Evidence map›Paper›PMID 31583529›Full record

ArticleCancer microenvironment : official journal of the International Cancer Microenvironment Society2019

Tumor-Infiltrating Immunosuppressive Cells in Cancer-Cell Plasticity, Tumor Progression and Therapy Response.

Laura Lorenzo-Sanz, Purificación Muñoz

Open access · bronzeAbstract read
In one paragraph

Article in Cancer microenvironment : official journal of the International Cancer Microenvironment Society, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

48 citing papers in PubMed, 73 citations in OpenAlex.

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  13. IGF1R signaling induces epithelial-mesenchymal plasticity via ITGAV in cutaneous carcinoma.Journal of experimental & clinical cancer research : CR · 2024
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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

2 authors at 1 institution in 1 country.

Laura Lorenzo-SanzAging and Cancer Group, Oncobell Program, Bellvitge Biomedical Research Institute (IDIBELL), Av. Gran Vía de L'Hospitalet 199-203, 08908, Barcelona, Spain.
Purificación MuñozAging and Cancer Group, Oncobell Program, Bellvitge Biomedical Research Institute (IDIBELL), Av. Gran Vía de L'Hospitalet 199-203, 08908, Barcelona, Spain. p.munoz@idibell.cat.ORCID http://orcid.org/0000-0002-3751-2099
Institut d'Investigació Biomédica de Bellvitge · ES

Funding

EARLY DIAGNOSIS OF CANCER: THE CANFIND CONSORTIUMU01CA084976 · NCI · GENETICA, INC. · PI BEACH, DAVID H. · 1999 to 2002
$2.0M
Agència de Gestió d'Ajuts Universitaris i de Recerca 2017SGR565IDIBELL FellowshipMinisterio de Ciencia e Innovación SAF2017-84976R
6 · The paper itself

Abstract

In most tumors, cancer cells show the ability to dynamically transit from a non-cancer stem-like cell to a cancer stem-like cell (CSC) state and vice versa. This cell plasticity has been associated with the epithelial-to-mesenchymal transition program (EMT) and can be regulated by tumor cell-intrinsic mechanisms and complex interactions with various tumor microenvironment (TME) components. These interactions favor the generation of a specific "CSC niche" that helps maintain the main properties, phenotypic plasticity and metastatic potential of this subset of tumor cells. For this reason, TME has been recognized as an important promoter of tumor progression and therapy resistance. Tumors have evolved a network of immunosuppressive mechanisms that limits the cytotoxic T cell response to cancer cells. Some key players in this network are tumor-associated macrophages, myeloid-derived suppressor cells and regulatory T cells, which not only favor a pro-tumoral and immunosuppressive environment that supports tumor growth and immune evasion, but also negatively influences immunotherapy. Here, we review the relevance of cytokines and growth factors provided by immunosuppressive immune cells in regulating cancer-cell plasticity. We also discuss how cancer cells remodel their own niche to promote proliferation, stemness and EMT, and escape immune surveillance. A better understanding of CSC-TME crosstalk signaling will enable the development of effective targeted or immune therapies that block tumor growth and metastasis.

Indexed as

Cancer-cell plasticityCancer stem cellsEMTImmunosuppressive immune cellsMetastasisTherapy response

Identifiers

PMID31583529
PMCPMC6937363
OpenAlexW2978132006

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.