Evidence map›Paper›PMID 41023204›Full record

ReviewCell research2025

Lineage plasticity and histological transformation: tumor histology as a spectrum.

Xiaoling Li, Eric E Gardner, Sonia Molina-Pinelo, Clare Wilhelm, Ping Mu, Álvaro Quintanal-Villalonga

Abstract readReview
In one paragraph

Review in Cell research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing 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

22 citing papers in PubMed.

  1. Article
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  10. Game of clones: decipher lineage plasticity in hormone-driven cancers.Cellular and molecular life sciences : CMLS · 2026
    Review
  11. Article
  12. Review
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  15. Review
  16. Review
  17. Targeting tumor transition windows.Exploration of targeted anti-tumor therapy · 2026
    Review
  18. Review
  19. Article
  20. Review
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

6 authors.

Xiaoling LiDepartment of Urology, Yale School of Medicine, Yale University, New Haven, CT, USA.ORCID 0000-0002-1554-1569
Eric E GardnerMeyer Cancer Center, Weill Cornell Medicine, New York, NY, USA.
Sonia Molina-PineloInstitute of Biomedicine of Seville (IBiS), HUVR, CSIC, Universidad de Sevilla, Seville, Spain.
Clare WilhelmDepartment of Medicine, Thoracic Oncology Service, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Ping MuDepartment of Urology, Yale School of Medicine, Yale University, New Haven, CT, USA.ORCID 0000-0003-0955-0896
Álvaro Quintanal-VillalongaDepartment of Medicine, Thoracic Oncology Service, Memorial Sloan Kettering Cancer Center, New York, NY, USA. quintaa1@mskcc.org.ORCID 0000-0002-7234-3446

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI SELWYN M VICKERS · 1985 to 2026
$347.4M
Elucidating the Molecular Role of SYNCRIP in Prostate Cancer and AR Targeted Therapy ResistanceR37CA258730 · NCI · YALE UNIVERSITY · PI Ping Mu · 2021 to 2026
$2.7M
Unveiling the Role of UBE2J1 as the E2 Ubiquitin Conjugating Enzyme in Androgen Receptor DegradationR01CA292949 · NCI · YALE UNIVERSITY · PI Ping Mu · 2024 to 2026
$2.1M
Translational Research in Oncology Training ProgramT32CA160001 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI SAWYERS, CHARLES L. · 2011 to 2020
$2.0M
Deciphering the Impact of ZNF397-deficiency in Promoting TET2-driven Epigenetic Rewiring, Lineage Plasticity, and Therapy Resistance in Prostate CancerR01CA288820 · NCI · YALE UNIVERSITY · PI Ping Mu · 2024 to 2026
$820k
NCI NIH HHS P30 CA008748NCI NIH HHS R01 CA288820NCI NIH HHS R01 CA292949NCI NIH HHS R37 CA258730NCI NIH HHS T32 CA160001
6 · The paper itself

Abstract

Lineage plasticity, the ability of cells to transition to an alternative phenotype as a means for adaptation, is an increasingly recognized mechanism of tumor evolution and a driver of resistance to anticancer therapies. The most extensively described clinical settings impacted by such molecular phenomena include neuroendocrine transformation in androgen receptor-dependent prostate adenocarcinoma, and adenocarcinoma-to-neuroendocrine and adenocarcinoma-to-squamous transdifferentiation in epidermal growth factor receptor-driven lung adenocarcinoma, affecting 10%-20% of patients treated with targeted therapy. Recent analyses of human tumor samples and in vivo models of histological transformation have led to insights into the biology of lineage plasticity, including biomarkers predictive of high risk of transformation. However, no clinically available therapies aimed to prevent or revert plasticity are currently available. In the present review, we will provide a biological and therapeutic overview of the current understanding of common and divergent molecular drivers of neuroendocrine and squamous transdifferentiation in tumors from different origins, including descriptive analysis of previously known and recently described molecular events associated with histological transformation, and propose evidence-based alternative models of transdifferentiation. A clear definition of the commonalities and differences of transforming tumors in different organs and to different histological fates will be important to translate molecular findings to the clinical setting.

Indexed as

Cell LineageCell PlasticityCell Transformation, NeoplasticNeoplasmsAnimalsCell TransdifferentiationHumans

Identifiers

PMID41023204
PMCPMC12589604

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.