Evidence map›Paper›PMID 34191627›Full record

ReviewAmerican journal of physiology. Cell physiology2021

Heterogeneity within molecular subtypes of breast cancer.

Kevin M Turner, Syn Kok Yeo, Tammy M Holm, Elizabeth Shaughnessy, Jun-Lin Guan

Abstract readReview
In one paragraph

Review in American journal of physiology. Cell physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
95citing papers in PubMed, 1 pooled it
–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

95 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  14. Association of Post-Neoadjuvant Chemotherapy MRI andDiagnostics (Basel, Switzerland) · 2026
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35 more citing papers are in PubMed but not listed here.

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

5 authors.

Kevin M TurnerDepartment of Cancer Biology, University of Cincinnati College of Medicine, Cincinnati, Ohio.
Syn Kok YeoDepartment of Cancer Biology, University of Cincinnati College of Medicine, Cincinnati, Ohio.
Tammy M HolmDepartment of Surgery, University of Cincinnati College of Medicine, Cincinnati, Ohio.
Elizabeth ShaughnessyDepartment of Surgery, University of Cincinnati College of Medicine, Cincinnati, Ohio.
Jun-Lin GuanDepartment of Cancer Biology, University of Cincinnati College of Medicine, Cincinnati, Ohio.ORCID 0000-0001-8720-8338

Funding

Mechanisms of progression of vascular malformation to lymphangiosarcomaR01HL073394 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI GUAN, JUN-LIN · 2003 to 2025
$8.4M
Regulation of Neural Stem Cells and Neurogenesis by Autophagy GenesR01NS094144 · NINDS · UNIVERSITY OF CINCINNATI · PI GUAN, JUN-LIN · 2015 to 2024
$3.6M
Mechanisms of FIP200 regulation of breast cancer through its autophagy and non-autophagy functionsR01CA211066 · NCI · UNIVERSITY OF CINCINNATI · PI JUN-LIN GUAN · 2017 to 2026
$3.4M
NCI NIH HHS R01 CA211066NHLBI NIH HHS R01 HL073394NINDS NIH HHS R01 NS094144
6 · The paper itself

Abstract

Breast cancer is the quintessential example of how molecular characterization of tumor biology guides therapeutic decisions. From the discovery of the estrogen receptor to current clinical molecular profiles to evolving single-cell analytics, the characterization and compartmentalization of breast cancer into divergent subtypes is clear. However, competing with this divergent model of breast cancer is the recognition of intratumoral heterogeneity, which acknowledges the possibility that multiple different subtypes exist within a single tumor. Intratumoral heterogeneity is driven by both intrinsic effects of the tumor cells themselves as well as extrinsic effects from the surrounding microenvironment. There is emerging evidence that these intratumoral molecular subtypes are not static; rather, plasticity between divergent subtypes is possible. Interconversion between seemingly different subtypes within a tumor drives tumor progression, metastases, and treatment resistance. Therapeutic strategies must, therefore, contend with changing phenotypes in an individual patient's tumor. Identifying targetable drivers of molecular heterogeneity may improve treatment durability and disease progression.

Indexed as

Tumor MicroenvironmentBiomarkers, TumorBreast NeoplasmsHumansPrognosisReceptors, EstrogenSingle-Cell AnalysisBiomarkers, TumorReceptors, Estrogencell-state heterogeneitydynamic interconversionhierarchical heterogeneityintratumoral heterogeneityplasticity

Identifiers

PMID34191627
PMCPMC8424677

What OpenQuestion holds

Textmetadata
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.