ArticleOncotarget2017
The effect of the JAK2 inhibitor TG101209 against T cell acute lymphoblastic leukemia (T-ALL) is mediated by inhibition of JAK-STAT signaling and activation of the crosstalk between apoptosis and autophagy signaling.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 29 citations in OpenAlex.
- Ruxolitinib reverses alopecia areata via a triple mechanism: JAK-STAT inhibition, localized oxidative stress attenuation and selective apoptosis modulation.Journal of translational autoimmunity · 2026Article
- Crosstalk Between Autophagy and Oxidative Stress in Hematological Malignancies: Mechanisms, Implications, and Therapeutic Potential.Antioxidants (Basel, Switzerland) · 2025Review
- Integrated UPLC-ESI-MS/MS, network pharmacology, and transcriptomics to reveal the material basis and mechanism of Schisandra chinensis Fruit Mixture against diabetic nephropathy.Frontiers in immunology · 2024Article
- Acute T-cell lymphoblastic leukemia: chimeric antigen receptor technology may offer a new hope.Frontiers in immunology · 2024Review
- BP‑1‑102 exerts antitumor effects on T‑cell acute lymphoblastic leukemia cells by suppressing the JAK2/STAT3/c‑Myc signaling pathway.Experimental and therapeutic medicine · 2023Article
- JAK/STAT pathway: Extracellular signals, diseases, immunity, and therapeutic regimens.Frontiers in bioengineering and biotechnology · 2023Review
- Review
- Second-Generation Jak2 Inhibitors for Advanced Prostate Cancer: Are We Ready for Clinical Development?Cancers · 2021Review
- The JAK2 inhibitor TG101209 exhibits anti-tumor and chemotherapeutic sensitizing effects on Burkitt lymphoma cells by inhibiting the JAK2/STAT3/c-MYB signaling axis.Cell death discovery · 2021Article
- Therapeutic afucosylated monoclonal antibody and bispecific T-cell engagers for T-cell acute lymphoblastic leukemia.Journal for immunotherapy of cancer · 2021Article
- FV-429 induces autophagy blockage and lysosome-dependent cell death of T-cell malignancies via lysosomal dysregulation.Cell death & disease · 2021Article
- MiR-126 promotes esophageal squamous cell carcinoma via inhibition of apoptosis and autophagy.Aging · 2020Observational
- Pharmacological Inhibition of Oncogenic STAT3 and STAT5 Signaling in Hematopoietic Cancers.Cancers · 2020Review
- NVP-BSK805, an Inhibitor of JAK2 Kinase, Significantly Enhances the Radiosensitivity of Esophageal Squamous Cell Carcinoma in vitro and in vivo.Drug design, development and therapy · 2020Article
- Targeting the JAK/STAT Pathway in T Cell Lymphoproliferative Disorders.Current hematologic malignancy reports · 2019Review
- Role of Autophagy and Apoptosis in Acute Lymphoblastic Leukemia.Cancer control : journal of the Moffitt Cancer CenterReview
- The Crosstalk Between Long Non-Coding RNAs and Various Types of Death in Cancer Cells.Technology in cancer research & treatmentReview
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous reports have shown that active JAK2 contributes to T cell acute lymphoblastic leukaemia (T-ALL) development and that JAK inhibitors may be a potential treatment for T-ALL. In the current study, the JAK2 inhibitor TG101209 was used to treat T-ALL cell lines and primary T-ALL cells. The effects of TG101209 on T-ALL cells were determined, and the signaling proteins related to cell growth, apoptosis and autophagy were analysed. The results indicated that TG101209 significantly inhibited T-ALL cell proliferation and induced cell apoptosis in a dose-dependent manner. The mechanisms involved the suppression of the JAK2-STAT signaling pathway and activation of apoptosis or autophagy. Additionally, a JAK2 gene copy gain (FISH) and up-regulated JAK2, LC3 and Beclin1 expression (western blotting) were observed in T-ALL samples compared with healthy controls, which implied that JAK2 is a target for T-ALL treatment. TG101209 initiated apoptosis and autophagy in T-ALL cells; therefore, this JAK2 inhibitor may be a potential drug or alternative therapy for T-ALL.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.