ABL1 (ABL proto-oncogene 1)

The rare genetic co-occurrence of t(15;17)/PML::RARA and t(9;22)/BCR::ABL1 translocations may be identified in a single patient with acute promyelocytic leukaemia (APL).Successful induction using all-trans retinoic acid (ATRA) together with imatinib achieved effective control of both leukemic clones.The patient demonstrated rapid haematologic remission and favourable clinical recovery, suggesting a positive outcome with this therapeutic approach.

5-fluorouracil and VEGF (vascular endothelial growth factor) inhibitors are the agents most commonly linked to abnormal vasoreactivity, whereas BCR-ABL (breakpoint cluster region-Abelson murine leukemia viral oncogene homolog) inhibitors and immune checkpoint inhibitors have been associated with accelerated atherosclerosis...Key contributors include endothelial injury and dysfunction, oxidative stress, and inflammation. An understanding of the mechanisms of vascular toxicities may facilitate optimal treatment and preventive strategies in patients with cancer.

The visual and texture features of the Siamese architecture help in the capture of molecular similarities based on electrostatic and non-covalent interaction profiles. Therefore, the developed protocol offers a suitable approach in computational drug discovery, being a promising framework for virtual screening, drug repositioning, and the identification of novel therapeutic candidates.

One of the mutations that is still an on-going challenge in clinical and scientific field is the T315I mutation, since it gives patients a poor prognosis attributable to acquired resistance to therapy. In the following narrative review, we will discuss the current knowledge on the T315I mutation, explore the most suitable treatment options, examine the role of third-generation tyrosine kinase inhibitors, and outline potential future therapeutic strategies.

These findings establish OSM as a key mediator linking oncogenic STAT5 activation to remodeling of the microenvironment and immune suppression. Targeting OSM signaling therefore represents a promising therapeutic strategy to alleviate disease progression in myeloproliferative neoplasms and related malignancies.

Pin1 may convert the mature form BCR::ABL1 to an immature form for Bag1 recognition leading to CHIP-mediated ubiquitination and degradation. These findings may lead to provide a molecular basis for the development of new Pin1 related therapeutic strategies against TKI resistance.

Since 2004, patients receiving imatinib with relapse in non-marrow sites were given dasatinib to preserve control of leukemic marrow. Dasatinib is a potentially practice-changing targeted therapy for EML. Finding and eradicating EML could increase the possibility of lengthy disease-free survival.

However, the toxicity and resistance associated with the use of imatinib, a first-generation Bcr-Abl inhibitor, in cases where the T315I mutation exists, necessitates the need for new tyrosine kinase inhibitors...However, investigating different combined scaffolds enhances the chance of successfully developing novel drug candidates. Overall, the information provided in this review can be beneficial to researchers with an interest in chronic myeloid leukemia and tyrosine kinase inhibitors.

These findings underscore the necessity for vigilant, protocol-driven monitoring of blood counts and cardiac function (including echocardiography) during dasatinib therapy. Proactive management strategies should be considered to mitigate these risks and improve treatment safety.

At present, there is no established consensus on the treatment of Ph + MPAL, and reports on cases with the atypical e13a3 BCR::ABL1 fusion are particularly scarce. This finding will bring new insights and references for the diagnosis and treatment of Ph + MPAL.

The rates of non-relapse mortality at one, three, and five years were 22%, 26%, and 30%, while the cumulative incidences of relapse were 7%, 10%, and 14%, respectively. In summary, 8 Gy TBI conditioning in ALL patients was feasible and resulted in outcomes similar to those previously reported for 12 Gy conditioning regimens.

In conclusion, MSI2 inhibition, in combination with TKI therapy, has shown to overcome drug resistance and mitigate senescence in preclinical CML models, and suggesting a potential strategy to target CML LSCs.