Evidence map›Paper›PMID 36859337›Full record

ArticleBreast cancer research : BCR2023

Lineage plasticity enables low-ER luminal tumors to evolve and gain basal-like traits.

Gadisti Aisha Mohamed, Sundis Mahmood, Nevena B Ognjenovic, Min Kyung Lee, Owen M Wilkins, Brock C Christensen, Kristen E Muller, Diwakar R Pattabiraman

Open access · goldAbstract read
In one paragraph

Article in Breast cancer research : BCR, 2023. 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
6.2field-weighted citation impact, top 3% 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.

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, 27 citations in OpenAlex.

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  9. Collective migration modes in development, tissue repair and cancer.Nature reviews. Molecular cell biology · 2025
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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

8 authors at 2 institutions in 1 country.

Gadisti Aisha MohamedDepartment of Molecular and Systems Biology, Geisel School of Medicine at Dartmouth, Hanover, NH, 03755, USA.
Sundis MahmoodDepartment of Pathology, Dartmouth-Hitchcock Medical Center, Lebanon, NH, 03756, USA.
Nevena B OgnjenovicDepartment of Molecular and Systems Biology, Geisel School of Medicine at Dartmouth, Hanover, NH, 03755, USA.
Min Kyung LeeDepartment of Epidemiology, Geisel School of Medicine at Dartmouth, Hanover, NH, 03755, USA.
Owen M WilkinsDepartment of Biomedical Data Science, Geisel School of Medicine at Dartmouth, Hanover, NH, 03755, USA.
Brock C ChristensenDepartment of Molecular and Systems Biology, Geisel School of Medicine at Dartmouth, Hanover, NH, 03755, USA.
Kristen E MullerDepartment of Pathology, Dartmouth-Hitchcock Medical Center, Lebanon, NH, 03756, USA. Kristen.E.Muller@hitchcock.org.
Diwakar R PattabiramanDepartment of Molecular and Systems Biology, Geisel School of Medicine at Dartmouth, Hanover, NH, 03755, USA. raman@dartmouth.edu.
Dartmouth College · USDartmouth–Hitchcock Medical Center · US

Funding

Translational Engineering in Cancer (TEC)P30CA023108 · NCI · DARTMOUTH COLLEGE · PI Fred W Kolling IV · 1985 to 2026
$91.3M
Zhao - Proj 2P20GM130454 · NIGMS · DARTMOUTH COLLEGE · PI MICHAEL L WHITFIELD · 2019 to 2026
$27.2M
Uncovering the basis and implications of lineage plasticity in breast cancerR01CA267691 · NCI · MEDICAL COLLEGE OF WISCONSIN · PI Todd W. Miller · 2022 to 2026
$1.8M
Exploiting the epithelial-to-mesenchymal transition for the differentiation of cancer stem cellsR00CA201574 · NCI · DARTMOUTH COLLEGE · PI PATTABIRAMAN, DIWAKAR R · 2018 to 2020
$686k
10X Genomics Chromium Single-cell Sequencing to Expand Research At DartmouthS10OD025235 · OD · DARTMOUTH COLLEGE · PI TOMLINSON, CRAIG R · 2018 to 2018
$125k
NCI NIH HHS P30 CA023108NCI NIH HHS R00 CA201574NCI NIH HHS R01 CA267691NIGMS NIH HHS P20 GM130454NIH HHS 5R00CA201574-05NIH HHS S10 OD025235
6 · The paper itself

Abstract

Stratifying breast cancer into specific molecular or histologic subtypes aids in therapeutic decision-making and predicting outcomes; however, these subtypes may not be as distinct as previously thought. Patients with luminal-like, estrogen receptor (ER)-expressing tumors have better prognosis than patients with more aggressive, triple-negative or basal-like tumors. There is, however, a subset of luminal-like tumors that express lower levels of ER, which exhibit more basal-like features. We have found that breast tumors expressing lower levels of ER, traditionally considered to be luminal-like, represent a distinct subset of breast cancer characterized by the emergence of basal-like features. Lineage tracing of low-ER tumors in the MMTV-PyMT mouse mammary tumor model revealed that basal marker-expressing cells arose from normal luminal epithelial cells, suggesting that luminal-to-basal plasticity is responsible for the evolution and emergence of basal-like characteristics. This plasticity allows tumor cells to gain a new lumino-basal phenotype, thus leading to intratumoral lumino-basal heterogeneity. Single-cell RNA sequencing revealed SOX10 as a potential driver for this plasticity, which is known among breast tumors to be almost exclusively expressed in triple-negative breast cancer (TNBC) and was also found to be highly expressed in low-ER tumors. These findings suggest that basal-like tumors may result from the evolutionary progression of luminal tumors with low ER expression.

Indexed as

Mammary Neoplasms, AnimalReceptors, EstrogenAnimalsDisease Models, AnimalGene ExpressionMicePhenotypeReceptors, EstrogenBreast cancerLineage plasticityLow-ERLumino-basal heterogeneityMMTV-PyMTSingle-cell RNA sequencingSOX10

Identifiers

PMID36859337
PMCPMC9979432
OpenAlexW4322754753

What Socratic 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 Socratic graph.