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Exacerbated T cell lymphoma in NOD.Stat5bTg mice is caused by selective activation of Stat5b in CD8+ thymocytes and can be prevented by inhibition of the Stat5b signaling pathway with chemoprevention agents

ABSTRACT: This study demonstrated that genetic background is critical to the STAT5B-mediated lymphomagenesis probably through regulation of STAT5B activation, which results in the alteration of many tumorigenic genes. Chemopreventive compounds that can reduce STAT5B phosphorylation and/or the STAT5B signaling pathway can efficiently block lymphomagenesis, demonstrating that the NOD.Stat5bTg mouse is an excellent model for testing novel chemopreventive strategies.

ORGANISM(S): Mus musculus

PROVIDER: GSE31526 | GEO | 2012/04/10

SECONDARY ACCESSION(S): PRJNA145519

REPOSITORIES: GEO

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Exacerbated T cell lymphoma in NOD.Stat5bTg mice is caused by selective activation of Stat5b in CD8+ thymocytes and can be prevented by inhibition of the Stat5b signaling pathway with chemoprevention agents

Project description:This study demonstrated that genetic background is critical to the STAT5B-mediated lymphomagenesis probably through regulation of STAT5B activation, which results in the alteration of many tumorigenic genes. Chemopreventive compounds that can reduce STAT5B phosphorylation and/or the STAT5B signaling pathway can efficiently block lymphomagenesis, demonstrating that the NOD.Stat5bTg mouse is an excellent model for testing novel chemopreventive strategies. To elucidate the molecular mechanism underlying the activation of Stat5b upon lymphoma onset, we profiled gene expression in thymocytes of NOD.Stat5b mice, Gene expression was analyzed with the Illumina's MouseRef-8 v2.0 Expression beadchips

2012-04-09 | E-GEOD-31526 | biostudies-arrayexpress

Genetic STAT5B immunodysregulatory disorder

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Sex-dependent and STAT5b-dependent Liver Gene Expression

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Microarray mRNA expression profiling in Stat5b knockdown pancreatic beta cell line

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2022-12-31 | GSE85496 | GEO

Enhanced T cell lymphoma in NOD.Stat5b transgenic mice is caused by hyperactivation of Stat5b in CD8+ thymocytes.

Project description:Activation of signal transducers and activators of transcription (STAT) proteins may be critical to their oncogenic functions as demonstrated by the development of B-cell lymphoma/leukemia in transgenic (TG) mice overexpressing a constitutively activated form of Stat5b. However, low incidence of CD8(+) T cell lymphoma was observed in B6 transgenic mice overexpressing a wild-type Stat5b (B6.Stat5b(Tg)) despite of undetectable Stat5b phosphorylation and the rate of lymphomagenesis was markedly enhanced by immunization or the introduction of TCR transgenes [1]. Here, we report that the wild-type Stat5b transgene leads to the acceleration and high incidence (74%) of CD8(+) T cell lymphoblastic lymphomas in the non-obese-diabetic (NOD) background. In contrast to the B6.Stat5b(Tg) mice, Stat5b in transgenic NOD (NOD.Stat5b(Tg)) mice is selectively and progressively phosphorylated in CD8(+) thymocytes. Stat5 phosphorylation also leads to up-regulation of many genes putatively relevant to tumorigenesis. Treatment of NOD.Stat5b(Tg) mice with cancer chemopreventive agents Apigenin and Xanthohumol efficiently blocked lymphomagenesis through reduction of Stat5 phosphorylation and genes up-regulated in the NOD.Stat5b(Tg) mice. These results suggest that NOD genetic background is critical to the Stat5b-mediated lymphomagenesis through regulation of Stat5 hyperactivation. NOD.Stat5b(Tg) mouse is an excellent model for studying the molecular mechanisms underlying lymphomagenesis and testing novel chemoprevention strategies.

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Prolactin-inducible Stat5a-mediated and Stat5b-mediated gene profiles

Project description:Stat5a and Stat5b proteins are highly homologous with greater than 90% amino acid identity and share binding to the palindromic Stat5 consensus sequence, TTCNNNGAA, but individual roles of each transcription factor in breast cancer have not been thoroughly evaluated. To determine the degree of similarity between transcripts modulated by Stat5a and Stat5b proteins in human breast cancer, we utilized genome-wide transcript profiling to identify genes regulated specifically by Stat5a or Stat5b in response to prolactin. Stat5a or Stat5b was transiently overexpressed using adenoviral gene delivery in MCF7 breast cancer cells followed 16 hr serum starvation and a brief 4 hr exposure to 10nM human prolactin to identify immediate-early transcripts modulated by each transcription factor. Basal activation of Stat5a or Stat5b was not present in cells not stimulated with prolactin. mRNA from each condition was harvested and validated using the Agilent bioanalyzer. cDNA was generated and genome-wide transcript profiling was performed in triplicate using the Affymetrix HuGene 1.0 ST array.

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Prolactin-inducible Stat5a-mediated and Stat5b-mediated gene profiles

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Mouse colon expression in wild type and STAT5b deficient mice

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2010-05-25 | E-GEOD-8942 | biostudies-arrayexpress

Sex-dependent and STAT5b-dependent Liver Gene Expression

Project description:A series of dual-channel gene expression profiles obtained using Rosetta/Merck Mouse TOE 75k microarrays was used to examine the sex-dependent and STAT5b-dependent differences in gene expression in adult mouse liver. This series is comprised of 4 pools of 3 randomly chosen independent wildtype male and female mouse liver cDNA samples and 4 pools of 3 randomly chosen independent STAT5b-deficient male and female mouse liver cDNA samples, totaling 16 pools. The pools were paired randomly to generate 4 comparisons of M-WT:F-WT, M-WT:M-KO, F-KO:F-WT, and F-KO:M-KO. Comparison of the set of sex-dependent genes with the set of genes responsive to the loss of STAT5b in males shows that 75% of the sex-specific genes were also regulated by STAT5b in males. Only 20% of the sex-specific genes retained sex-specificity in the absence of STAT5b, indicating a large role for STAT5b in sex-specific liver gene expression. A pool of cDNA from 3 mice is Cy3-labeled and compared to another pool of cDNA from 3 mice that is Cy5-labeled. The pools are then dye-swapped and compared again. The two pairs of data are averaged together, the averages are normalized across the fluorescent reverse pairings, and the log2 value is reported for each average as well as the anti-log. This is replicated 3 times with independent pools of cDNA for each pair of conditions being compared. There are a total of 4 pairs of conditions compared for a grand total of 12 samples.

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