Evidence map›Paper›PMID 25920797›Full record

ReviewSeminars in cancer biology2015

Cell intrinsic and extrinsic activators of the unfolded protein response in cancer: Mechanisms and targets for therapy.

Feven Tameire, Ioannis I Verginadis, Constantinos Koumenis

Abstract readReview
In one paragraph

Review in Seminars in cancer biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
–field-weighted citation impact
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

67 citing papers in PubMed.

  1. Article
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  13. Review
  14. A PERK-Specific Inhibitor Blocks Metastatic Progression by Limiting Integrated Stress Response-Dependent Survival of Quiescent Cancer Cells.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023
    Article
  15. Dual RNase activity of IRE1 as a target for anticancer therapies.Journal of cell communication and signaling · 2023
    Review
  16. Article
  17. Article
  18. ER chaperone GRP78/BiP translocates to the nucleus under stress and acts as a transcriptional regulator.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  19. Targeting Myc-driven stress addiction in colorectal cancer.Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy · 2023
    Review
  20. Article

7 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.

Feven TameireDepartment of Radiation Oncology, Perelman University School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA; Program in Cell and Molecular Biology, Perelman University School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
Ioannis I VerginadisDepartment of Radiation Oncology, Perelman University School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
Constantinos KoumenisDepartment of Radiation Oncology, Perelman University School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. Electronic address: costas.koumenis@uphs.upenn.edu.

Funding

UPR, interferon signaling and tumorigenesisP01CA165997 · NCI · UNIVERSITY OF PENNSYLVANIA · PI WILEYTO, E. PAUL · 2013 to 2023
$10.9M
The Role of ATF4 in Promoting c-Myc Induced LymphomagenesisF31CA183569 · NCI · UNIVERSITY OF PENNSYLVANIA · PI TAMEIRE, FEVEN · 2013 to 2017
$159k
NCI NIH HHS 1P01-CA165997NCI NIH HHS F31 CA183569NCI NIH HHS F31CA183569NCI NIH HHS P01 CA165997
6 · The paper itself

Abstract

A variety of cell intrinsic or extrinsic stresses evoke perturbations in the folding environment of the endoplasmic reticulum (ER), collectively known as ER stress. Adaptation to stress and re-establishment of ER homeostasis is achieved by activation of an integrated signal transduction pathway called the unfolded protein response (UPR). Both ER stress and UPR activation have been implicated in a variety of human cancers. Although at early stages or physiological conditions of ER stress, the UPR generally promotes survival, when the stress becomes more stringent or prolonged, its role can switch to a pro-cell death one. Here, we discuss historical and recent evidence supporting an involvement of the UPR in malignancy, describe the main mechanisms by which tumor cells overcome ER stress to promote their survival, tumor progression and metastasis and discuss the current state of efforts to develop therapeutic approaches of targeting the UPR.

Indexed as

Unfolded Protein ResponseAdaptation, PhysiologicalAnimalsApoptosisAutophagyCell LineageCellular SenescenceEndoplasmic ReticulumEndoplasmic Reticulum StressEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHomeostasisHumansHypoxiaMiceMice, TransgenicBRAF protein, humanProto-Oncogene Proteins B-rafProto-Oncogene Proteins c-mycras ProteinsCancerER stressTherapeutic approachesTumorigenesisUPR

Identifiers

PMID25920797
PMCPMC4523493

What OpenQuestion holds

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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.