Evidence map›Paper›PMID 36168057›Full record

ReviewNature reviews. Urology2022

The endoplasmic reticulum stress response in prostate cancer.

Claire M de la Calle, Kevin Shee, Heiko Yang, Peter E Lonergan, Hao G Nguyen

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Urology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.9field-weighted citation impact, top 5% 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

21 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Protein disulfide isomerases regulate androgen receptor stability and promote prostate cancer cell growth and survival.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  8. Article
  9. NXP800 Activates the Unfolded Protein Response, Altering AR and E2F Function to Impact Castration-Resistant Prostate Cancer Growth.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025
    Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
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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

5 authors at 1 institution in 2 countries.

Claire M de la CalleDepartment of Urology, Helen Diller Comprehensive Cancer Center, University of California, San Francisco, San Francisco, CA, USA.ORCID 0000-0003-1770-7953
Kevin SheeDepartment of Urology, Helen Diller Comprehensive Cancer Center, University of California, San Francisco, San Francisco, CA, USA.ORCID 0000-0001-5378-7650
Heiko YangDepartment of Urology, Helen Diller Comprehensive Cancer Center, University of California, San Francisco, San Francisco, CA, USA.
Peter E LonerganDepartment of Urology, Helen Diller Comprehensive Cancer Center, University of California, San Francisco, San Francisco, CA, USA.ORCID 0000-0001-7233-8156
Hao G NguyenDepartment of Urology, Helen Diller Comprehensive Cancer Center, University of California, San Francisco, San Francisco, CA, USA. hao.nguyen@ucsf.edu.
University of California, San Francisco · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In order to proliferate in unfavourable conditions, cancer cells can take advantage of the naturally occurring endoplasmic reticulum-associated unfolded protein response (UPR) via three highly conserved signalling arms: IRE1α, PERK and ATF6. All three arms of the UPR have key roles in every step of tumour progression: from cancer initiation to tumour growth, invasion, metastasis and resistance to therapy. At present, no cure for metastatic prostate cancer exists, as targeting the androgen receptor eventually results in treatment resistance. New research has uncovered an important role for the UPR in prostate cancer tumorigenesis and crosstalk between the UPR and androgen receptor signalling pathways. With an improved understanding of the mechanisms by which cancer cells exploit the endoplasmic reticulum stress response, targetable points of vulnerability can be uncovered.

Indexed as

Endoplasmic Reticulum StressProstatic NeoplasmsEndoribonucleasesHumansMaleProtein Serine-Threonine KinasesReceptors, AndrogenEndoribonucleasesProtein Serine-Threonine KinasesReceptors, Androgen

Identifiers

PMID36168057
OpenAlexW4297327204

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.