Activation of signal transducer and activator of transcription 5 is required for progression of autochthonous prostate cancer: evidence from the transgenic adenocarcinoma of the mouse prostate system.

No abstract is available for this paper.

• Publication year

  2003

• Venue

  Cancer Research

• Publication date

  2003-12-15

• Fields of study

  Biology, Medicine

• Identifiers
  PMID 14695191
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• Inhibition of Transcription Factor Stat5 Induces Cell Death of Human Prostate Cancer Cells*

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• Molecular characterization of prostate hyperplasia in prolactin‐transgenic mice by using cDNA representational difference analysis *

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• STAT3 exerts two-way regulation in the biological effects of IL-6 in M1 leukemia cells.

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• Constitutive activation of JAK–STAT3 signaling by BRCA1 in human prostate cancer cells

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• Divergent roles of STAT1 and STAT5 in malignancy as revealed by gene disruptions in mice

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• Differential Effects of Prolactin andsrc/abl Kinases on the Nuclear Translocation of STAT5B and STAT5A*

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• Activation of STAT3 by the c-Fes Protein-tyrosine Kinase*

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• Transgenic mice overexpressing the prolactin gene develop dramatic enlargement of the prostate gland.

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• Redesigning an FKBP-ligand interface to generate chemical dimerizers with novel specificity.

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• Stat3 Activation by Src Induces Specific Gene Regulation and Is Required for Cell Transformation

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• Development of a bicistronic vector driven by the human polypeptide chain elongation factor 1alpha promoter for creation of stable mammalian cell lines that express very high levels of recombinant proteins.

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• Lyn physically associates with the erythropoietin receptor and may play a role in activation of the Stat5 pathway.

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• Constitutive activation of Stat3 in fibroblasts transformed by diverse oncoproteins and in breast carcinoma cells.

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  1995cited by this paper
• Regulation of mammary gland factor/Stat5a during mammary gland development.

  1995influential reference
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  1995cited by this paper
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  1993cited by this paper
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  1989cited by this paper

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• Asymmetrically Substituted m‐Terphenyl Phosphates Inhibit the Transcription Factor STAT5a

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• Prospects for Clinical Development of Stat5 Inhibitor IST5-002: High Transcriptomic Specificity in Prostate Cancer and Low Toxicity In Vivo

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