Evidence map›Paper›PMID 27874061›Full record

ReviewNature reviews. Clinical oncology2017

Strategies to avoid treatment-induced lineage crisis in advanced prostate cancer.

Guilhem Roubaud, Bobby C Liaw, William K Oh, David J Mulholland

Registry-linked trialAbstract readReview
In one paragraph

Review in Nature reviews. Clinical oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06056791 (An Open-label, Phase I/IIa Dose Escalation and Expansion Study to Determine the Safety and Clinical Activity of an Immune Priming Cell Therapy), which is not on this map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.6field-weighted citation impact, top 10% 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.

NCT06056791 phase1 / phase2completednot on this mapstarted 2023, after this paper: background citation

An Open-label, Phase I/IIa Dose Escalation and Expansion Study to Determine the Safety and Clinical Activity of an Immune Priming Cell Therapy (INKmune) in Patients With Metastatic Castration Resistant Prostate Cancer (mCRPC)

TypeinterventionalSponsorInmune Bio, Inc.Ran2023 to 2025Enrolled12ConditionsCancer, Metastatic Castration-resistant Prostate Cancer, mCRPCArmsINKmune
3 · Its place in the literature

Who cites it

29 citing papers in PubMed, 48 citations in OpenAlex.

  1. Trial
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  4. ARNature communications · 2025
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  16. Molecules (Basel, Switzerland) · 2022
    Article
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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

4 authors at 3 institutions in 2 countries.

Guilhem RoubaudDepartment of Medical Oncology, Institut Bergonié, 229 Cours de l'Argonne, Bordeaux 33076, France.
Bobby C LiawIcahn School of Medicine at Mount Sinai, Tisch Cancer Institute, 1470 Madison Avenue, New York, New York 10029, USA.
William K OhIcahn School of Medicine at Mount Sinai, Tisch Cancer Institute, 1470 Madison Avenue, New York, New York 10029, USA.
David J MulhollandIcahn School of Medicine at Mount Sinai, Tisch Cancer Institute, 1470 Madison Avenue, New York, New York 10029, USA.
Icahn School of Medicine at Mount Sinai · USInstitut Bergonié · FRTisch Cancer Institute

Funding

Chronic inhibition of androgen receptor signaling leads to neuroendocrine prostate cancer by trans differentiation of stem/progenitor cellsR01CA197910 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI MULHOLLAND, DAVID · 2015 to 2019
$2.0M
NCI NIH HHS R01 CA197910
6 · The paper itself

Abstract

The increasing potency of therapies that target the androgen receptor (AR) signalling axis has correlated with a rise in the proportion of patients with prostate cancer harbouring an adaptive phenotype, termed treatment-induced lineage crisis. This phenotype is characterized by features that include soft-tissue metastasis and/or resistance to standard anticancer therapies. Potent anticancer treatments might force cancer cells to evolve and develop alternative cell lineages that are resistant to primary therapies, a mechanism similar to the generation of multidrug- resistant microorganisms after continued antibiotic use. Herein, we assess the hypothesis that treatment-adapted phenotypes harbour reduced AR expression and/or activity, and acquire compensatory strategies for cell survival. We highlight the striking similarities between castration-resistant prostate cancer and triple-negative breast cancer, another poorly differentiated endocrine malignancy. Alternative treatment paradigms are needed to avoid therapy-induced resistance. Herein, we present a new clinical trial strategy designed to evaluate the potential of rapid drug cycling as an approach to delay the onset of resistance and treatment-induced lineage crisis in patients with metastatic castration-resistant prostate cancer.

Indexed as

Antineoplastic AgentsDrug Resistance, NeoplasmHumansMaleModels, BiologicalMolecular Targeted TherapyProstatic NeoplasmsProstatic Neoplasms, Castration-ResistantReceptors, AndrogenSignal TransductionAntineoplastic AgentsReceptors, Androgen

Identifiers

PMID27874061
PMCPMC5567685
OpenAlexW2555743815

What OpenQuestion holds

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LicenceTDM
Read underepoch 390

Registered trials

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.