The industry is again raising concerns that new EU health technology assessment rules coming into force on Jan. 12, 2025, will have the opposite of the desired effect and slow down access to innovative therapies.
Researchers from Incyte Corp. and collaborators presented the preclinical profile of INCB-160058, an ATP-competitive small-molecule inhibitor of the JAK2 V617F mutant sparing its wild-type (WT) form, designed for the treatment of JAC2 V617F mutation-positive myeloproliferative neoplasms with potential as a first-in-class JAK2 V617-inhibiting drug.
Bispecific CD20×CD3 T-cell engagers have shown efficacy in hematological malignancies; however, associated toxicities such as cytokine release syndrome and immune effector-associated neurotoxicity syndrome limit their use.
Residual leukemic stem cells (LSCs) are leukemia relapse-initiating cells that mediate treatment resistance in response to therapy stress. Different from normal hematopoietic stem cells (HSCs), both blasts and LSCs express T-cell immunoglobulin mucin-3 (TIM-3) on the surface.
Targeting topoisomerase 2 (TOP2) is crucial in AML, and researchers from Wakunaga Pharmaceutical Co. Ltd. have developed and tested racemic WAC-224, a quinolone TOP2 inhibitor, and (R)-WAC-224 as a potential approach for AML treatment.
Among the acquired mutations in the calreticulin (CALR) gene, both 52 bp deletion (del52) and 5 bp insertion (ins5) are among the most frequent and are linked to two different types of myeloproliferative neoplasms (MPNs).
During the basic science morning track on the last day of this year’s Annual Congress of the European Hematology Association (EHA), the attention was focused on oncogenic transcription factors and complexes considered turning points within the acute myeloid leukemia (AML) arena.
Angiogenesis plays a crucial role in multiple myeloma and its prognosis, with the success of antiangiogenic therapies being limited. Exosomes mediate cell-to-cell cross talk during the progression of cancer by transporting their molecular cargo, which include long non-coding RNAs (lncRNAs); their role in multiple myeloma was investigated.
The development of resistance and relapse during the blast phase of chronic myeloid leukemia poses a challenge in the management of this pathology, with half of the cases accounting for FLT3 pathway activation that, in turn, contributes to tyrosine kinase inhibitor resistance.
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