Acute Promyelocytic Leukemia

MSC-l levels were lower in patients receiving myeloablative conditioning compared with non-transplanted patients, suggesting transplant intensity may influence MSC dynamics. Higher post-treatment MSC-l proportions are associated with poorer survival, independent of ELN risk and age, supporting their potential as a prognostic biomarker in AML.

This study confirmed well-known gene-disease associations in myeloid malignancies but found no significant link between parvovirus B19 infection and specific somatic mutations or disease subtypes. These findings suggest that B19 infection may be incidental, underscoring the need for larger-scale studies to clarify its clinical relevance in patients with myeloid malignancies.

Additionally, YW3-56 suppressed the downstream mTOR pathway, inducing caspase-3/PARP-mediated apoptosis and inhibiting cell proliferation. Our study demonstrated that YW3-56 exerts multimodal antileukemic effects in APL by simultaneously targeting PAD4-mediated epigenetic regulation, AKT-driven metabolic reprogramming and cellular differentiation, highlighting PAD4-AKT signaling as a promising target for APL combination therapy.

EWSR1 could be a powerful prognostic indicator for clinical strategy selection in AML. The prediction model may effectively predict the OS of non-APL AML.

P1, N=66, Completed, National Cancer Institute (NCI) | Active, not recruiting --> Completed

In recent years, a novel type of tripartite retinoic acid receptor (RAR) fusion genes has been identified in atypical APL (aAPL), exhibiting distinct structural characteristics and pathogenic mechanisms compared to the classical bipartite fusion. This article systematically introduces relevant content in this field: it begins by outlining the long-standing scientific puzzle of inconsistent clinical resistance versus in vitro sensitivity in aAPL patients; subsequently, it describes the discovery process and structural features of tripartite fusion genes in all RARG and specific RARA-related cases, and elucidates the key molecular mechanism by which tripartite fusion leads to all-trans retinoic acid (ATRA) resistance at the protein conformational level; finally, the discovery of transposon involvement in the formation of tripartite fusions and its implications for the mechanism of fusion gene are discussed.

P1, N=12, Completed, SDK Therapeutics, Inc. | Phase classification: P1/2 --> P1

In summary, our data confirm that CEBPA bZIPinf mutation is an independent factor of favorable prognosis in AML patients.

The former partner gene is RARG, with clinical manifestations, bone marrow morphology, and immunophenotype similar to APL. The latter partner gene is HOXC13, with the characteristics of NUP98-AML patients.

ATRA accelerates growth plate closure through the ITGB2-YAP axis, disrupting Wnt/β-catenin signaling. These findings establish a mechanistic framework for developing therapeutic strategies targeting ITGB2 or YAP to delay premature growth plate senescence in pediatric disorders.

Our findings reveal that TTMV integrates exclusively within intron 2 of the RARA gene via microhomology-mediated end joining (MMEJ), forming functional TTMV::RARA transcripts. Clinically, patients harboring this fusion were predominantly pediatric (72.

Collectively, our results suggest that tamibarotene may elicit detrimental effects in patients with EBA by abolishing the recruitment of Tregs into skin. This warrants great caution when using tamibarotene in patients with EBA and possibly other pemphigoid diseases.