Evidence map›Paper›PMID 28105371›Full record

ReviewJournal for immunotherapy of cancer2017

Unfolding anti-tumor immunity: ER stress responses sculpt tolerogenic myeloid cells in cancer.

Juan R Cubillos-Ruiz, Eslam Mohamed, Paulo C Rodriguez

Open access · goldAbstract readReview
In one paragraph

Review in Journal for immunotherapy of cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

51 citing papers in PubMed, 96 citations in OpenAlex.

  1. Review
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  4. Margin-enriched CD4International journal of biological sciences · 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.

Juan R Cubillos-RuizWeill Cornell Medicine, Department of Obstetrics & Gynecology, Sandra and Edward Meyer Cancer Center, 1300 York Ave, E-907, New York, NY 10065 USA.
Eslam MohamedGeorgia Cancer Center, 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.
National Cancer Center of Georgia · GEWeill Cornell Medicine · 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

Established tumors build a stressful and hostile microenvironment that blocks the development of protective innate and adaptive immune responses. Different subsets of immunoregulatory myeloid populations, including dendritic cells, myeloid-derived suppressor cells (MDSCs) and macrophages, accumulate in the stressed tumor milieu and represent a major impediment to the success of various forms of cancer immunotherapy. Specific conditions and factors within tumor masses, including hypoxia, nutrient starvation, low pH, and increased levels of free radicals, provoke a state of "endoplasmic reticulum (ER) stress" in both malignant cells and infiltrating myeloid cells. In order to cope with ER stress, cancer cells and tumor-associated myeloid cells activate an integrated signaling pathway known as the Unfolded Protein Response (UPR), which promotes cell survival and adaptation under adverse environmental conditions. However, the UPR can also induce cell death under unresolved levels of ER stress. Three branches of the UPR have been described, including the activation of the inositol-requiring enzyme 1 (IRE1), the pancreatic ER kinase (PKR)-like ER kinase (PERK), and the activating transcription factor 6 (ATF6). In this minireview, we briefly discuss the role of ER stress and specific UPR mediators in tumor development, growth and metastasis. In addition, we describe how sustained ER stress responses operate as key mediators of chronic inflammation and immune suppression within tumors. Finally, we discuss multiple pharmacological approaches that overcome the immunosuppressive effect of the UPR in tumors, and that could potentially enhance the efficacy of cancer immunotherapies by reprogramming the function of tumor-infiltrating myeloid cells.

Indexed as

Activating Transcription Factor 6AnimalseIF-2 KinaseEndoplasmic Reticulum StressEndoribonucleasesHumansMyeloid CellsNeoplasmsProtein Serine-Threonine KinasesSignal TransductionUnfolded Protein ResponseActivating Transcription Factor 6ATF6 protein, humanEIF2AK3 protein, humaneIF-2 KinaseEndoribonucleasesERN1 protein, humanProtein Serine-Threonine KinasesCHOPER stressImmunotherapyIRE1Myeloid cellsPERKTumor immunologyUnfolded Protein ResponsesXBP1

Identifiers

PMID28105371
PMCPMC5240216
OpenAlexW2576425501

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.