An intensification strategy guided by response and MRD deepened remissions in individuals with residual disease and spared early responders further treatment. This approach merits further study as an alternative to fixed-duration triplet therapy.
P2, N=160, Active, not recruiting, French Innovative Leukemia Organisation | Recruiting --> Active, not recruiting | Trial primary completion date: Jan 2026 --> Aug 2025
1 day ago
Enrollment closed • Trial primary completion date
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TP53 (Tumor protein P53) • IGH (Immunoglobulin Heavy Locus)
The combination of the B-cell lymphoma 2 inhibitor venetoclax with CIT has emerged as a new first-line benchmark with promising response rates and overall survival...Pirtobrutinib has demonstrated responses even in heavily pretreated patients...For R/R disease, novel BTK inhibitors, bispecific antibodies, and cellular therapies are demonstrating substantial efficacy. Ongoing trials investigating combinations of these agents are poised to further transform RT management.
Despite containing SLL deposits, the harvested melanoma produced a CD8+ T cell-predominant tumor-reactive TIL infusion product containing stem-like CD39negCD69neg CD8+ T cells. A strong overlap (60%) in the TCRβ sequences between this infusion product and peripheral blood mononuclear cells collected at the 9-month follow-up visit was evidence of long-term persistence of TIL in this patient.
A subset of patients who were exposed to and were found to be relapsed, refractory, resistant, or intolerant to both BTKi and BCL2i-based regimens (n = 25) had high rates of progressive disease at first assessment (15.0%) and death (44.0%). These findings highlight an unmet clinical need for patients with CLL and underscore the urgency to develop effective new strategies to treat those patients who have already received covalent BTKi and BCL2i.
To identify the most relevant source of Mif in CLL, we generated two CLL mouse strains with B-lymphoid- or myeloid-lineage-specific Mif deletion. In contrast to the global Mif knockout, neither conditional Mif knockout significantly altered CLL progression, illustrating that the cellular source of Mif is less critical than its systemic presence in the tissue environment.