Evidence map›Paper›PMID 37966552›Full record

ReviewClinical and experimental medicine2023

EMT-induced immune evasion: connecting the dots from mechanisms to therapy.

Sikiru O Imodoye, Kamoru A Adedokun

Abstract readReview
PubMed Publisher
In one paragraph

Review in Clinical and experimental medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
5.4field-weighted citation impact, top 4% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

  1. Necroptosis in pancreatic cancer: Molecular mechanisms and therapeutic implications.Apoptosis : an international journal on programmed cell death · 2026
    Pooled it
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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 2 institutions in 1 country.

Sikiru O ImodoyeDepartment of Oncological Sciences, Huntsman Cancer Institute, University of Utah, Salt Lake City, USA. Yemi.imodoye@hci.utah.edu.
Kamoru A AdedokunDepartment of Immunology, Roswell Park Comprehensive Cancer Center, Buffalo, NY, 14263, USA.
Roswell Park Comprehensive Cancer Center · USUniversity of Utah · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epithelial-mesenchymal transition (EMT) is a dynamic program crucial for organismal development and tissue regeneration. Unfortunately, this program is often hijacked by epithelial tumors to facilitate metastasis. Beyond its role in cancer spread, EMT increases cancer cell survival by activating stem cell programs and bypassing apoptotic programs. Importantly, the capacity of EMT to enforce tumor progression by altering the tumor cell phenotype without triggering immune responses opens the intriguing possibility of a mechanistic link between EMT-driven cancers and immune evasion. Indeed, EMT has been acknowledged as a of driver immune evasion, but the mechanisms are still evolving. Here, we review recent insights into the influence of EMT on tumor immune evasion. Specifically, we focus on the mechanistic roles of EMT in immune escape as the basis that may provide a platform for innovative therapeutic approaches in advanced tumors. We summarize promising therapeutic approaches currently in clinical trials and trending preclinical studies aimed at reinvigorating the tumor microenvironment to create immune-permissive conditions that facilitates immune-mediated tumor clearance. We anticipate that this will assist researchers and pharmaceutical companies in understanding how EMT compromises the immune response, potentially paving the way for effective cancer therapies.

Indexed as

Immune EvasionNeoplasmsEpithelial-Mesenchymal TransitionHumansTumor MicroenvironmentCytotoxic T lymphocyteEpithelial–mesenchymal transitionImmune evasionImmunotherapyNK cellsTumor microenvironment

Identifiers

PMID37966552
OpenAlexW4388702453

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.