Evidence map›Paper›PMID 24762632›Full record

ArticleCancers2014

STAT3 Activity and Function in Cancer: Modulation by STAT5 and miR-146b.

Sarah R Walker, Michael Xiang, David A Frank

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

16 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
  2. Epigenetic Signaling of Cancer Stem Cells During Inflammation.Frontiers in cell and developmental biology · 2021
    Review
  3. Article
  4. MicroRNA expression profile in Treg cells in the course of primary immune thrombocytopenia.Journal of investigative medicine : the official publication of the American Federation for Clinical Research · 2019
    Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. The Novel Nutraceutical KJS018A Prevents Hepatocarcinogenesis Promoted by Inflammation.Evidence-based complementary and alternative medicine : eCAM · 2018
    Article
  12. STAT3 in the systemic inflammation of cancer cachexia.Seminars in cell & developmental biology · 2016
    Review
  13. Article
  14. Article
  15. Article
  16. 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

3 authors at 1 institution in 1 country.

Sarah R WalkerDepartment of Medical Oncology, Dana-Farber Cancer Institute, and Departments of Medicine, Brigham and Women's Hospital and Harvard Medical School, 450 Brookline Avenue, Boston, MA 02215, USA. sarah_walker@dfci.harvard.edu.
Michael XiangDepartment of Medical Oncology, Dana-Farber Cancer Institute, and Departments of Medicine, Brigham and Women's Hospital and Harvard Medical School, 450 Brookline Avenue, Boston, MA 02215, USA. mxiang@mit.edu.
David A FrankDepartment of Medical Oncology, Dana-Farber Cancer Institute, and Departments of Medicine, Brigham and Women's Hospital and Harvard Medical School, 450 Brookline Avenue, Boston, MA 02215, USA. david_frank@dfci.harvard.edu.
Dana-Farber Brigham Cancer Center · US

Funding

Medical Scientist Training ProgramT32GM007753 · NIGMS · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI WALENSKY, LOREN DAVID · 1985 to 2021
$50.0M
Dual STAT3/NF-kB Inhibitors for Targeted Cancer TherapyR01CA160979 · NCI · DANA-FARBER CANCER INST · PI FRANK, DAVID A. · 2012 to 2016
$1.8M
MiR-146b, a novel STAT target: regulatory mechanisms and role in cancerF30CA165740 · NCI · HARVARD MEDICAL SCHOOL · PI XIANG, MICHAEL · 2012 to 2013
$67k
NCI NIH HHS F30 CA165740NCI NIH HHS R01 CA160979NIGMS NIH HHS T32 GM007753
6 · The paper itself

Abstract

The transcription factor STAT3 regulates genes that control critical cellular processes such as proliferation, survival, pluripotency, and motility. Thus, under physiological conditions, the transcriptional function of STAT3 is tightly regulated as one part of a complex signaling matrix. When these processes are subverted through mutation or epigenetic events, STAT3 becomes highly active and drives elevated expression of genes underlying these phenotypes, leading to malignant cellular behavior. However, even in the presence of activated STAT3, other cellular modulators can have a major impact on the biological properties of a cancer cell, which is reflected in the clinical behavior of a tumor. Recent evidence has suggested that two such key modulators are the activation status of other STAT family members, particularly STAT5, and the expression of STAT3-regulated genes that are part of negative feedback circuits, including microRNAs such as miR-146b. With attention to these newly emerging areas, we will gain greater insight into the consequence of STAT3 activation in the biology of human cancers. In addition, understanding these subtleties of STAT3 signaling in cancer pathogenesis will allow the development of more rational molecular approaches to cancer therapy.

Identifiers

PMID24762632
PMCPMC4074811
OpenAlexW2070947781

What OpenQuestion holds

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LicenceCC BY
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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.