Evidence map›Paper›PMID 28752247›Full record

ReviewCancer metastasis reviews2017

Breast cancer complexity: implications of intratumoral heterogeneity in clinical management.

Brittany Haynes, Ashapurna Sarma, Pratima Nangia-Makker, Malathy P Shekhar

Abstract readReview
In one paragraph

Review in Cancer metastasis reviews, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing 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

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

  1. Pooled it
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  8. Intricate ribosome composition and translational reprogramming in epithelial-mesenchymal transition.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  9. MEF2D Functions as a Tumor Suppressor in Breast Cancer.International journal of molecular sciences · 2024
    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.

Brittany HaynesDepartment of Oncology, Wayne State University School of Medicine, 421 E. Canfield Avenue, Detroit, MI, 48201, USA.
Ashapurna SarmaDepartment of Oncology, Wayne State University School of Medicine, 421 E. Canfield Avenue, Detroit, MI, 48201, USA.
Pratima Nangia-MakkerDepartment of Oncology, Wayne State University School of Medicine, 421 E. Canfield Avenue, Detroit, MI, 48201, USA.
Malathy P ShekharDepartment of Oncology, Wayne State University School of Medicine, 421 E. Canfield Avenue, Detroit, MI, 48201, USA. shekharm@karmanos.org.

Funding

THE ROLE OF CNS INSULIN AS A MODULATOR OF DIABETIC COMPLICATIONSR25GM058905 · NIGMS · WAYNE STATE UNIVERSITY · PI CHOW, CHRISTINE S, DUNBAR, JOSEPH C · 1999 to 2020
$14.4M
TRAINING PROGRAM IN THE BIOLOGY OF CANCERT32CA009531 · NCI · WAYNE STATE UNIVERSITY · PI Larry H Matherly · 1985 to 2026
$5.3M
Targeting Rad6 Postreplication DNA Repair to Treat Triple Negative Breast CancerR21CA178117 · NCI · WAYNE STATE UNIVERSITY · PI SHEKHAR, MALATHY PV · 2013 to 2015
$358k
National Cancer Institute T32-CA009531NCI NIH HHS R21 CA178117NCI NIH HHS T32 CA009531NIGMS NIH HHS R25 GM058905U.S. Department of Defense DAMD-17-02-1-0618 and W81XWH-09-1-0608
6 · The paper itself

Abstract

Generation of intratumoral phenotypic and genetic heterogeneity has been attributed to clonal evolution and cancer stem cells that together give rise to a tumor with complex ecosystems. Each ecosystem contains various tumor cell subpopulations and stromal entities, which, depending upon their composition, can influence survival, therapy responses, and global growth of the tumor. Despite recent advances in breast cancer management, the disease has not been completely eradicated as tumors recur despite initial response to treatment. In this review, using data from clinically relevant breast cancer models, we show that the fates of tumor stem cells/progenitor cells in the individual tumor ecosystems comprising a tumor are predetermined to follow a limited (unipotent) and/or unlimited (multipotent) path of differentiation which create conditions for active generation and maintenance of heterogeneity. The resultant dynamic systems respond differently to treatments, thus disrupting the delicate stability maintained in the heterogeneous tumor. This raises the question whether it is better then to preserve stability by preventing takeover by otherwise dormant ecosystems in the tumor following therapy. The ultimate strategy for personalized therapy would require serial assessments of the patient's tumor for biomarker validation during the entire course of treatment that is combined with their three-dimensional mapping to the tumor architecture and landscape.

Indexed as

AnimalsBreast NeoplasmsFemaleHeterograftsHumansNeoplastic Stem CellsBreast cancerClinical modelsHeterogeneityStem cellsTumor ecosystem

Identifiers

PMID28752247
PMCPMC5693662

What OpenQuestion holds

Textmetadata
LicenceTDM
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.