Evidence map›Paper›PMID 34680248›Full record

ArticleCancers2021

Impact of Epithelial-Mesenchymal Transition on the Immune Landscape in Breast Cancer.

Fatima-Zohra Khadri, Marianne Samir Makboul Issac, Louis Arthur Gaboury

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.7field-weighted citation impact, top 26% 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

10 citing papers in PubMed, 11 citations in OpenAlex.

  1. Suppression of NGALR impedes TNBC cell survival, proliferation, invasion, and migration through Akt/mTOR and JAK/STAT3 pathway inhibition.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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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

3 authors at 2 institutions in 2 countries.

Fatima-Zohra KhadriInstitute for Research in Immunology and Cancer (IRIC), Université de Montréal, Montréal, QC H3T 1J4, Canada.ORCID 0000-0002-7686-0539
Marianne Samir Makboul IssacInstitute for Research in Immunology and Cancer (IRIC), Université de Montréal, Montréal, QC H3T 1J4, Canada.ORCID 0000-0003-1113-9270
Louis Arthur GabouryInstitute for Research in Immunology and Cancer (IRIC), Université de Montréal, Montréal, QC H3T 1J4, Canada.ORCID 0000-0002-7093-8139
Institute for Research in Immunology and Cancer · CACairo University · EG

Funding

This research was funded by Internal Research funds, Department of Pathology and Cell Biology, Faculty of Medicine, Université de Montréal 0
6 · The paper itself

Abstract

The impact of epithelial-mesenchymal transition (EMT) signature on the immune infiltrate present in the breast cancer tumor microenvironment (TME) is still poorly understood. Since there is mounting interest in the use of immunotherapy for the treatment of subsets of breast cancer patients, it is of major importance to understand the fundamental tumor characteristics which dictate the inter-tumor heterogeneity in immune landscapes. We aimed to assess the impact of EMT-related markers on the nature and magnitude of the inflammatory infiltrate present in breast cancer TME and their association with the clinicopathological parameters. Tissue microarrays were constructed from 144 formalin-fixed paraffin-embedded invasive breast cancer tumor samples. The protein expression patterns of Snail, Twist, ZEB1, N-cadherin, Vimentin, GRHL2, E-cadherin, and EpCAM were examined by immunohistochemistry (IHC). The inflammatory infiltrate in the TME was assessed semi-quantitatively on hematoxylin and eosin (H&E)-stained whole sections and was characterized using IHC. The inflammatory infiltrate was more intense in poorly differentiated carcinomas and triple-negative carcinomas in which the expression of E-cadherin and GRHL2 was reduced, while EpCAM was overexpressed. Most EMT-related markers correlated with plasma cell infiltration of the TME. Taken together, our findings reveal that the EMT signature might impact the immune response in the TME.

Indexed as

biomarkersbreast cancerepithelial–mesenchymal transition (EMT)immune landscapeimmunohistochemistryinflammatory infiltrateprotein expressiontumor microenvironment (TME)

Identifiers

PMID34680248
PMCPMC8533811
OpenAlexW3207646209

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.