Evidence map›Paper›PMID 24469394›Full record

ArticleMolecular and cellular biology2014

Stat5 regulates the phosphatidylinositol 3-kinase/Akt1 pathway during mammary gland development and tumorigenesis.

Jeffrey W Schmidt, Barbara L Wehde, Kazuhito Sakamoto, Aleata A Triplett, Steven M Anderson, Philip N Tsichlis, Gustavo Leone, Kay-Uwe Wagner

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

38 citing papers in PubMed, 64 citations in OpenAlex.

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  15. Review
  16. Role of the JAK-STAT Pathway in Bovine Mastitis and Milk Production.Animals : an open access journal from MDPI · 2020
    Review
  17. Article
  18. Article
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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

8 authors at 4 institutions in 1 country.

Jeffrey W SchmidtEppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, Nebraska, USA.
Barbara L Wehde
Kazuhito Sakamoto
Aleata A Triplett
Steven M Anderson
Philip N Tsichlis
Gustavo Leone
Kay-Uwe Wagner
University of Nebraska Medical Center · USCancer Genetics (United States) · USTufts Medical Center · USUniversity of Colorado Denver · US

Funding

Suppression of Mammary Tumorigenesis by Stromal p53P01CA097189 · NCI · OHIO STATE UNIVERSITY · PI FERNANDEZ, SOLEDAD A · 2004 to 2016
$16.1M
The functional role of microRNAs in the normal mammary glandP01HD038129 · NICHD · UNIVERSITY OF COLORADO DENVER · PI ANDERSON, STEVEN M · 2000 to 2015
$15.2M
CHEMICAL CARCINOGENESIS &CANCER BIOLOGYT32CA009476 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI Jennifer D. Black · 1988 to 2026
$6.2M
Growth-Regulatory Signaling Networks in Breast CancerR01CA117930 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI WAGNER, KAY-UWE · 2006 to 2016
$2.5M
NCI NIH HHS BC100147NCI NIH HHS CA009476NCI NIH HHS CA117930NCI NIH HHS P01 CA097189NCI NIH HHS R01 CA117930NCI NIH HHS T32 CA009476NICHD NIH HHS HD38129NICHD NIH HHS P01 HD038129
6 · The paper itself

Abstract

Stat5 (signal transducer and activator of transcription 5) is an essential mediator of cytokine receptor signaling and plays important roles in the proliferation of alveolar progenitors and the survival of functionally differentiated epithelial cells in the mammary gland. A deregulated expression and activation of Stat5 leads to precocious alveolar development in the absence of pregnancy hormones, impaired mammary gland remodeling following the cessation of lactation, and mammary tumor formation. We reported previously that Stat5 induces the transcription of the Akt1 gene from a novel promoter. In this report, we provide experimental evidence that Akt1 is an essential mediator for the biological function of Stat5 as a survival factor. Additionally, Stat5 controls the expression of the regulatory and catalytic subunits of the phosphatidylinositol 3-kinase (PI3K) (p85α and p110α), thereby greatly augmenting signaling through the prosurvival PI3K/Akt pathway. In agreement with this model, we observed that the constitutive activation of Stat5 cooperates with the loss of function of the tumor suppressor PTEN by accelerating the formation of preneoplastic lesions and mammary tumors. The mammary gland-specific ablation of Stat5 is sufficient to prevent mammary carcinogenesis in a genuine mouse model for Cowden syndrome. Therefore, targeting the Jak2/Stat5 pathway might be a suitable strategy to prevent breast cancer in patients that carry a mutant PTEN allele.

Indexed as

AnimalsCell LineClass Ia Phosphatidylinositol 3-KinaseClass I Phosphatidylinositol 3-KinasesFemaleGene Knockout TechniquesHamartoma Syndrome, MultipleHumansJanus Kinase 2Mammary Glands, AnimalMammary Neoplasms, ExperimentalMiceMice, KnockoutMice, Mutant StrainsMice, TransgenicPhosphatidylinositol 3-Kinases1-phosphatidylinositol 3-kinase p110 subunit, mouseAkt1 protein, mouseClass Ia Phosphatidylinositol 3-KinaseClass I Phosphatidylinositol 3-KinasesJak2 protein, mouseJanus Kinase 2Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePten protein, mouseRNA, MessengerSTAT5 Transcription Factor

Identifiers

PMID24469394
PMCPMC3993568
OpenAlexW2034408892

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.