Evidence map›Paper›PMID 22804234›Full record

ArticleCurrent molecular medicine2012

HSF1, a versatile factor in tumorogenesis.

S K Calderwood

Open access · greenAbstract read
In one paragraph

Article in Current molecular medicine, 2012. 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
1.7field-weighted citation impact, top 15% 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, 33 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. NRF2 transcriptionally activates theThe Journal of biological chemistry · 2018
    Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Heat shock in the springtime.Cell stress & chaperones · 2014
    Article
  19. Article
  20. Review
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

1 author at 1 institution in 1 country.

S K CalderwoodDepartment of Radiation Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA. scalderw@bidmc.harvard.edu
Harvard University · US

Funding

TRANSMEMBRANE SIGNAL MODULATION BY HYPERTHERMIAR01CA047407 · NCI · DANA-FARBER CANCER INSTITUTE · PI CALDERWOOD, STUART KEITH · 1988 to 2014
$4.3M
Extracellular Hsp70 and hyperthermia in tumor therapyR01CA119045 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI CALDERWOOD, STUART KEITH · 2007 to 2016
$3.1M
Gene Repression by HSF1 during hyperthermia and stressesR01CA094397 · NCI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI CALDERWOOD, STUART KEITH · 2002 to 2006
$1.5M
NCI NIH HHS R01 CA047407NCI NIH HHS R0-1CA047407NCI NIH HHS R01 CA094397NCI NIH HHS R0-1CA094397NCI NIH HHS R01 CA119045NCI NIH HHS R01CA119045
6 · The paper itself

Abstract

HSF1 is an essential factor in the acute response to proteotoxic stress, in which it causes rapid transcription of heat shock protein (HSP) genes in order to permit survival of cells and restoration of global protein quality. In addition to this property however, HSF1 is chronically activated or overexpressed in a wide range of cancers and is essential for multiple pathways of malignant transformation. Studies in recent years indicate a remarkable pleiotropy in the properties of HSF1 in cancer. HSF1 functions as a transcription factor for HSP genes, reminiscent of its role in the stress response, and the resultant elevation in HSP levels leads to a reduction in programmed cell death and senescence and permits overexpression of mutated oncogenic protein clients required to fuel tumor growth. In addition HSF1 plays a role as a signal modulator, stimulating kinase activity, regulating energy metabolism and permitting the development of polyploidy in cancer cells. HSF1 can also function as an inhibitor of transcription and in cooperation with NuRD family factors can repress genes that oppose metastasis. Inhibitors of HSF1 are undergoing selection and future studies may see the testing of HSF1 as a target in cancer therapy.

Indexed as

AgingCell DeathCell Transformation, NeoplasticDNA-Binding ProteinsHeat Shock Transcription FactorsHumansMi-2 Nucleosome Remodeling and Deacetylase ComplexMutationNeoplasmsTranscription FactorsDNA-Binding ProteinsHeat Shock Transcription FactorsHSF1 protein, humanMi-2 Nucleosome Remodeling and Deacetylase ComplexTranscription Factors

Identifiers

PMID22804234
PMCPMC4075975
OpenAlexW2322809234

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.