Evidence map›Paper›PMID 18508994›Full record

ReviewEndocrine-related cancer2008

Signal transducer and activator of transcription 5A/B in prostate and breast cancers.

Shyh-Han Tan, Marja T Nevalainen

Open access · bronzeAbstract readReview
In one paragraph

Review in Endocrine-related cancer, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

50 citing papers in PubMed, 115 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Growth hormone and gastrointestinal malignancy: An intriguing link.World journal of gastrointestinal pathophysiology · 2023
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Colonic Cancer and Acromegaly.Frontiers in endocrinology · 2019
    Review
  16. Article
  17. Review
  18. Article
  19. Review
  20. Article
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

2 authors at 1 institution in 1 country.

Shyh-Han TanDepartment of Cancer Biology, Kimmel Cancer Center, Thomas Jefferson University, 233 South 10th Street, BLSB 309, Philadelphia, Pennsylvania 19107, USA.
Marja T Nevalainen
Thomas Jefferson University · US

Funding

Stat5 in Progression of Prostate CancerR01CA113580 · NCI · THOMAS JEFFERSON UNIVERSITY · PI NEVALAINEN, MARJA T · 2006 to 2015
$2.7M
Novel Strategy to Sensitize Prostate Cancer Cells to RadiationR21CA178755 · NCI · THOMAS JEFFERSON UNIVERSITY · PI NEVALAINEN, MARJA T · 2013 to 2014
$365k
NCI NIH HHS 1R01CA113580-01A1NCI NIH HHS R01 CA113580NCI NIH HHS R21 CA178755
6 · The paper itself

Abstract

Protein kinase signaling pathways, such as Janus kinase 2-Signal transducer and activator of transcription 5A/B (JAK2-STAT5A/B), are of significant interest in the search for new therapeutic strategies in both breast and prostate cancers. In prostate cancer, the components of the JAK2-STAT5A/B signaling pathway provide molecular targets for small-molecule inhibition of survival and growth signals of the cells. At the same time, new evidence suggests that the STAT5A/B signaling pathway is involved in the transition of organ-confined prostate cancer to hormone-refractory disease. This implies that the active JAK2-STAT5A/B signaling pathway potentially provides the means for pharmacological intervention of clinical prostate cancer progression. In addition, active STAT5A/B may serve as a prognostic marker for identification of those primary prostate cancers that are likely to progress to aggressive disease. In breast cancer, the role of STAT5A/B is more complex. STAT5A/B may have a dual role in the regulation of malignant mammary epithelium. Data accumulated from mouse models of breast cancer suggest that in early stages of breast cancer STAT5A/B may promote malignant transformation and enhance growth of the tumor. This is in contrast to established breast cancer, where STAT5A/B may mediate the critical cues for maintaining the differentiation of mammary epithelium. In addition, present data suggest that activation of STAT5A/B in breast cancer predicts favorable clinical outcome. The dual nature of STAT5A/B action in breast cancer makes the therapeutic use of STAT5 A/B more complex.

Indexed as

Breast NeoplasmsFemaleHumansMaleProstatic NeoplasmsSignal TransductionSTAT5 Transcription FactorTumor Suppressor ProteinsSTAT5A protein, humanSTAT5B protein, humanSTAT5 Transcription FactorTumor Suppressor Proteins

Identifiers

PMID18508994
PMCPMC6036917
OpenAlexW2171837966

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.