ABL1 fusion

We will discuss how these factors may help shape therapeutic choices. Finally, we will highlight innovative research avenues aiming at improving prognostication of CML.

Post-transplant TKI maintenance improved outcomes in BCR-ABL+ BCP-ALL. EudraCT: 2012-0032-22; ClinicalTrials.gov: NCT01949129.

Moreover, epigenetic silencing of miR-203 enhances BCR::ABL1 expression, further contributing to TKI resistance. These small regulatory RNAs consequently act for promising candidates both as therapeutic targets and as prognostic biomarkers, with the potential to fill treatment gaps that persist even in the TKI era.

Through a systematic review of published e8a2 BCR::ABL1 cases, we summarized the classification, treatment outcomes, and prognostic characteristics associated with this rare genotype. This analysis aims to provide additional evidence to facilitate improved diagnosis and therapeutic strategies for e8a2-positive CML patients.

Notably, the presence of NUP214::ABL1 identified a clinically actionable target, supporting the use of tyrosine kinase inhibitors (TKIs) such as imatinib. This case underscores the critical role of integrated sequencing approaches in identifying cryptic genetic alterations in B-ALL for precise classification of oncogenic drivers and for targeted therapeutic strategies to improve patient outcomes.

Cytogenetic anomalies such as trisomy 8, trisomy 19, and complex karyotypes may contribute to TKI resistance. Further study is needed to understand additional abnormalities observed.

In contrast, Patients 2 and 3 tolerated the regimen well without significant adverse events. The treatment of MPAL with Ven combined with HMAs achieved a high remission rate and can be used as an alternative treatment for MPAL.

She ultimately achieved Major Molecular Response (MMR) after haploidentical hematopoietic stem-cell transplantation (haplo-HSCT). This case highlights the importance of comprehensive molecular profiling at diagnosis and the need to develop alternative therapeutic strategies for rare BCR::ABL1 variants.

These interconnected circuits offer novel insights into treatment resistance and stem cell persistence, identifying promising therapeutic targets. Future validation of these interactions may guide the development of non-coding RNA-targeted therapies for resistant CML.

Low-dose dasatinib (20 mg/day) reduced BCR::ABL1 levels (FISH negative, RT-PCR positive), but had no effect on anemia, dysplasia, or transfusion frequency...In Ph-positive de novo MDS, BCR::ABL1 transcript responses alone may not reflect disease control when an adverse founder clone persists. Integrating panel-based NGS with fusion transcript monitoring may improve therapeutic decision-making and prognostic assessment.

It is noteworthy that imatinib was more effective than dasatinib in our case, although the duration of remission was short. Our findings suggest that other therapies like allogeneic hematopoietic stem cell transplantation may need to be combined to improve long-term survival in ALL cases with BCR::PDGFRA.