Please use this identifier to cite or link to this item: https://doi.org/10.3390/cancers13205147
Title: Janus Kinase Signaling: Oncogenic Criminal of Lymphoid Cancers
Authors: Li, Boheng
Wan, Qin
Li, Zhubo
Chng, Wee-Joo 
Keywords: Science & Technology
Life Sciences & Biomedicine
Oncology
<p>JAK/STAT</p>
lymphoma
myeloma
inhibitor
B-CELL LYMPHOMA
CLASSICAL HODGKIN LYMPHOMA
JAK-STAT PATHWAY
MULTIPLE-MYELOMA CELLS
IN-VITRO
KAPPA-B
ANTITUMOR-ACTIVITY
JAK/STAT PATHWAY
GENE-REGULATION
PHASE-I
Issue Date: 1-Oct-2021
Publisher: MDPI
Citation: Li, Boheng, Wan, Qin, Li, Zhubo, Chng, Wee-Joo (2021-10-01). Janus Kinase Signaling: Oncogenic Criminal of Lymphoid Cancers. CANCERS 13 (20). ScholarBank@NUS Repository. https://doi.org/10.3390/cancers13205147
Abstract: The Janus kinase (JAK) family are known to respond to extracellular cytokine stimuli and to phosphorylate and activate signal transducers and activators of transcription (STAT), thereby modulating gene expression profiles. Recent studies have highlighted JAK abnormality in inducing over-activation of the JAK/STAT pathway, and that the cytoplasmic JAK tyrosine kinases may also have a nuclear role. A couple of anti-JAK therapeutics have been developed, which effectively harness lymphoid cancer cells. Here we discuss mutations and fusions leading to JAK deregulations, how up-stream nodes drive JAK expression, how classical JAK/STAT pathways are represented in lymphoid malignancies and the noncanonical and nuclear role of JAKs. We also summarize JAK inhibition therapeutics applied alone or synergized with other drugs in treating lymphoid malignancies.
Source Title: CANCERS
URI: https://scholarbank.nus.edu.sg/handle/10635/228997
ISSN: 20726694
DOI: 10.3390/cancers13205147
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