Articles related to CHRONIC LYMPHOCYTIC LEUKEMIA (CLL)

As reported at the at the AACR Annual Meeting 2023, the combination of Ianalumab and ibrutinib showed promising results in treating chronic lymphocytic leukemia (CLL) in a phase 1b, dose-escalation and expansion trial. Ianalumab, an anti-BAFF-R monoclonal antibody, works by inhibiting B-cell differentiation, proliferation, and survival, and depleting B-cells through antibody-dependent cellular cytotoxicity within the tumor microenvironment. The trial treated 15 patients with CLL who were already receiving ibrutinib with different doses of Ianalumab for 6 cycles, with patients continuing the combination up to cycle 8 if they showed evidence of disease, and then followed up every 3 months for 2 years. The ORR at cycle 9 or before treatment discontinuation was 56.7%, with a complete response (CR) rate of 37.8%. Patients who were in their first line of treatment showed better outcomes than patients who had relapsed or refractory disease, with the ORR for previously-untreated patients being 81.8% with a CR of 54.5% and a CR + CRi of 63.6%. Additionally, 45.9% of patients achieved undetectable minimal residual disease (uMRD) in blood or bone marrow by cycle 9 of treatment, including 63.6% of patients in their first line of therapy and 38.5% of patients with relapsed/refractory disease. There were […]

In patients with R/R MDS/AML, the combination ipilimumab + decitabine (IPI + DEC) therapy shows a favorable safety profile and significant therapeutic activity that doesn’t seem to require T cell-mediated alloreactivity. Potential transplant candidates may find that IPI + DEC therapy acts as a less strenuous transition to transplant. Future research is necessary to determine logical IPI-based treatment plans that can provide persistent responses without causing significant immune damage.

In this video, Dr. Talha Munir, a hematology consultant at St. James’s Hospital in Leeds, UK, discusses the treatment options for a 76-year-old gentleman with Binet stage C and Rai stage 3 CLL with unmutated IGHV status and ATM gene deletion. Chemoimmunotherapy is excluded due to the patient’s condition, and the chosen treatment is venetoclax with obinutuzumab as fixed-duration therapy for 12 months. Continuous BTK-inhibitor therapy may also be an option, but the patient preferred fixed-duration therapy. The patient’s history of ischemic heart disease and need for antiplatelet therapy were also considered, with aspirin use indicating acalabrutinib or ibrutinib may be reasonable. Fixed-duration ibrutinib with venetoclax is also an option, though not yet licensed, and targeted drugs can mitigate the negative impact of ATM gene deletion.

This CME program discusses how Bruton’s tyrosine kinase inhibitors (BTKi) have improved treatment for chronic lymphocytic leukemia (CLL), mantle cell lymphoma (MCL), and other B-cell malignancies. However, due to adverse events and treatment resistance, many patients discontinue treatment. A new generation of BTKi with a different mechanism of action (MOA) is emerging as a possible alternative. The program presents four modules that discuss the MOAs of covalent and non-covalent BTKi, current practices for using BTKi in treatment of CLL and MCL, the efficacy and safety data for novel BTKi, and the potential role of non-covalent BTKi in future treatment plans.

CLL affects more than 200,000 people in the United States, and it is responsible for approximately 4,410 deaths each year. Approximately two-thirds of patients require treatment at some point. BTK inhibitors such as acalabrutinib, zanubrutinib, ibrutinib, and pirtobrutinib, as well as BCL2 inhibitors such as venetoclax, are examples of highly effective novel targeted agents.

Researchers studying acute myeloid leukemia (AML) have been able to better characterize the disease, improve risk-stratification methods, and create new treatments thanks to the era of genomic medicine. Despite major advancements, AML’s extremely intricate and plastic cellular architecture means that it is still a fatal malignancy. Because it makes it difficult to pinpoint and then eliminate the cells that cause leukemogenesis and therapy failure, this level of heterogeneity continues to be a significant obstacle. Single-cell genomics has made unheard-of advancements in the study of cellular heterogeneity in recent years, and it shows promise for the investigation of AML.