Myeloproliferative Neoplasm

Readily assessable clinical and laboratory parameters can refine risk prediction for thrombosis and survival outcomes in ET. Further research is warranted to validate findings and inform individualized management approaches.

Additionally, on mathematical models of the BCR::ABL1 transcripts after initiation of TFR, distinct patterns in the kinetics in sustained and relapsed patients was identified. Our findings support a modified, risk-adapted TFR monitoring strategy for low- and middle-income countries (LMICs) to enhance surveillance while optimizing resource utilization.

Overexpression of CD123 and CD86 in CBFB::MYH11 may have diagnostic and therapeutic relevance. The online version contains supplementary material available at 10.1007/s12288-025-02150-4.

Demographic characteristics were comparable across groups, though comorbidities were more frequent in MPNs. Laboratory analyses confirmed expected disease-specific differences, including elevated leukocyte, neutrophil, and platelet counts in MPNs and prolonged activated partial thromboplastin time in hemophilia A. Circulating citrullinated histone H3 (cit-H3) levels differed significantly among groups (p < 0.001), being lowest in controls, intermediate in MPNs, and highest in hemophilia A. Within disease groups, cit-H3 levels were unaffected by clinical variables such as MPN subtype, aspirin use, phlebotomy history, or factor replacement regimen.ConclusionsElevated circulating cit-H3 levels, suggestive of increased NETosis activity, were observed in both thrombosis-prone MPNs and bleeding-prone hemophilia A. These exploratory findings suggest a possible association between NET formation and thromboinflammatory processes across distinct hemostatic disorders.

The patient was treated with cytoreductive therapy, followed by imatinib, with a favorable clinical and hematologic response. This case highlights the potential for massive splenomegaly to mask CML and emphasizes the importance of early molecular testing. Splenectomy may unmask underlying hematologic malignancy through significant postoperative hematologic changes.

P3, N=340, Active, not recruiting, Merck Sharp & Dohme LLC | Recruiting --> Active, not recruiting

Maternal and neonatal outcomes were favorable. With careful multidisciplinary management, pregnancy in women with stable BCS is feasible.

P1/2, N=83, Active, not recruiting, Ryvu Therapeutics S.A. | Recruiting --> Active, not recruiting

In recent years, oral therapy with the JAK1/2 inhibitor ruxolitinib has become the standard of care. Since 2021, the JAK2/FLT3 inhibitor fedratinib has also been approved in the EU (note: in Switzerland, fedratinib will no longer be available as of February 28, 2025, as Swissmedic did not extend its time-limited approval)...Compared to the other two JAK inhibitors, momelotinib is particularly effective in patients with clinically symptomatic moderate to severe anemia. Results from studies investigating additional JAK inhibitors, combination therapies, and novel agents have also demonstrated significant efficacy and point toward future therapeutic developments, although these approaches are not yet available for routine clinical practice.

Moreover, N-acetylcysteine inhibited CCCP-induced reactive oxygen species production, prevented mitochondrial translocation of p210 BCR-ABL, and fully restored ERK-activation. These findings suggest that intercellular relocation of p210 BCR-ABL dynamically rewires downstream signaling networks, potentially optimizing the signaling balance required for CML cell survival and proliferation.

Our literature review identified three previously reported cases of HU-associated digital gangrene, though limited to the lower extremities - two in chronic myeloid leukemia (CML) and one in sickle cell disease (SCD). In each case, gangrene developed after prolonged HU exposure, alternative etiologies were not substantiated, and stabilization or clinical improvement followed HU withdrawal. The present case aligns with this pattern while extending the reported phenotype to well-controlled PV and upper-extremity digits. Given the small number of reported cases, the pathophysiology remains incompletely defined and is largely extrapolated from studies of more frequently described HU-associated ulceration, histopathologic reports of HU-related tissue injury, and in vitro studies of HU effects on endothelial and circulating cells. Plausible mechanisms include cumulative endothelial injury, localized thrombo-occlusive microvascular dysfunction, impaired vascular and cutaneous repair, and interaction with PV-related microvascular susceptibility. Clinicians should include HU-associated vasculopathy in the differential diagnosis of otherwise unexplained digital ischemia, as prompt drug cessation may limit progression and improve digit salvage.