specificity and sensitivity of different agents; and off-target and toxic effects associated with these agents. Understanding the dynamic nature of cell-surface targets and non-overlapping expression patterns might also lead to future combinational strategies.

Indexed as

Prostatic NeoplasmsHumansMaleMolecular Targeted Therapy

Identifiers

PMID40169837
PMCPMC12954637

What Socratic 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 Socratic graph.