Evidence map›Paper›PMID 35817701›Full record

ReviewTrends in cancer2022

Decoding endoplasmic reticulum stress signals in cancer cells and antitumor immunity.

Camilla Salvagno, Jessica K Mandula, Paulo C Rodriguez, Juan R Cubillos-Ruiz

Open access · greenAbstract readReview
In one paragraph

Review in Trends in cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed
11.1field-weighted citation impact, top 1% 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

80 citing papers in PubMed, 108 citations in OpenAlex.

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  16. TRMT6/TRMT61A-mediated tRNA mCellular & molecular biology letters · 2026
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20 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

4 authors at 2 institutions in 1 country.

Camilla SalvagnoDepartment of Obstetrics and Gynecology, Weill Cornell Medicine, New York, NY, USA; Sandra and Edward Meyer Cancer Center, Weill Cornell Medicine, New York, NY, USA.
Jessica K MandulaDepartment of Immunology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, USA.
Paulo C RodriguezDepartment of Immunology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, USA. Electronic address: Paulo.Rodriguez@Moffitt.org.
Juan R Cubillos-RuizDepartment of Obstetrics and Gynecology, Weill Cornell Medicine, New York, NY, USA; Sandra and Edward Meyer Cancer Center, Weill Cornell Medicine, New York, NY, USA; Weill Cornell Graduate School of Medical Sciences, Cornell University, New York, NY, USA. Electronic address: jur2016@med.cornell.edu.
Cornell University · USMoffitt Cancer Center · US

Funding

TRANSLATIONAL RESEARCHP30CA076292 · NCI · UNIVERSITY OF SOUTH FLORIDA · PI John L. Cleveland · 1998 to 2026
$93.5M
Project 4P01CA250984 · NCI · H. LEE MOFFITT CANCER CTR & RES INST · PI RODRIGUEZ, PAULO CESAR · 2021 to 2025
$10.1M
Plant-derived extracts regulate immunosuppressive myelopoiesis in Breast cancer patientsR01CA262121 · NCI · H. LEE MOFFITT CANCER CTR & RES INST · PI RODRIGUEZ, PAULO CESAR · 2021 to 2025
$2.1M
Endoplasmic Reticulum Stress Responses in PainR01NS114653 · NINDS · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI BOADA, MARIO DANILO, ROMERO-SANDOVAL, E. ALFONSO · 2020 to 2024
$2.0M
Functional reprogramming of tumor-MDSC through antibody-based therapies targeting Notch ligandsR01CA233512 · NCI · H. LEE MOFFITT CANCER CTR & RES INST · PI RODRIGUEZ, PAULO CESAR · 2019 to 2023
$2.0M
Mitochondrial stress promotes immunosuppressive potential of myeloid subsets in tumorsR01CA273034 · NCI · H. LEE MOFFITT CANCER CTR & RES INST · PI RODRIGUEZ, PAULO CESAR · 2022 to 2025
$1.9M
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
IRE1a-XBP1 Signaling as a Driver of Chemotherapy-Induced Peripheral NeuropathyR21CA248106 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI CUBILLOS-RUIZ, JUAN R, ROMERO-SANDOVAL, E. ALFONSO · 2020 to 2021
$420k
NCI NIH HHS P01 CA250984NCI NIH HHS P30 CA076292NCI NIH HHS R01 CA184185NCI NIH HHS R01 CA233512NCI NIH HHS R01 CA262121NCI NIH HHS R01 CA273034NCI NIH HHS R21 CA248106NINDS NIH HHS R01 NS114653
6 · The paper itself

Abstract

The tumor microenvironment (TME) provokes endoplasmic reticulum (ER) stress in malignant cells and infiltrating immune populations. Sensing and responding to ER stress is coordinated by the unfolded protein response (UPR), an integrated signaling pathway governed by three ER stress sensors: activating transcription factor (ATF6), inositol-requiring enzyme 1α (IRE1α), and protein kinase R (PKR)-like ER kinase (PERK). Persistent UPR activation modulates malignant progression, tumor growth, metastasis, and protective antitumor immunity. Hence, therapies targeting ER stress signaling can be harnessed to elicit direct tumor killing and concomitant anticancer immunity. We highlight recent findings on the role of the ER stress responses in onco-immunology, with an emphasis on genetic vulnerabilities that render tumors highly sensitive to therapeutic UPR modulation.

Indexed as

Endoplasmic Reticulum StressNeoplasmsEndoribonucleasesHumansInositolProtein Serine-Threonine KinasesTumor MicroenvironmentEndoribonucleasesInositolProtein Serine-Threonine Kinasescancer therapyER stressimmune cellstumor microenvironmentunfolded protein response

Identifiers

PMID35817701
PMCPMC9588488
OpenAlexW4284959679

What OpenQuestion holds

Textmetadata
LicenceTDM
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.