ZNF384 (Zinc Finger Protein 384)

DNA hypermethylation in the promoter region of ZNF382 and low ZNF382 mRNA expression are closely related to the occurrence and progression of DLBCL. Moreover, ZNF382 overexpression significantly increased apoptosis and inhibited cell proliferation, migration, and clone formation. Therefore, ZNF382 has potential as a therapeutic target in the treatment of DLBCL.

Furthermore, patients with TCF3::PBX1 or MEF2D fusion and high EVI1 expression had RFS and OS similar to those without the corresponding fusions, and patients with ZNF384 fusion and low EVI1 expression had RFS and OS comparable to those without ZNF384 fusions (all p > 0.05). Low EVI1 transcript levels at diagnosis are related to poor prognosis in adult Ph-negative B-ALL, and EVI1 expression may improve fusion gene-defined risk stratification.

SLC31A1 plays a crucial role in the proliferation and invasion of breast cancer cells, and its expression is regulated by ZNF384. These findings highlight SLC31A1 as a potential therapeutic target and suggest that modulation of copper metabolism may offer novel strategies for breast cancer treatment.

Advances in molecular characterization have enhanced classification techniques and have the potential to inform personalized treatment strategies. Considering the rarity and heterogeneity of MPAL, extensive prospective multicenter trials are imperative to develop evidence-based therapeutic protocols.

Finally, in vivo animal models confirmed that targeted silencing of INTS13 significantly impeded cervical cancer xenograft growth in nude mice, reduced cellular proliferation, and augmented apoptosis, consistently accompanied by a reduction in hnRNPC expression. These findings collectively establish INTS13 as a crucial precancerous gene in cervical cancer, promoting malignant phenotypes primarily through the ZNF384-INTS13-hnRNPC signaling axis.

CD10, CD19 and MPO in one flow cytometry tube facilitated distinguishing B-cell acute lymphoblastic leukemia with dim expression of MPO versus B/myeloid mixed phenotype acute leukemia. B-ALL chemotherapy followed by blinatumomab bridging to allogeneic stem cell transplantation was successful in our patient.

The implementation of FLT3 expression profiling and full-coding mutation screening in ALL (and in AML) diagnostics could unlock precision medicine approaches. By bridging the AML experience with ALL innovations, this review outlines a roadmap for FLT3-targeted therapies and combination strategies, underscoring the urgency of biomarker-driven clinical trials to optimize FLT3-directed interventions in acute leukemias.

This rare presentation underlines the diagnostic challenges of acute leukaemias. The patient was finally treated with azacitidine and venetoclax.

Our results suggest ALAL-RUNX1 is associated with younger age, higher blasts, and more karyotypic abnormalities, but has similar clinical and genetic features and outcomes to AML-RUNX1. Our findings suggest, like other MR mutations, RUNX1-mutated ALALs should be included within AML-MR.

The use of lineage-specific targeted approaches may result in therapeutic pressure and lineage switch in patients with acute leukaemia with multi-phenotypic potential. The role and optimal platform for minimal residual disease surveillance in ALAL to guide therapy, and inform transplantation is unclear, given the paucity of prospective controlled data.

Remarkably, Hinokitiol exhibits stage-dependent efficacy, with superior suppression of metastatic (stage IV) tumors linked to heightened ferroptosis sensitivity. This study not only elucidates the transcriptional machinery governing ISC biogenesis in LUAD but also highlights Hinokitiol's dual mechanism as a promising stage-specific therapeutic agent, offering novel strategies for advanced disease management.

These findings indicate that SYTL5 acts as a potential oncogene in TC and may serve as a biomarker for TC diagnosis. Moreover, this study enhances our understanding of TC's underlying mechanisms and highlights SYTL5 as a promising target for immunotherapy.