Leukemia

This study established causal relationships between specific immune cell phenotypes, inflammatory cytokines, and AA. Importantly, LIF partially mediated the effects of immune cells on AA, suggesting the LIF-LIFR axis as a potential therapeutic target.

In the TFR phase, MR4.0 rates at 12 months (Arm 1: 31.9%, Arm 2: 37.5%; p = 0.383) and 24 months (Arm 1: 29.4%, Arm 2: 30.8%) revealed no differences in TFR success between 2 and 3 years of nilotinib. Irrespective of the consolidation duration, switching to nilotinib 300 mg BID provided the opportunity to achieve TFR if patients were unable to reach stable DMR with first-line imatinib.

The study demonstrated a high ratio of abnormal CD marker expression in AL cases, aligning previous data from various area around the world. Identifying aberrant antigen expression patterns through immunophenotyping aids in diagnosing leukemia and distinguishing neoplastic cells from normal hematopoietic precursors.

Histology revealed CD3+ mononuclear cell infiltration in alveolar septa and peribronchiolar regions in HAB and HAM, consistent with T cell-mediated alveolitis and bronchiolitis, and CXCL10 expression was elevated in infiltrated lesions. Collectively, these findings implicate the CXCR3/CXCL10 axis as a common pathway for pulmonary T cell recruitment in HTLV-1-associated diseases.

Overall, our findings showed that an adjustment of the initial asciminib dose may be needed based on genotyping information for the NR1I2 -25385C > T polymorphism and the body weight of the patient; however, further prospective studies are necessary.

The uniqueness of the case is the presence of an additional population of bonafide promonocytes in an otherwise typical case of Philadelphia-positive B-ALL expressing CD13 and CD33. This case underscores the importance of morphology and cytochemistry in detecting and confirming minor blast populations, which may manifest as the dominant or the only clone at relapse.

FCM on intact LNs is a robust tool with high pathologic concordance. Integrating genetic mutation data with FCM provides a powerful, multi-parameter strategy. This approach moves beyond standard immunophenotyping to include mutation-associated antigens, thereby refining lymphoma classification and enhancing diagnostic accuracy.

She was initially treated with low-dose acetylsalicylic acid, with partial improvement, but microvascular symptoms persisted, and platelet counts remained >1,000 × 10⁹/L. Hydroxyurea was initiated, leading to progressive platelet reduction and marked clinical benefit...Cytoreductive therapy may be indicated in cases with extreme thrombocytosis or refractory symptoms, and long-term follow-up is crucial to monitor disease evolution and treatment outcomes. This case highlights the need for multicenter studies and international registries to have pediatric-specific evidence that can better inform diagnostic and therapeutic strategies.

Multivariate analysis identified Day 1 concurrent IT administration as an independent risk factor (OR = 12.5; 95% CI: 1.45-131; p = 0.023). Initiating IT chemotherapy on the same day as blinatumomab infusion significantly increases the risk of neurotoxicity in pediatric ALL patients.

These findings suggest that Teniposide activates STING through a previously unrecognized, cGAS-independent mechanism, while retaining potential for canonical cGAS-STING stimulation. Our combined computational and experimental evidence supports repurposing Teniposide as a STING agonist, highlighting new therapeutic possibilities for innate immune stimulation.

Genetic ablation of the IL-6 receptor in AML cells significantly attenuated AML growth in osteoblast-specific mTORC1-activated mice. Collectively, our results suggest that the mTORC1/IL-6 axis in osteoblastic niche non-autonomously contributes to the AML progression, suggesting a viable therapeutic target for AML.

We found that forced expression of scaRNA12 in BCP-ALL increased p53 activity and significantly enhanced the sensitivity of BCP-ALL to chemotherapeutic reagents. Together, our results suggest a tumour-suppressing role for scaRNA12 in BCP-ALL.