Evidence map›Paper›PMID 32633727›Full record

ArticleAging2020

Essential role of STAT5a in DCIS formation and invasion following estrogen treatment.

Sundee Dees, Laura Pontiggia, Jean-Francois Jasmin, Federica Sotgia, Michael P Lisanti, Isabelle Mercier

Open access · greenAbstract read
In one paragraph

Article in Aging, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.2field-weighted citation impact, top 50% 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

4 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. 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

6 authors at 2 institutions in 2 countries.

Sundee DeesDepartment of Pharmaceutical Sciences, Philadelphia College of Pharmacy, University of the Sciences, Philadelphia, PA, USA.
Laura PontiggiaDepartment of Mathematics, Physics and Statistics, Misher College of Arts and Sciences, University of the Sciences, Philadelphia, PA, USA.
Jean-Francois JasminDepartment of Pharmaceutical Sciences, Philadelphia College of Pharmacy, University of the Sciences, Philadelphia, PA, USA.
Federica SotgiaTranslational Medicine, School of Science, Engineering and Environment (SEE), Biomedical Research Centre (BRC), University of Salford, Greater Manchester, United Kingdom.
Michael P LisantiTranslational Medicine, School of Science, Engineering and Environment (SEE), Biomedical Research Centre (BRC), University of Salford, Greater Manchester, United Kingdom.
Isabelle MercierDepartment of Pharmaceutical Sciences, Philadelphia College of Pharmacy, University of the Sciences, Philadelphia, PA, USA.
University of the Sciences · USUniversity of Salford · GB

Funding

CAV-1, Stat5a Signaling, and Estrogen-Dependent Breast CancerR01CA098779 · NCI · YESHIVA UNIVERSITY · PI FRANK, PHILIPPE G. · 2003 to 2012
$3.5M
NCI NIH HHS R01 CA098779
6 · The paper itself

Abstract

Ductal carcinoma in situ (DCIS) is one of the earliest stages of breast cancer (BCa). The mechanisms by which DCIS lesions progress to an invasive state while others remain indolent are yet to be fully characterized and both diagnosis and treatment of this pre-invasive disease could benefit from better understanding the pathways involved. While a decreased expression of Caveolin-1 (Cav-1) in the tumor microenvironment of patients with DCIS breast cancer was linked to progression to invasive breast cancer (IBC), the downstream effector(s) contributing to this process remain elusive. The current report shows elevated expression of Signal Transducer and Activator of Transcription 5a (STAT5a) within the DCIS-like lesions in Cav-1 KO mice following estrogen treatment and inhibition of STAT5a expression prevented the formation of these mammary lesions. In addition, STAT5a overexpression in a human DCIS cell line (MCF10DCIS.com) promoted their invasion, a process accelerated by estrogen treatment and associated with increased levels of the matrix metalloproteinase-9 (MMP-9) precursor. In sum, our results demonstrate a novel regulatory axis (Cav-1♦STAT5a♦MMP-9) in DCIS that is fully activated by the presence of estrogen. Our sudies suggest to further study phosphorylated STAT5a (Y694) as a potential biomarker to guide and predict outcome of DCIS patient population.

Indexed as

Breast NeoplasmsCarcinoma, Intraductal, NoninfiltratingEstrogensNeoplasm InvasivenessAnimalsBiomarkers, TumorCaveolin 1Cell Line, TumorDisease ProgressionFemaleGene Expression Regulation, NeoplasticHumansMatrix Metalloproteinase 9MicePhosphorylationSTAT5 Transcription FactorBiomarkers, TumorCaveolin 1EstrogensMatrix Metalloproteinase 9STAT5 Transcription FactorCav-1DCISestrogeninvasionSTAT5a

Identifiers

PMID32633727
PMCPMC7425506
OpenAlexW3041479608

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.