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4D-DIA-based proteomics analysis reveals the protective effects of Pidanjiangtang granules in IGT rat model.
J Ethnopharmacol
February 2025
Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing, China. Electronic address:
Article Synopsis
- The Pidanjiangtang (PDJT) formula, based on traditional theories, is used clinically to treat impaired glucose tolerance (IGT) but lacks clarity on its bioactive ingredients and mechanisms.
- A study was conducted using IGT rats to assess PDJT's therapeutic effects and mechanisms through various tests and proteomic analysis after treatment with different doses.
- Results showed that PDJT improves glucose metabolism, restores islet function, and influences key proteins and pathways, particularly the JAK2/STAT1 pathway, suggesting its effectiveness in managing IGT.
JAK2V617F-dependent down regulation of SHP-1 expression participates in the selection of myeloproliferative neoplasm cells in the presence of TGF-β.
J Cell Mol Med
October 2024
Inserm UMRS_1131, Institut de Recherche Saint-Louis, Université de Paris, Paris, France.
Myeloproliferative neoplasms (MPNs) are characterized by an increased production of blood cells due to the acquisition of mutations such as JAK2. TGF-β, whose secretion is increased in MPN patients, is known to negatively regulate haematopoietic stem cell (HSC) proliferation. Using an isogenic JAK2 or JAK2 wild-type UT-7 cell line we observed that JAK2 cells resist to TGF-β antiproliferative activity.
View Article and Find Full Text PDFTransformation into acute myeloid leukemia with t(8;21)(q22;q22.1); RUNX1::RUNX1T1 from JAK2-mutated essential thrombocythemia: a case report.
J Med Case Rep
August 2024
Department of Hematology, Saitama Medical University Hospital, 38 Morohongo, Iruma-gun, Moroyama, Saitama, 350-0495, Japan.
Article Synopsis
- A 74-year-old woman in Japan had a blood disorder called essential thrombocythemia (ET), which made her blood platelets too high.
- After two years, she developed a more serious condition called secondary acute myeloid leukemia (AML) with specific chromosome changes (t(8;21)).
- She received treatment with special medicines and after the first round, her harmful blood cells started to disappear.
Molecular biomarkers of leukemia: convergence-based drug resistance mechanisms in chronic myeloid leukemia and myeloproliferative neoplasms.
Front Pharmacol
July 2024
Department of Hematology and Oncology, University Medical Center Schleswig-Holstein, Lübeck, Germany.
Leukemia represents a diverse group of hematopoietic neoplasms that can be classified into different subtypes based on the molecular aberration in the affected cell population. Identification of these molecular classification is required to identify specific targeted therapeutic approaches for each leukemic subtype. In general, targeted therapy approaches achieve good responses in some leukemia subgroups, however, resistance against these targeted therapies is common.
View Article and Find Full Text PDFConsistency of Spleen and Symptom Reduction Regardless of Cytopenia in Patients With Myelofibrosis Treated With Pacritinib.
Clin Lymphoma Myeloma Leuk
November 2024
Transplantation Program, Fred Hutchinson Cancer Research Center, Seattle, WA.
Background: Pacritinib is a JAK2/IRAK1/ACVR1 inhibitor that is approved in the United States for the treatment of patients with myelofibrosis who have a platelet count < 50 × 109/L. Phase 3 clinical studies of pacritinib included patients across a wide range of baseline platelet and hemoglobin levels.
Patients And Methods: In order to assess the impact of baseline blood counts on pacritinib efficacy, an analysis of efficacy outcomes by baseline platelet and hemoglobin levels was performed using data pooled from 2 Phase 3 studies of pacritinib in patients with MF (PERSIST-1 and PERSIST-2).
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