Evidence map›Paper›PMID 31376430›Full record

ReviewSeminars in cancer biology2020

The pan-therapeutic resistance of disseminated tumor cells: Role of phenotypic plasticity and the metastatic microenvironment.

Bo Ma, Alan Wells, Amanda M Clark

Abstract readReview
In one paragraph

Review in Seminars in cancer biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing 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

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

  1. Pooled it
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  8. Mediator kinase inhibitors suppress triple-negative breast cancer growth and extend tumor suppression by mTOR and AKT inhibitors.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
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  14. Tumor biomarkers for diagnosis, prognosis and targeted therapy.Signal transduction and targeted therapy · 2024
    Review
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  20. Observational
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

3 authors.

Bo MaDepartment of Pathology, University of Pittsburgh, Pittsburgh, PA 15261, USA; VA Pittsburgh Healthcare System, Pittsburgh, PA 15213, USA.
Alan WellsDepartment of Pathology, University of Pittsburgh, Pittsburgh, PA 15261, USA; VA Pittsburgh Healthcare System, Pittsburgh, PA 15213, USA; Department of Bioengineering, University of Pittsburgh, Pittsburgh, PA 15260, USA; Department of Computational & Systems Biology, University of Pittsburgh, Pittsburgh, PA 15260, USA; UPMC Hillman Cancer Center, University of Pittsburgh, Pittsburgh, PA 15213, USA.
Amanda M ClarkDepartment of Pathology, University of Pittsburgh, Pittsburgh, PA 15261, USA; VA Pittsburgh Healthcare System, Pittsburgh, PA 15213, USA. Electronic address: amc235@pitt.edu.

Funding

VECTOR CORE FACILITYP30CA047904 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI JOHN C. BYRD · 1988 to 2026
$158.0M
Spatial Segregation of Cell Functioning During MotilityR01GM069668 · NIGMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI WELLS, ALAN · 2004 to 2019
$4.7M
Dermal-Epidermal Communication during Wound HealingR01GM063569 · NIGMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI WELLS, ALAN · 2003 to 2018
$3.7M
Probing the Role of the Tumor Microenvironment on Mechanistic Biomarkers for Chemotherapeutic ResistanceUH3TR000496 · NCATS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI GRIFFITH, LINDA G · 2014 to 2016
$3.5M
Dermal-Epidermal Communication during Wound HealingR56GM063569 · NIGMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI WELLS, ALAN · 2008 to 2008
$341k
Molecular Regulation of Breast Cancer ProgressionI01BX003368 · VA · VETERANS HEALTH ADMINISTRATION · PI WELLS, ALAN · 2016 to 2023
–
BLRD VA I01 BX003368NCATS NIH HHS UH3 TR000496NCI NIH HHS P30 CA047904NIGMS NIH HHS R01 GM063569NIGMS NIH HHS R01 GM069668NIGMS NIH HHS R56 GM063569
6 · The paper itself

Abstract

Cancer metastasis is the leading cause of mortality in patients with solid tumors. The majority of these deaths are associated with metastatic disease that occurs after a period of clinical remission, anywhere from months to decades following removal of the primary mass. This dormancy is prominent in cancers of the breast and prostate among others, leaving the survivors uncertain about their longer-term prognosis. The most daunting aspect of this dormancy and re-emergence is that the micrometastases in particular, and even large lethal outgrowths are often show resistance to agents to which they have not been exposed. This suggests that in addition to specific mutations that target single agents, there also exist adaptive mechanisms that provide this pan-resistance. Potential molecular underpinnings of which are the topic of this review.

Indexed as

Drug Resistance, NeoplasmTumor MicroenvironmentAdaptation, PhysiologicalAnimalsCell PlasticityDisease ProgressionEpithelial-Mesenchymal TransitionHumansImmunomodulationNeoplasm MetastasisNeoplasmsNeoplasm StagingTumor EscapeDisseminated tumor cellsDormancyEpithelial-mesenchymal plasticityMetastasisMetastatic microenvironmentTherapeutic resistance

Identifiers

PMID31376430
PMCPMC6992520

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.