Myelofibrosis, a Philadelphia-negative myeloproliferative neoplasm, is in a new treatment era after the discovery of the JAK2V617F mutation in 2005. JAK inhibitors boast improvements in disease-related symptoms, splenomegaly, and overall survival; however, treatment of myelofibrosis remains a challenge, given the lack of improvement in cytopenias with these agents. Second-generation immunomodulatory agents, such as pomalidomide, have shown efficacy in myelofibrosis-associated anemia within multiple clinical trials. Five major pomalido-mide clinical trials have been completed to date, and demonstrate tolerability and efficacy with low-dose pomalidomide (0.5 mg/day) in the treatment of myelofibrosis, and no clinical benefit of elevated dosing regimens (≥2.5 mg/day). Anemia responses ranged from 17% to 36% as per the International Working Group for Myelofibrosis Research and Treatment consensus guidelines, while improvements in splenomegaly were rare, and observed in <1% of most clinical trials. In comparison with earlier immunomodulatory agents, pomalidomide was associated with an improved toxicity profile, with substantially lower rates of myelosuppression and neuropathy. Given the low overall response rate to pomalidomide as a single agent, combination strategies are of particular interest for future studies. Pomalidomide is currently being tested in combination with ruxolitinib, and other novel combinations are likely on the horizon.
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http://dx.doi.org/10.2147/TCRM.S69211 | DOI Listing |
Oncol Ther
January 2025
Hematology, Department of Translational and Precision Medicine, Policlinico Umberto I-Sapienza University, Via Benevento 6, 00161, Rome, Italy.
Introduction: Myelofibrosis (MF) is often characterized by a multifactorial anemia determined, in part, by bone marrow (BM) fibrosis, extramedullary erythropoiesis and splenomegaly. Ruxolitinib (RUX) is the first-in-class janus kinase 2 (JAK2) inhibitor approved for treatment of MF, proved to reduce spleen volume and decrease symptom burden. The red cell distribution width (RDW) is the measure of erythrocyte volume variability (anisocytosis).
View Article and Find Full Text PDFBlood Adv
January 2025
Univ Angers, Nantes Université, CHU Angers, Inserm, CNRS, CRCI2NA, F-49000, Angers, France, ANGERS, France.
Patients with essential thrombocythemia (ET) have a chronic evolution with a risk of hematological transformation associated with a dismal outcome. Since patients with resistance or intolerance have an adverse prognosis, it is important to identify which patient will respond to first-line treatment. We therefore aim to describe the association between additional mutations and response to first-line treatment in patients with ET.
View Article and Find Full Text PDFIntern Med
January 2025
Department of Internal Medicine 1, Shimane University Faculty of Medicine, Japan.
We herein report a 56-year-old man with severe hypocalcemia during ruxolitinib therapy for myelofibrosis transitioning from JAK2 mutation-positive polycythemia vera. Blood transfusions were administered every one to two weeks for ruxolitinib-induced anemia. Blood tests revealed hypocalcemia with low TRACP-5b, 25-hydroxyvitamin D (25 (OH) D), and 1,25-dihydroxyvitamin D (1,25 (OH) D) levels within the lower reference range.
View Article and Find Full Text PDFJ Transl Med
January 2025
Department of Biomedical and Biotechnological Sciences, Division of Medical Biochemistry, University of Catania, Catania, Italy.
Background: Clonal myeloproliferation and fibrotic transformation of the bone marrow (BM) are the pathogenetic events most commonly occurring in myelofibrosis (MF). There is great evidence indicating that tumor microenvironment is characterized by high lactate levels, acting not only as an energetic source, but also as a signaling molecule.
Methods: To test the involvement of lactate in MF milieu transformation, we measured its levels in MF patients' sera, eventually finding a massive accumulation of this metabolite, which we showed to promote the expansion of immunosuppressive subsets.
Blood Cancer J
January 2025
School of Medicine, Faculty of Medicine and Health Sciences, Tel Aviv University, Tel Aviv, Israel.
Fedratinib is a predominantly JAK2 inhibitor that has shown efficacy in untreated and ruxolitinib-exposed patients with myelofibrosis (MF). Based on randomized clinical trial data, it is approved for use in patients with International Prognostic Scoring System (IPSS) or Dynamic International Prognostic Scoring System (DIPSS) intermediate-2 or high-risk disease and is distinguished from ruxolitinib in that it can be administered without dose reduction in patients with thrombocytopenia, to a platelet count above 50,000/µL. In these trials, fedratinib achieved significant spleen volume reduction in ~30-45% of patients and improvement in total symptom scores in 35-40% with good tolerability.
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