- |||||||||| Tavalisse (fostamatinib) / Rigel
ITALIAN REAL-WORLD EXPERIENCE WITH FOSTAMATINIB IN ADULT PATIENTS WITH CHRONIC IMMUNE THROMBOCYTOPENIA (Poster Area (Hall 7)) - May 15, 2024 - Abstract #EHA2024EHA_2907; Fosta was used in most cases as fourth or further line of therapy, after failure of TPO-RAs. Our findings indicate that a significant proportion of patients (nearly 40% of the overall population)benefit from fosta after 6 months, suggesting that this treatment may be considered as a manageable andeffective therapeutic option in the real-world practice.
- |||||||||| EFFECT OF NOVEL AGENTS ON THE MECHANISM OF FIBROCYTE-MEDIATED INDUCTION OF MYELOFIBROSIS (Poster Area (Hall 7)) - May 15, 2024 - Abstract #EHA2024EHA_2712;
In vitro experiments demonstrated that the novel agents examined in this studyeffectively inhibited monocyte differentiation into fibrocytes and reduced certain profibrotic cytokinelevels in the culture supernatant. Further investigation into these mechanisms is anticipated to provideinsights into the antifibrotic mechanisms underlying the action of these novel agents.
- |||||||||| Prolia (denosumab) / Amgen
CHARACTERIZATION OF BONE MARROW NICHE AND IMMUNOPHENOTYPING IN A MULTIPLE MYELOMA MOUSE MODEL DRIVEN BY COMBINED EXPRESSION OF ACTIVE RANK AND TCL1 (Poster Area (Hall 7)) - May 15, 2024 - Abstract #EHA2024EHA_2375; It offers a detailed understanding of the bone marrow niche dynamics,immunosurveillance mechanisms, and genomic alterations, establishing a significant advancement in MMresearch. Our findings not only closely mirror human myeloma, but also unveil potential novel targets fortherapeutic intervention, such as the microenvironment-modulating protein CD39, and allow furtherexploration of the autophagy-linked protein p62, shedding light on its role in drug resistance to proteasomalinhibition.
- |||||||||| Undisclosed CDK4/6 inhibitor / CS Group, narazaciclib (HX301) / Traws Pharma
THE MULTIKINASE CDK4/6 INHIBITOR NARAZACICLIB OVERCOMES BTK-I RESISTANCE IN MANTLE CELL LYMPHOMA BY TARGETING USP24-P53 SIGNALING AXIS (Poster Area (Hall 7)) - May 15, 2024 - Abstract #EHA2024EHA_2120; Our findings demonstrate that narazaciclib is safe and effective as a single agent in preclinical models of MCL,including BTKi-resistant cases. Its combination with ibrutinib achieved a synergistic tumoricidal effect in vitroand in vivo, accelerating cell cycle blockade and, specifically in the BTK-resistant cases, promoting thephosphorylation of USP24, followed by the activation of P53 and the modulation of DNA repair pathway.
- |||||||||| Ibrance (palbociclib) / Pfizer, Verzenio (abemaciclib) / Eli Lilly
INHIBITION OF CDK4/6 AUGMENTS ATRA-INDUCED DIFFERENTIATION ACROSS ACUTE MYELOID LEUKAEMIA SUBTYPES () - May 15, 2024 - Abstract #EHA2024EHA_1065; Additionally, we observed that ATRA-induced differentiation isenhanced when in combination with CDK4/6 inhibitors across a wide range of AML subtypes. Although theseresults should be validated in additional AML models, they show that a primary mechanism of action ofCDK4/6 inhibitors is cell cycle arrest accompanied by the induction of differentiation, and that, in combinationwith ATRA, this effect can be augmented.
- |||||||||| Ibrance (palbociclib) / Pfizer
DUAL TARGETING OF FLT3-ITD AND CLK BY SCREENED DONATED CHEMICAL PROBES IN ACUTE MYELOID LEUKEMIA (Poster Area (Hall 7)) - May 15, 2024 - Abstract #EHA2024EHA_1039; The unexpected discovery of potent FLT3 signalinginhibition specifically in FLT3-ITD mutated AML cases introduces a dual-targeting approach that couldsignificantly improve AML treatment. This finding not only highlights the utility of DCPs in therapeutic discoverybut also paves the way for innovative, more effective AML treatment protocols.
- |||||||||| Blincyto (blinatumomab) / Astellas, Amgen, Besponsa (inotuzumab ozogamicin) / Pfizer, UCB
TARGETED- AND IMMUNO-BASED THERAPIES FOR ADULTS WITH TP53-MUTATED ACUTE LYMPHOBLASTIC LEUKEMIA (Poster Area (Hall 7)) - May 15, 2024 - Abstract #EHA2024EHA_871; Our results show that novel therapies are effective in ALL withTP53 mutations, leading to high remission rates and MRD- responses. Previous exposure to novel therapies didnot seem to impact response to subsequent novel therapies.
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