Evidence map›Paper›PMID 28577085›Full record

ReviewCancer immunology, immunotherapy : CII2017

Endoplasmic reticulum stress regulates tumor growth and anti-tumor immunity: a promising opportunity for cancer immunotherapy.

Eslam Mohamed, Yu Cao, Paulo C Rodriguez

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Cancer immunology, immunotherapy : CII, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed, 1 pooled it
3.9field-weighted citation impact, top 6% 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

63 citing papers in PubMed, 1 synthesis or guideline pooled it, 108 citations in OpenAlex.

  1. Pooled it
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  13. Harnessing myeloid cells in cancer.Molecular cancer · 2025
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3 more citing papers are in PubMed but not listed here.

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 1 country.

Eslam MohamedGeorgia Cancer Center, Medical College of Georgia, Augusta University, 1410 Laney Walker Blvd, Room CN-4125A, Augusta, GA, 30912, USA. emohamed@augusta.edu.
Yu CaoGeorgia Cancer Center, Medical College of Georgia, Augusta University, 1410 Laney Walker Blvd, Room CN-4125A, Augusta, GA, 30912, USA.
Paulo C RodriguezDepartment of Medicine, Georgia Cancer Center, Augusta University, 1410 Laney Walker Blvd, Room CN-4114, Augusta, GA, 30912, USA. paurodriguez@augusta.edu.
Augusta University · USAugusta University Health · US

Funding

Stress Pathways in Tumors Drive Global MDSC Activity and Survival through ChopR01CA184185 · NCI · LSU HEALTH SCIENCES CENTER · PI RODRIGUEZ, PAULO CESAR · 2015 to 2019
$1.8M
NCI NIH HHS R01 CA184185
6 · The paper itself

Abstract

The endoplasmic reticulum (ER) stress is a cellular process that occurs as a consequence of several stress circumstances, such as the accumulation of unfolded proteins in the lumen of the ER or distinct insults that disturb the ER normal function. Different conditions in the tumor microenvironment (TME), including hypoxia, nutrient deprivation, and the elevated production of reactive oxygen and nitrogen species destabilize the loading and dispatching of the newly synthesized proteins, triggering ER stress in cancer cells and tumor-infiltrating leukocytes. In order to cope with TME-induced ER stress, tumor and stromal cells initiate an adaptive response process that aims to resolve ER stress and to restore cellular homeostasis, which is referred as the unfolded protein responses (UPR). Paradoxically, the UPR can also induce cell death under severe and/or permanent ER stress. The UPR is started through three mediators, the activation of the inositol-requiring enzyme-1α, the pancreatic ER kinase-like ER kinase, and the activating transcription factor 6. In this minireview, we will discuss the pro- and anti-tumorigenic role of the UPR in cancer cells. In addition, we will describe the effects of the TME-induced ER stress in the immunosuppressive activity of tumor-infiltrating myeloid cells. Also, we will review the results of emerging therapeutic interventions that target ER stress and the UPR mediators in cancer. We postulate that the inhibition of ER stress or the UPR-related elements could represent a significant approach to increase the efficacy of various forms of cancer immunotherapy.

Indexed as

ImmunityAnimalsCarcinogenesisEndoplasmic ReticulumEndoplasmic Reticulum StressHumansImmunomodulationImmunotherapyMyeloid-Derived Suppressor CellsNeoplasmsTumor MicroenvironmentUnfolded Protein ResponseEndoplasmic reticulum stressMyeloid-derived suppressor cellsRegulatory myeloid suppressor cellsT cellsTumor microenvironmentUnfolded protein responses

Identifiers

PMID28577085
PMCPMC5700458
OpenAlexW2621111540

What OpenQuestion holds

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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.