Inactivated STAT5 pathway underlies a novel inhibitory role of EBF1 in chronic lymphocytic leukemia

Wang, Chong; Li, Mengya; Shen, Xiaohui; Liu, Yanfang; Wang, Shujuan

doi:10.1016/j.yexcr.2020.112371

Cited by 2 publications

(1 citation statement)

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“…The same mutation has been commonly found in pediatric T-cell acute lymphoblastic leukemia (T-ALL) and is linked to a higher risk of relapse (Bandapalli et al, 2014). Recently, a key contributor to B-cell lymphopoiesis, Early B cell factor 1 (EBF1), has been shown to possess an inhibitory role in chronic lymphocytic leukemia (CLL) through inactivation of the STAT5 pathway (Wang et al, 2021).…”

Section: Jak-stat In Hematologic Malignanciesmentioning

confidence: 99%

JAK-STAT in Early Hematopoiesis and Leukemia

Fasouli

Katsantoni

2021

Front. Cell Dev. Biol.

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Hematopoietic stem cells (HSCs) produce all the terminally differentiated blood cells and are controlled by extracellular signals from the microenvironment, the bone marrow (BM) niche, as well as intrinsic cell signals. Intrinsic signals include the tightly controlled action of signaling pathways, as the Janus kinase-signal transducer and activator of transcription (JAK-STAT) pathway. Activation of JAK-STAT leads to phosphorylation of members of the STAT family to regulate proliferation, survival, and self-renewal of HSCs. Mutations in components of the JAK-STAT pathway are linked with defects in HSCs and hematologic malignancies. Accumulating mutations in HSCs and aging contribute to leukemia transformation. Here an overview of hematopoiesis, and the role of the JAK-STAT pathway in HSCs and in the promotion of leukemic transformation is presented. Therapeutic targeting of JAK-STAT and clinical implications of the existing research findings are also discussed.

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Section: Jak-stat In Hematologic Malignanciesmentioning

confidence: 99%