Epigenetic regulation of signal transducer and activator of transcription 3 in acute myeloid leukemia

Ghoshal, Sampa; Baumann, Heinz; Wetzler, Meir

doi:10.1016/j.leukres.2007.11.035

Cited by 23 publications

(10 citation statements)

References 88 publications

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“…Also, the 5′ flanking site of SOCS‐1 contains Sp‐1 binding sites, but the presence of IFN‐stimulated responsive element and IFNγ‐activated site promoter elements determines IFNγ‐induced SOCS1 expression. In this context, it is interesting to note that both SOCS proteins can be differentially regulated by transcription factors and epigenetic changes at the transcription level (23–25).…”

Section: Discussionmentioning

confidence: 99%

Enhanced suppressor of cytokine signaling 3 in arthritic cartilage dysregulates human chondrocyte function

Loo¹,

Veenbergen²,

Brand³

et al. 2012

Arthritis & Rheumatism

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Objective. To determine the expression of suppressor of cytokine signaling 3 (SOCS-3) in human articular chondrocytes and its functional consequences.Methods. Chondrocytes were isolated from the cartilage of patients with osteoarthritis (OA), patients with rheumatoid arthritis (RA), and trauma patients and from the healthy cartilage of patients with a femoral neck fracture. The human chondrocyte cell line G6 and primary bovine chondrocytes were used in validation experiments. SOCS-3 messenger RNA (mRNA) expression was measured by quantitative polymerase chain reaction, and SOCS-3 protein levels were determined by Western blotting and immunohistochemical analysis. Conclusion. This study demonstrated that both SOCS-3 mRNA and SOCS-3 protein are expressed in human arthritic chondrocytes and affect cellular responses involved in cartilage pathology.

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Section: Discussionmentioning

confidence: 99%

Enhanced suppressor of cytokine signaling 3 in arthritic cartilage dysregulates human chondrocyte function

Loo¹,

Veenbergen²,

Brand³

et al. 2012

Arthritis & Rheumatism

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“… 7 Studies of solid and hematological malignancies have also highlighted the role of signal transducer and activator of transcription 3 (STAT3) in the stimulation of cellular proliferation and survival. 11 , 12 , 13 Enhanced tyrosine phosphorylation of STAT3 whether due to increased secretion of cytokines, such as IL-6(ref. 14 ) or mutations in receptor tyrosine kinases (for example, FLT3 duplications 15 or less frequently JAK2) 16 is seen in up to 50% of AML cases and signifies a worse prognosis.…”

Section: Pathophysiologymentioning

confidence: 99%

‘Acute myeloid leukemia: a comprehensive review and 2016 update’

Kouchkovsky

Abdul-Hay

2016

Blood Cancer Journal

1,029

884

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Acute myeloid leukemia (AML) is the most common acute leukemia in adults, with an incidence of over 20 000 cases per year in the United States alone. Large chromosomal translocations as well as mutations in the genes involved in hematopoietic proliferation and differentiation result in the accumulation of poorly differentiated myeloid cells. AML is a highly heterogeneous disease; although cases can be stratified into favorable, intermediate and adverse-risk groups based on their cytogenetic profile, prognosis within these categories varies widely. The identification of recurrent genetic mutations, such as FLT3-ITD, NMP1 and CEBPA, has helped refine individual prognosis and guide management. Despite advances in supportive care, the backbone of therapy remains a combination of cytarabine- and anthracycline-based regimens with allogeneic stem cell transplantation for eligible candidates. Elderly patients are often unable to tolerate such regimens, and carry a particularly poor prognosis. Here, we review the major recent advances in the treatment of AML.

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“…Increased activity of STAT3 has been reported in 20-50% of AML patients while STAT5 and STAT1 activation is uncommon [49,50]. The pathologic value of activated STAT3 in AML is unclear.…”

Section: Myeloid Leukemiamentioning

confidence: 99%

Dysregulation of JAK-STAT pathway in hematological malignancies and JAK inhibitors for clinical application

Furqan

Mukhi

Lee³

et al. 2013

Biomark Res

154

123

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JAK-STAT (Janus associated kinase-signal transducer and activator of transcription) pathway plays a critical role in transduction of extracellular signals from cytokines and growth factors involved in hematopoiesis, immune regulation, fertility, lactation, growth and embryogenesis. JAK family contains four cytoplasmic tyrosine kinases, JAK1-3 and Tyk2. Seven STAT proteins have been identified in human cells, STAT1-6, including STAT5a and STAT5b. Negative regulators of JAK–STAT pathways include tyrosine phosphatases (SHP1 and 2, CD45), protein inhibitors of activated STATs (PIAS), suppressors of cytokine signaling (SOCS) proteins, and cytokine-inducible SH2-containing protein (CIS). Dysregulation of JAK-STAT pathway have been found to be key events in a variety of hematological malignancies. JAK inhibitors are among the first successful agents reaching clinical application. Ruxolitinib (Jakafi), a non-selective inhibitor of JAK1 & 2, has been approved by FDA for patients with intermediate to high risk primary or secondary myelofibrosis. This review will also summarize early data on selective JAK inhibitors, including SAR302503 (TG101348), lestaurtinib (CEP701), CYT387, SB1518 (pacritinib), LY2784544, XL019, BMS-911543, NS-018, and AZD1480.

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Epigenetic regulation of signal transducer and activator of transcription 3 in acute myeloid leukemia

Cited by 23 publications

References 88 publications

Enhanced suppressor of cytokine signaling 3 in arthritic cartilage dysregulates human chondrocyte function

Enhanced suppressor of cytokine signaling 3 in arthritic cartilage dysregulates human chondrocyte function

‘Acute myeloid leukemia: a comprehensive review and 2016 update’

Dysregulation of JAK-STAT pathway in hematological malignancies and JAK inhibitors for clinical application

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