Role of STAT3 Locus in autoimmune diseases

Jabalameli, M. Reza

doi:10.1038/gene.2010.55

Cited by 2 publications

(1 citation statement)

References 5 publications

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“…For example, Guillem et al (2012) showed that SNPs in SOCS1 (rs243327) and PTPN22 (rs2476601) genes correlated with the risk of primary resistance to IM were adverse prognostic factors for failure-free survival in CML patients. Polymorphism in the STAT3 gene has already been shown to co-relate with higher proclivity in patients for asthma, inflammation, and autoimmune diseases, so it is attractive to speculate that SNPs affecting the expression levels of STAT3 protein may also predict the treatment outcome when utilizing immune therapy like IFN-α in CML (Litonjua et al, 2005; Ferguson et al, 2010; Jabalameli, 2011). For example, IFN-α therapy is very effective in inducing hematological remission and a sustained cytogenetic response in CML (Talpaz et al, 1986, 1991).…”

Section: Regulation Of the Stat3 Activation Pathwaymentioning

confidence: 99%

Role of STAT3 in Transformation and Drug Resistance in CML

Nair¹,

Tolentino²,

Hazlehurst³

2012

Front. Oncol.

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Chronic myeloid leukemia (CML) is initially driven by the bcr–abl fusion oncoprotein. The identification of bcr–abl led to the discovery and rapid translation into the clinic of bcr–abl kinase inhibitors. Although, bcr–abl inhibitors are efficacious, experimental evidence indicates that targeting bcr–abl is not sufficient for elimination of minimal residual disease found within the bone marrow (BM). Experimental evidence indicates that the failure to eliminate the leukemic stem cell contributes to persistent minimal residual disease. Thus curative strategies will likely need to focus on strategies where bcr–abl inhibitors are given in combination with agents that specifically target the leukemic stem cell or the leukemic stem cell niche. One potential target to be exploited is the Janus kinase (JAK)/signal transducers and activators of transcription 3 (STAT3) pathway. Recently using STAT3 conditional knock-out mice it was shown that STAT3 is critical for initiating the disease. Interestingly, in the absence of treatment, STAT3 was not shown to be required for maintenance of the disease, suggesting that STAT3 is required only in the tumor initiating stem cell population (Hoelbl et al., 2010). In the context of the BM microenvironment, STAT3 is activated in a bcr–abl independent manner by the cytokine milieu. Activation of JAK/STAT3 was shown to contribute to cell survival even in the event of complete inhibition of bcr–abl activity within the BM compartment. Taken together, these studies suggest that JAK/STAT3 is an attractive therapeutic target for developing strategies for targeting the JAK–STAT3 pathway in combination with bcr–abl kinase inhibitors and may represent a viable strategy for eliminating or reducing minimal residual disease located in the BM in CML.

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Section: Regulation Of the Stat3 Activation Pathwaymentioning

confidence: 99%

Role of STAT3 in Transformation and Drug Resistance in CML

Nair¹,

Tolentino²,

Hazlehurst³

2012

Front. Oncol.

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Genetic update on inflammatory factors in ulcerative colitis: Review of the current literature

Patrícia

Kövesdi

Magyari

et al. 2014

WJGP

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Ulcerative colitis (UC) is one of the main types of inflammatory bowel disease, which is caused by dysregulated immune responses in genetically predisposed individuals. Several genetic factors, including interleukin and interleukin receptor gene polymorphisms and other inflammation-related genes play central role in mediating and modulating the inflammation in the human body, thereby these can be the main cause of development of the disease. It is clear these data are very important for understanding the base of the disease, especially in terms of clinical utility and validity, but summarized literature is exiguous for challenge health specialist that can used in the clinical practice nowadays. This review summarizes the current literature on inflammation-related genetic polymorphisms which are associated with UC. We performed an electronic search of Pubmed Database among publications of the last 10 years, using the following medical subject heading terms: UC, ulcerative colitis, inflammation, genes, polymorphisms, and susceptibility.

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Role of STAT3 Locus in autoimmune diseases

Cited by 2 publications

References 5 publications

Role of STAT3 in Transformation and Drug Resistance in CML

Role of STAT3 in Transformation and Drug Resistance in CML

Genetic update on inflammatory factors in ulcerative colitis: Review of the current literature

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