ArticleNPJ precision oncology2024
PIM1 is a potential therapeutic target for the leukemogenic effects mediated by JAK/STAT pathway mutations in T-ALL/LBL.
Article in NPJ precision oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- PIM1 in myeloproliferative neoplasms: potential pathogenic and therapeutic implications.Leukemia · 2026Review
- BRD4 regulation of PIM1 identifies a novel therapeutic vulnerability in acute megakaryoblastic leukemia.Cancer cell international · 2026Article
- Combination of artesunate and ruxolitinib suppresses T cell leukemia/lymphoma proliferation via the JAK STAT pathway.Scientific reports · 2026Article
- Pharmacological Blockade of NMUR2 Suppresses Glioma Growth by Inhibiting STAT5-Mediated Transcription of Cell Cycle-associated Genes.International journal of biological sciences · 2026Article
- KPT-330, A New Candidate Drug for Targeting NOTCH1 Overexpression in T-cell Acute Lymphoblastic Leukemia, An In Vitro and Silico Study.Cell biochemistry and biophysics · 2025Article
- Successful treatment of multi-hit TP53-mutated myelodysplastic syndromes with erythroid predominance using allogeneic stem cell transplantation and ruxolitinib.Annals of hematology · 2025Article
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Authors and funding
9 authors.
Funding
Abstract
Precursor T-cell neoplasms (T-ALL/LBL) are aggressive hematological malignancies that arise from the malignant transformation of immature thymocytes. Despite the JAK/STAT pathway is recurrently altered in these neoplasms, there are not pharmacological inhibitors officially approved for the treatment of T-ALL/LBL patients that present oncogenic JAK/STAT pathway mutations. In the effort to identify potential therapeutic targets for those patients, we followed an alternative approach and focused on their transcriptional profile. We combined the analysis of molecular data from T-ALL/LBL patients with the generation of hematopoietic cellular models to reveal that JAK/STAT pathway mutations are associated with an aberrant transcriptional profile. Specifically, we demonstrate that JAK/STAT pathway mutations induce the overexpression of the PIM1 gene. Moreover, we show that the pan-PIM inhibitor, PIM447, significantly reduces the leukemogenesis, as well as the aberrant activation of c-MYC and mTOR pathways in cells expressing different JAK/STAT pathway mutations, becoming a potential therapeutic opportunity for a relevant subset of T-ALL/LBL patients.
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Registered trials
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 Socratic graph.