Evidence map›Paper›PMID 42557372›Full record

ArticleProstate cancer and prostatic diseases2026

Clinical and genomic determinants of extraordinary response and resistance to androgen receptor pathway inhibitors in men with metastatic androgen pathway modulator sensitive (APMS) prostate cancer.

Jane McKenzie, Lauren Howard, Joseph J Park, Bilal Ashraf, Tara Seibert, Kallie White, Sundhar Ramalingam, Jeffrey W Shevach, Michael R Harrison, Christopher Hoimes and 6 more

Abstract read
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In one paragraph

Article in Prostate cancer and prostatic diseases, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0cells of the map it votes in
0citing papers in PubMed
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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

16 authors.

Jane McKenzieDuke Cancer Institute Center for Prostate and Urologic Cancers, Department of Medicine, Division of Medical Oncology, Duke University, Durham, NC, 27710, USA.ORCID http://orcid.org/0000-0003-2126-2838
Lauren HowardDuke Cancer Institute Center for Prostate and Urologic Cancers, Department of Medicine, Division of Medical Oncology, Duke University, Durham, NC, 27710, USA.ORCID http://orcid.org/0000-0003-3355-4483
Joseph J ParkDuke Cancer Institute Center for Prostate and Urologic Cancers, Department of Medicine, Division of Medical Oncology, Duke University, Durham, NC, 27710, USA.
Bilal AshrafDuke Cancer Institute Center for Prostate and Urologic Cancers, Department of Medicine, Division of Medical Oncology, Duke University, Durham, NC, 27710, USA.ORCID http://orcid.org/0009-0008-2892-9184
Tara SeibertDuke Cancer Institute Center for Prostate and Urologic Cancers, Department of Medicine, Division of Medical Oncology, Duke University, Durham, NC, 27710, USA.
Kallie WhiteDuke Cancer Institute Center for Prostate and Urologic Cancers, Department of Medicine, Division of Medical Oncology, Duke University, Durham, NC, 27710, USA.
Sundhar RamalingamDuke Cancer Institute Center for Prostate and Urologic Cancers, Department of Medicine, Division of Medical Oncology, Duke University, Durham, NC, 27710, USA.
Jeffrey W ShevachDuke Cancer Institute Center for Prostate and Urologic Cancers, Department of Medicine, Division of Medical Oncology, Duke University, Durham, NC, 27710, USA.
Michael R HarrisonDuke Cancer Institute Center for Prostate and Urologic Cancers, Department of Medicine, Division of Medical Oncology, Duke University, Durham, NC, 27710, USA.ORCID http://orcid.org/0000-0003-3776-8892
Christopher HoimesDuke Cancer Institute Center for Prostate and Urologic Cancers, Department of Medicine, Division of Medical Oncology, Duke University, Durham, NC, 27710, USA.
Matthew LabriolaDuke Cancer Institute Center for Prostate and Urologic Cancers, Department of Medicine, Division of Medical Oncology, Duke University, Durham, NC, 27710, USA.ORCID http://orcid.org/0000-0003-0919-9864
Jordan InfieldDuke Cancer Institute Center for Prostate and Urologic Cancers, Department of Medicine, Division of Medical Oncology, Duke University, Durham, NC, 27710, USA.
Dillon CockrellDuke Cancer Institute Center for Prostate and Urologic Cancers, Department of Medicine, Division of Medical Oncology, Duke University, Durham, NC, 27710, USA.ORCID http://orcid.org/0000-0002-5399-6329
Hannah D McManusDuke Cancer Institute Center for Prostate and Urologic Cancers, Department of Medicine, Division of Medical Oncology, Duke University, Durham, NC, 27710, USA.
Daniel J GeorgeDuke Cancer Institute Center for Prostate and Urologic Cancers, Department of Medicine, Division of Medical Oncology, Duke University, Durham, NC, 27710, USA.ORCID http://orcid.org/0000-0002-0836-8542
Andrew J ArmstrongDuke Cancer Institute Center for Prostate and Urologic Cancers, Department of Medicine, Division of Medical Oncology, Duke University, Durham, NC, 27710, USA. andrew.armstrong@duke.edu.ORCID http://orcid.org/0000-0001-7012-1754

Funding

U.S. Department of Health & Human Services | National Institutes of Health (NIH) 5R01CA233585 - 05
6 · The paper itself

Abstract

backgroundIdentifying clinical and genomic predictors of response to androgen deprivation therapy (ADT) and androgen receptor pathway inhibitors (ARPI) for metastatic androgen pathway modulator sensitive (APMS) prostate cancer is essential for improving therapeutic decision-making. Divergent outcomes are observed in practice, with some achieving exceptional responses (ER) while others experience early resistance or non-response (NR), the biologic basis of which remains unclear.

methodsA retrospective review was conducted of patients with APMS prescribed ADT/ARPI from 2015-2024. ER and NR were defined by upper ( > 53.36 months) and lower ( < 10.41 months) quartiles of progression-free survival (PFS). Objectives were to associate baseline genomic and clinical factors with ER/NR status, PFS, overall survival (OS) and PSA kinetics..

resultsAmong 3363 prescribed ADT/ARPI, 224 were treated for APMS, with 154 (69%) undergoing temporal molecular testing. Alteration of ≥1 tumor suppressor gene with or without proliferative gene co-alteration was associated with NR while no single alteration predicted achieving ER. ECOG < 1, lack of pain, low-volume disease, higher hemoglobin and albumin, and normal alkaline phosphatase were associated with improved PFS, OS, and PSA nadir <0.2 ng/mL at 12 months. Alterations in TP53 (HR 1.60 [95%CI 1.02-2.50], p = 0.039; HR 1.91 [95%CI 1.05-3.49], p = 0.035) and MYC (HR 2.01 [95%CI 1.03-3.91], p = 0.040; HR 3.81 [95%CI 1.81-7.99], p < 0.001) were associated with inferior PFS and OS, while BRCA2 (HR 2.12 [95%CI 1.02-4.42], p = 0.045) additionally associated with PFS, and RAD21 (HR 2.55 [95%CI 1.13-5.77], p = 0.024) with OS. On multivariable analysis, MYC gain associated with OS (HR 4.41 [95%CI 1.24-15.7], p = 0.022). Pathway-level analysis showed proliferative gene alterations were associated with failure to achieve PSA nadir <0.2 ng/mL at 12 months (HR 0.49 [95%CI 0.24, 0.98], p = 0.047).

conclusionsIn this real-world APMS cohort, we identified pre-treatment clinical and genomic predictors of patient benefits and long-term survival with ADT/ARPI therapy.

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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.