The Acute Myeloid Leukemia Channel on VJHemOnc is an independent medical education platform, supported with funding from BMS (Silver), and through an educational grant from Jazz Pharmaceuticals. Supporters have no influence on the production of content. The levels of sponsorship listed are reflective of the amount of funding given.
ASH 2024 | A tool to predict response to quizartinib by analyzing gene expression profiles in AML
Adrian Mosquera-Orgueira, MD, PhD, Santiago Clinic Hospital CHUS, Santiago, Spain, discusses a tool to analyze the gene expression fingerprint downstream of FLT3-ITD or TKD mutations in acute myeloid leukemia (AML). This tool uses FLT3 clusterization to predict responses to quizartinib, showing that FLT3-ITD-like patients responded best in a clinical trial. This interview took place at the 66th ASH Annual Meeting and Exposition, held in San Diego, CA.
These works are owned by Magdalen Medical Publishing (MMP) and are protected by copyright laws and treaties around the world. All rights are reserved.
Transcript (AI-generated)
In 2021, we developed a project where we actually analyzed gene expression profiles from patients with acute myeloblastic leukemia. And the idea was to understand the genomic fingerprint, so the gene expression fingerprint downstream of FLT3-ITD or TKD mutation to gain insights about which are the pathways driving the proliferation of these tumor cells in this subtype of AML. Surprisingly to us, we discovered that a gene expression signature that could actually clusterize FLT3 ITD and TKD patients but additionally it’s clusterized in this set an additional 20-30 percent of patients who were FLT3 ITD negative and also TKD negative...
In 2021, we developed a project where we actually analyzed gene expression profiles from patients with acute myeloblastic leukemia. And the idea was to understand the genomic fingerprint, so the gene expression fingerprint downstream of FLT3-ITD or TKD mutation to gain insights about which are the pathways driving the proliferation of these tumor cells in this subtype of AML. Surprisingly to us, we discovered that a gene expression signature that could actually clusterize FLT3 ITD and TKD patients but additionally it’s clusterized in this set an additional 20-30 percent of patients who were FLT3 ITD negative and also TKD negative. So the next step was to evaluate this in a clinical trial which was being developed by Betema in Spain, whose PI is Pau Montesinos. And this trial was treating FLT3 ITD negative patients with quizartinib, which is a FLT3 inhibitor. And we analyzed initially 150 patients in this clinical trial, and we reproduced the FLT3 clusterization, and we observed that these patients were actually responding. So FLT3 ITD-like patients were the ones responding to quizartinib better than placebo. And in this ASH meeting, we are presenting an additional validation of this tool. So we have confirmed the validity of the FLT3-like clusterization to predict response to quizartinib with a hazard ratio in our new cohort of 0.08. So that’s a 98 risk reduction for death in patients who are FLT3-like if they are treated with quizartinib, this FLT3 inhibitor. So very promising to be honest, and already planning the next steps with this project.
This transcript is AI-generated. While we strive for accuracy, please verify this copy with the video.
Read more...
Disclosures
Takeda: Speakers Bureau; Roche: Consultancy; Pfizer: Consultancy; Abbvie: Membership on an entity’s Board of Directors or advisory committees, Speakers Bureau; AstraZeneca: Consultancy, Membership on an entity’s Board of Directors or advisory committees, Speakers Bureau; Janssen: Consultancy, Membership on an entity’s Board of Directors or advisory committees, Speakers Bureau; Incyte: Other; Biodigital THX: Current equity holder in private company; Novartis: Other; GSK: Consultancy.
