Evidence map›Paper›PMID 32824649›Full record

ReviewCancers2020

Extracellular Vesicle-Based Communication May Contribute to the Co-Evolution of Cancer Stem Cells and Cancer-Associated Fibroblasts in Anti-Cancer Therapy.

Gábor Valcz, Edit I Buzás, Anna Sebestyén, Tibor Krenács, Zoltán Szállási, Péter Igaz, Béla Molnár

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

13 citing papers in PubMed, 11 citations in OpenAlex.

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  13. New Insights into Therapy-Induced Progression of Cancer.International journal of molecular sciences · 2020
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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

7 authors at 2 institutions in 2 countries.

Gábor Valcz2nd Department of Internal Medicine and MTA-SE Molecular Medicine Research Group, 1051 Budapest, Hungary.
Edit I BuzásDepartment of Genetics, Cell- and Immunobiology, Semmelweis University, 1089 Budapest, Hungary.ORCID 0000-0002-3744-206X
Anna Sebestyén1st Department of Pathology and Experimental Cancer Research, Semmelweis University, 1085 Budapest, Hungary.
Tibor Krenács1st Department of Pathology and Experimental Cancer Research, Semmelweis University, 1085 Budapest, Hungary.ORCID 0000-0001-9164-065X
Zoltán SzállásiComputational Health Informatics Program (CHIP), Boston Children's Hospital and Harvard Medical School, Boston, MA 02115, USA.
Péter Igaz2nd Department of Internal Medicine and MTA-SE Molecular Medicine Research Group, 1051 Budapest, Hungary.ORCID 0000-0003-2192-554X
Béla Molnár2nd Department of Internal Medicine and MTA-SE Molecular Medicine Research Group, 1051 Budapest, Hungary.
Semmelweis University · HUBoston Children's Hospital · US

Funding

Higher Education Institutional Excellence Programme of the Ministry of Human Capacities in Hungary, within the framework of the molecular biology thematic programme of the Semmelweis University -Nemzeti Kutatási Fejlesztési és Innovációs Hivatal KMR-12-1-2012-0216Nemzeti Kutatási Fejlesztési és Innovációs Hivatal NVKP_16-1-2016-0004Nemzeti Kutatási Fejlesztési és Innovációs Hivatal NVKP_16-1-2016-0017Nemzeti Kutatási Fejlesztési és Innovációs Hivatal OTKA120237TRAIN EV H2020-MSCA-ITN-2017-722148
6 · The paper itself

Abstract

Analogously to the natural selective forces in ecosystems, therapies impose selective pressure on cancer cells within tumors. Some tumor cells can adapt to this stress and are able to form resistant subpopulations, parallel with enrichment of cancer stem cell properties in the residual tumor masses. However, these therapy-resistant cells are unlikely to be sufficient for the fast tumor repopulation and regrowth by themselves. The dynamic and coordinated plasticity of residual tumor cells is essential both for the conversion of their regulatory network and for the stromal microenvironment to produce cancer supporting signals. In this nursing tissue "niche", cancer-associated fibroblasts are known to play crucial roles in developing therapy resistance and survival of residual stem-like cells. As paracrine messengers, extracellular vesicles carrying a wide range of signaling molecules with oncogenic potential, can support the escape of some tumor cells from their deadly fate. Here, we briefly overview how extracellular vesicle signaling between fibroblasts and cancer cells including cancer progenitor/stem cells may contribute to the progression, therapy resistance and recurrence of malignant tumors.

Indexed as

cancer cell-fibroblast interactioncancer stem cellextracellular vesiclestherapy resistance

Identifiers

PMID32824649
PMCPMC7465064
OpenAlexW3049429462

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.