It has been previously demonstrated that the WNT gene/protein family member WNT5A is down-regulated in leukemia, and low expression of this tumor suppressor has been correlated with disease progression and poor prognosis. In a recent study, researchers from Universidade Estadual de Campina aimed to assess the role of WNT5A in leukemia and evaluate the effects of Foxy-5, (Wntresearch AB) a WNT5A-mimicking compound, on the progression of this disease.
Later this year, Mendus AB plans to move its allogeneic cell-based cancer vaccine, vididencel, into a phase II combination trial with oral azacitidine to evaluate the regimen’s potential as a maintenance therapy in patients with acute myeloid leukemia (AML).
The death of a patient caused Seattle Children's to pause its phase I study of relapsed/refractory pediatric acute myeloid leukemia (AML). It’s another hitch in the world of ground-breaking CAR T treatments that can have a serious downside.
Chia Tai Tianqing Pharmaceutical Group Co. Ltd. has identified proteolysis targeting chimeras (PROTACs) comprising cereblon (CRBN) ligands coupled to a Bruton tyrosine kinase (BTK) targeting moiety via linker and thus acting as BTK degradation inducers.
Part of the reason for CAR T cells’ astonishing success in B-cell cancers is that B cells are astonishingly easy to replace. CAR T cells are specific, yes. But they are not specific to tumor cells. They are specific to their target antigens. In the case of Yescarta (axicabtagene ciloleucel, Gilead Sciences Inc.) and Kymriah (tisagenlecleucel, Novartis AG), the first two clinically approved T cells, that target is CD19, which is expressed on B-cell precursors. And when it is successful, the treatment leaves patients without any B cells at all.
Researchers from City of Hope discussed preclinical data for CD33-targeted chimeric antigen receptor (CAR) T cells being developed for the treatment of acute myeloid leukemia (AML).
Although FMS-like tyrosine kinase 3 (FLT3) inhibitors have shown success treating FLT3-mutated acute myeloid leukemia (AML), around 30% to 50% of patients show primary resistance to both type I and type II inhibitors. Therefore, identifying therapeutic strategies to overcome this resistance and enhance the efficacy of FLT3 inhibitors remains an urgent need.
.webp?height=488&t=1670008838&width=650 "Acute myeloid leukemia")
