ArticleClinical cancer drugs2016
Transforming Mutations of Jak3 (A573V and M511I) Show Differential Sensitivity to Selective Jak3 Inhibitors.
Article in Clinical cancer drugs, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 19 citations in OpenAlex.
- Dual STAT3/STAT5 inhibition as a novel treatment strategy in T-prolymphocytic leukemia.Leukemia · 2025Article
- Spotlight on amino acid changing mutations in the JAK-STAT pathway: from disease-specific mutation to general mutation databases.Scientific reports · 2025Article
- Analysis of mutation profiles in extranodal NK/T-cell lymphoma: clinical and prognostic correlations.Annals of hematology · 2024Article
- Structural Analysis of Janus Tyrosine Kinase Variants in Hematological Malignancies: Implications for Drug Development and Opportunities for Novel Therapeutic Strategies.International journal of molecular sciences · 2023Article
- JAK3 Y841 Autophosphorylation Is Critical for STAT5B Activation, Kinase Domain Stability and Dimer Formation.International journal of molecular sciences · 2023Article
- JAK1 Pseudokinase V666G Mutant Dominantly Impairs JAK3 Phosphorylation and IL-2 Signaling.International journal of molecular sciences · 2023Article
- Article
- Untwining Anti-Tumor and Immunosuppressive Effects of JAK Inhibitors-A Strategy for Hematological Malignancies?Cancers · 2021Review
- Deregulation of the Interleukin-7 Signaling Pathway in Lymphoid Malignancies.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Identification of U937Frontiers in oncology · 2021Article
- Failure of tofacitinib to achieve an objective response in aCold Spring Harbor molecular case studies · 2020Article
- Article
- Are peptides a solution for the treatment of hyperactivated JAK3 pathways?Inflammopharmacology · 2019Review
- Oncogenic activation of the STAT3 pathway drives PD-L1 expression in natural killer/T-cell lymphoma.Blood · 2018Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundA medical need exists for successfully treating patients afflicted with leukemia and especially those that relapse and ultimately become refractory to front line chemotherapies. Leukemia cases are particularly high within Hispanic populations where this disease is among the most frequently occurring cancer. A possible cause is somatic mutations in Janus tyrosine kinase (Jak3). Fourteen somatic mutations have been reported in Jak3, including M511I and A573V, from patients with various forms of leukemia. While several of these Jak3 mutations have been shown to possess transforming ability in cell lines, whether these mutations are susceptible to Jak3 selective inhibitors remains less clear.
methodsThe IL-3 dependent pro-B cell line Ba/F3 was virally transduced with plasmids encoding GFP and different mutant forms of Jak3, some of which conferred IL-3 independence. Sensitivity to pre-clinical and clinical Jak3 selective inhibitors was assessed for cellular viability and growth.
resultsTwo Jak3 mutations conferred IL-3 independent growth in Ba/F3 cells. However, the level of drug sensitivity varied with respect to Jak3 inhibitors NC1153, CP-690,550, and EP-009.
conclusionJak3 inhibitors CP-690,550 and NC1153 showed efficacy in reducing viability of Ba/F3 cells transformed with mutant forms of Jak3, thus providing new therapeutic strategies to treat these types of cancer.
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