Cases harboring biallelic TET2 inactivation or TET2+SRSF2 co-mutation show the highest bone marrow monocyte burden, frequent classical monocyte (MO1; CD14+/CD16-) elevation, and highest progression risk representing biologically true OM-CMML, whereas SF3B1-mutated and biallelic TP53 mutated cases show MDS-directed biology and warrant reclassification. This review synthesizes current diagnostic frameworks, molecular heterogeneity, risk stratification approaches, and evolving classification proposals, thereby providing a practical guide for pathologists navigating OM-CMML in the modern genomic era.
Anti-CD69 monoclonal antibody treatment was associated with reduced generation of granulocyte-macrophage progenitor cells, prolonged survival, and decreased Treg accumulation in the BME. Our findings suggest that CD69 may serve as a biomarker of BME immunological dysfunction in CMML.
This study shows how competing-risk analysis complements standard Kaplan-Meier estimates of overall and progression-free survival when the cumulative incidence of a specific event, leukaemic transformation, is the quantity of interest. Although the modest, single-centre sample and non-randomised treatment allocation preclude definitive treatment recommendations, cytogenetic risk was the strongest disease-related prognostic factor, and molecular profiling provided additional risk discrimination within the NGS-tested subgroup. Cumulative incidence functions should therefore be reported routinely alongside Kaplan-Meier estimates in CMML and other myeloid neoplasms with non-negligible competing mortality.
6 days ago
Journal
|
TP53 (Tumor protein P53) • SETBP1 (SET Binding Protein 1)
P=N/A, N=50, Recruiting, Centre Hospitalier Universitaire de Nice | Unknown status --> Recruiting | Trial completion date: Nov 2018 --> Nov 2028 | Trial primary completion date: Nov 2018 --> Nov 2027
8 days ago
Enrollment open • Trial completion date • Trial primary completion date
DLI is an effective treatment strategy for post-transplant relapse of all myeloid malignancies, with specific genetic subtypes showing poorer outcomes and survival.
The 1p36.2 chromosomal region harbors tumor suppressors such as PR domain containing 16 (PRDM16), Tumor Protein 73 (TP73), Cadherin 5 or VE-cadherin (CHD5), and Kinase Family Member 1B (KIF1B), while the 3p12 chromosomal location plays a role in the malignant transformation and disruption of the tumor suppressors, focusing on the genomic instability observed in the case. These changes may partially harbor the capacity to contribute to the pathogenesis of aggressive behaviors in leukemia through failure of apoptosis, chromatin remodeling pathways, and enhanced self-renewal capabilities of stem cells.
18 days ago
Journal
|
TP73 (Tumor Protein P73) • CDH5 (Cadherin 5) • KIF1B (Kinesin Family Member 1B) • PRDM16 (PR/SET Domain 16)
Median OS was 27.2 vs. 17.2 months in AML and 16.7 vs. 23.7 months in MDS/CMML for clearance versus persistence groups, respectively. These findings suggest that SF mutation clearance does not significantly impact OS but may influence other clinical outcomes in patients with myeloid neoplasms harboring SF mutations.
HLA-DRB1 (Major Histocompatibility Complex, Class II, DR Beta 1) • HLA-B (Major Histocompatibility Complex, Class I, B) • HLA-C (Major Histocompatibility Complex, Class I, C)