Evidence map›Paper›PMID 21945472›Full record

ReviewMolecular and cellular endocrinology2012

Role of phosphorylation in progesterone receptor signaling and specificity.

Christy R Hagan, Andrea R Daniel, Gwen E Dressing, Carol A Lange

Abstract readReview
In one paragraph

Review in Molecular and cellular endocrinology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 7% 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, 1 synthesis or guideline pooled it, 88 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. The Role of Progesterone Receptors in Breast Cancer.Drug design, development and therapy · 2022
    Review
  16. Article
  17. LPACells · 2021
    Article
  18. Review
  19. Article
  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

4 authors at 1 institution in 1 country.

Christy R HaganUniversity of Minnesota, Departments of Medicine and Pharmacology, Division of Hematology, Oncology, and Transplantation, Women's Cancer Program, Masonic Cancer Center, Minneapolis, MN 55455, United States.
Andrea R Daniel
Gwen E Dressing
Carol A Lange
University of Minnesota · US

Funding

TRAINING GRANT IN MICROBIOLOGY/CANCER RESEARCHT32CA009138 · NCI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI Scott M. Dehm · 1985 to 2026
$11.3M
Progestin and growth factor cross-talk in breast cancerR01CA123763 · NCI · UNIVERSITY OF MINNESOTA · PI LANGE, CAROL A · 2006 to 2010
$1.1M
PROGESTIN AND GROWTH FACTOR CROSS-TALK IN BREAST CANCERR01DK053825 · NIDDK · UNIVERSITY OF MINNESOTA TWIN CITIES · PI LANGE, CAROL ANN · 1997 to 2004
$975k
MAPKs Regulate Progesterone Receptors by SUMO ModulationR21CA116790 · NCI · UNIVERSITY OF MINNESOTA · PI LANGE, CAROL ANN · 2006 to 2007
$294k
NCI NIH HHS R01 CA123763NCI NIH HHS R21 CA116790NCI NIH HHS T32 CA009138NIDDK NIH HHS R01 DK053825
6 · The paper itself

Abstract

Progesterone receptors (PR), in concert with peptide growth factor-initiated signaling pathways, initiate massive expansion of the epithelial cell compartment associated with the process of alveologenesis in the developing mammary gland. PR-dependent signaling events also contribute to inappropriate proliferation observed in breast cancer. Notably, PR-B isoform-specific cross talk with growth factor-driven pathways is required for the proliferative actions of progesterone. Indeed, PRs act as heavily phosphorylated transcription factor "sensors" for mitogenic protein kinases that are often elevated and/or constitutively activated in invasive breast cancers. In addition, phospho-PR-target genes frequently include the components of mitogenic signaling pathways, revealing a mechanism for feed-forward signaling that confers increased responsiveness of, PR +mammary epithelial cells to these same mitogenic stimuli. Understanding the mechanisms and isoform selectivity of PR/kinase interactions may yield further insight into targeting altered signaling networks in breast and other hormonally responsive cancers (i.e. lung, uterine and ovarian) in the clinic. This review focuses on PR phosphorylation by mitogenic protein kinases and mechanisms of PR-target gene selection that lead to increased cell proliferation.

Indexed as

Signal TransductionAnimalsHumansPhosphorylationReceptors, ProgesteroneReceptors, Progesterone

Identifiers

PMID21945472
PMCPMC3265648
OpenAlexW1989007353

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.