Evidence map›Paper›PMID 41906639›Full record

ReviewEndocrinology2026

Role of Janus kinase-signal transducer and activator of transcription signaling pathway in hormonal cancer therapeutic resistance and lineage plasticity.

Wendy Effah, Marjana Khalil, Sanskrita Sukla, Chenhao Zhao, Suriyan Ponnusamy, Lawrence M Pfeffer, Hyo Young Choi, Ramesh Narayanan

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Endocrinology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

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

8 authors.

Wendy EffahDepartment of Medicine, College of Medicine, University of Tennessee Health Science Center, Memphis, TN, USA.ORCID 0009-0001-5066-8119
Marjana KhalilDepartment of Medicine, College of Medicine, University of Tennessee Health Science Center, Memphis, TN, USA.ORCID 0000-0002-8596-6263
Sanskrita SuklaDepartment of Medicine, College of Medicine, University of Tennessee Health Science Center, Memphis, TN, USA.ORCID 0000-0001-6104-3600
Chenhao ZhaoDepartment of Preventive Medicine, College of Medicine, University of Tennessee Health Science Center, Memphis, TN, USA.ORCID 0000-0001-5607-7443
Suriyan PonnusamyDepartment of Medicine, College of Medicine, University of Tennessee Health Science Center, Memphis, TN, USA.
Lawrence M PfefferDepartment of Pathology, College of Medicine, University of Tennessee Health Science Center, Memphis, TN, USA.ORCID 0000-0003-2809-1234
Hyo Young ChoiDepartment of Preventive Medicine, College of Medicine, University of Tennessee Health Science Center, Memphis, TN, USA.ORCID 0000-0002-7627-8493
Ramesh NarayananDepartment of Medicine, College of Medicine, University of Tennessee Health Science Center, Memphis, TN, USA.ORCID 0000-0001-5490-0790

Funding

Racial Disparity in the Expression of Androgen Receptor Splice Variants (AR-SVs) in Prostate CancerR01CA229164 · NCI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI Ramesh Narayanan · 2019 to 2026
$3.2M
Discovery of Novel Selective Androgen Receptor Degraders (SARDs) for the Treatment of Spinobulbar Muscular Atrophy (SBMA) or Kennedy’s DiseaseR01NS131106 · NINDS · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI Ramesh Narayanan · 2024 to 2026
$1.1M
Department of Defense W81XWH-21-1-0055Eric Muirhead Chair of ExcellenceNational Institute of Neurological Diseases and Stroke R01-NS131106NCI NIH HHS R01 CA229164NCI NIH HHS R01-CA229164NINDS NIH HHS R01 NS131106UTHSC Center for Cancer Research
6 · The paper itself

Abstract

Cancers of the breast and prostate are one of the leading causes of cancer deaths in women and men, respectively. Although several treatment options have been developed to transform these cancers into manageable chronic diseases, they still contribute to over 70 000 deaths each year in the United States. Though majority of these cancers belong to slow growing differentiated subtypes, the cancers evolve over time due to treatment-related pressure into aggressive treatment-resistant types. A mechanism attributed to the transformation of hormonal and other cancers into aggressive treatment-refractory cancers is "lineage plasticity," a term used to describe a switch in the cell type or lineage. Evolving evidences suggest that the Janus kinase-signal transducer and activator of transcription (JAK-STAT) pathway plays a key role in driving lineage plasticity. This review discusses the role of JAK-STAT signaling pathway in hormonal cancers' evolution into aggressive cancers and in treatment resistance, with focus on treatment-induced lineage plasticity.

Indexed as

Breast NeoplasmsDrug Resistance, NeoplasmJanus KinasesProstatic NeoplasmsSignal TransductionSTAT Transcription FactorsAnimalsAntineoplastic Agents, HormonalCell LineageCell PlasticityFemaleHumansMaleAntineoplastic Agents, HormonalJanus KinasesSTAT Transcription Factorsbreast cancerhormonal cancerhormonesJAK-STATlineage plasticityprostate cancer

Identifiers

PMID41906639
PMCPMC13673697

What OpenQuestion holds

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Registered trials

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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 OpenQuestion graph.