Publications by authors named "B Cassinat"
The aim of our study was to analyze the potential survival benefit associated with HSCT according to clinico-biological scores which incorporate molecular data (MIPSS70 and MIPSS70+V2) to facilitate decision-making in this context. One transplant (n=241) and one non-transplant cohorts (n=239) were used to test the hypothesis that PMF patients with higher risk molecular score benefit from HSCT. A weighted propensity score was applied to balance confounding factors with the transplanted cohort as reference.
View Article and Find Full Text PDFDespite the advances in the understanding and treatment of myeloproliferative neoplasm (MPN), the disease remains incurable with the risk of evolution to acute myeloid leukemia or myelofibrosis (MF). Unfortunately, the evolution of the disease to MF remains poorly understood, impeding preventive and therapeutic options. Recent studies in solid tumor microenvironment and organ fibrosis have shed instrumental insights on their respective pathogenesis and drug resistance, yet such precise data are lacking in MPN.
View Article and Find Full Text PDFMyeloproliferative 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 PDFArticle Synopsis
- High-molecular risk (HMR) mutations, such as ASXL1 and IDH, are linked to poorer outcomes in myelofibrosis (MF) patients, particularly when combined with lower levels of the JAK2V617F variant allele frequency (VAF).
- Analysis of 124 MF patients showed that HMR mutations significantly impacted prognosis for those with lower JAK2V617F VAF, while this effect was not observed in patients with higher VAF levels.
- The study's findings indicate that having both HMR mutations and a lower JAK2V617F VAF (≤50%) serves as a strong independent risk factor for survival, improving existing prognostic models and prompting the need for further
Article Synopsis
- Acute myeloid leukaemia (AML) is a complex cancer marked by various genetic abnormalities and a heightened oxidative stress environment, making it a target for redox-based therapies.
- Research has shown that the combination of auranofin (AUF), a drug initially used for rheumatoid arthritis, and vitamin C (VC) effectively kills different leukemia cell lines by increasing reactive oxygen species and inhibiting protein synthesis.
- Testing on 22 primary AML samples revealed that this drug combination can effectively eliminate leukaemic cells while being less harmful to normal cells, suggesting a promising anti-AML treatment strategy.