ReviewJournal of mammary gland biology and neoplasia2006
The biological functions of the versatile transcription factors STAT3 and STAT5 and new strategies for their targeted inhibition.
Review in Journal of mammary gland biology and neoplasia, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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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.
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.
Who cites it
30 citing papers in PubMed, 91 citations in OpenAlex.
- The Roles of STAT3 and STAT5 in Breast Cancer.Cancers · 2025Review
- Mammalian Species-Specific Resistance to Mammary Cancer.Journal of mammary gland biology and neoplasia · 2025Review
- Photobiomodulation Improves the Inflammatory Response and Intracellular Signaling Proteins Linked to Vascular Function and Cell Survival in the Brain of Aged Rats.Molecular neurobiology · 2022Article
- Long non-coding RNAs as targets for immunosuppressive drug teriflunomide in anti-cancer potential for hepatocellular carcinoma.Journal of molecular histology · 2020Article
- Prognostic value of PD-L1 expression in patients with unresectable stage III non-small cell lung cancer treated with chemoradiotherapy.Radiation oncology (London, England) · 2020Article
- Insights into Molecular Classifications of Triple-Negative Breast Cancer: Improving Patient Selection for Treatment.Cancer discovery · 2019Review
- Oxymatrine Attenuates Tumor Growth and Deactivates STAT5 Signaling in a Lung Cancer Xenograft Model.Cancers · 2019Article
- Comparative analysis of TCDD-induced AhR-mediated gene expression in human, mouse and rat primary B cells.Toxicology and applied pharmacology · 2017Article
- Inhibition of STAT3 by Anticancer Drug Bendamustine.PloS one · 2017Article
- Review
- Article
- STAT3 genetic variant, alone and in combination with STAT5b polymorphism, contributes to breast cancer risk and clinical outcomes.Medical oncology (Northwood, London, England) · 2015Article
- Article
- JAK2-STAT5 signaling: A novel mechanism of resistance to targeted PI3K/mTOR inhibition.JAK-STAT · 2013Article
- Hypothermia enhances induction of protective protein metallothionein under ischemia.Journal of neuroinflammation · 2013Article
- Novel multiplexed assay for identifying SH2 domain antagonists of STAT family proteins.PloS one · 2013Article
- Signal transducer and activator of transcription 5 as a key signaling pathway in normal mammary gland developmental biology and breast cancer.Breast cancer research : BCR · 2011Review
- Phosphorylation of p27Kip1 by JAK2 directly links cytokine receptor signaling to cell cycle control.Oncogene · 2011Article
- Pharmacogenomics and cancer stem cells: a changing landscape?Trends in pharmacological sciences · 2011Review
- Singleminded-2s (Sim2s) promotes delayed involution of the mouse mammary gland through suppression of Stat3 and NFκB.Molecular endocrinology (Baltimore, Md.) · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Signal transducers and activators of transcription (STATs) comprise a unique family of transcription factors, which transmit the interactions of cytokines, hormones and growth factors with their cell surface receptors into transcriptional programs. The mechanism of STAT activation has been well-established and comprises tyrosine phosphorylation, dimerization, nuclear translocation, binding to specific DNA response elements, recruitment of co-activators or co-repressors and transcriptional induction or repression of target genes. Gene deletion, microarrays, proteomics and chromatin immunoprecipitation experiments have revealed target genes with a broad range of functions regulated by STAT3 and STAT5. In the mammary gland, STAT5-induced genes contribute mainly to the prolactin dependent lobulo-alveolar development, whereas STAT3 induced genes control apoptosis during involution. Crucial effects have also been observed in other tissues. The germ line deletion of STAT3 or STAT5 causes early embryonal or perinatal lethality in mice. STAT5 is also required for proliferation of T- and B-cells and hematopoietic stem cell self-renewal. Deregulated STAT activity is often found associated with tumorigenesis and activated STATs seem to be limiting components in tumor cells. This review summarizes the functions of STAT3 and STAT5 in different cell types and the strategies that are used to counteract their action in tumor cells.
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Registered trials
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.