SOHO 2025 | The current role of CAR T-cell therapy in high-risk B-ALL
Bijal Shah, MD, Moffitt Cancer Center, Tampa, FL, comments on the increasing role of CAR T-cell therapy in high-risk B-cell acute lymphoblastic leukemia (B-ALL), specifically those with measurable residual disease following induction chemotherapy. Dr Shah highlights that patients with high-risk B-ALL have poor long-term outcomes, and researchers are still learning which genotypes benefit from CAR T-cell therapy. This interview took place at the 13th Annual Meeting of the Society of Hematologic Oncology (SOHO 2025) in Houston, TX.
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Transcript
I think the current role of CAR T-cell therapy in high-risk B-ALL is increasing and I want to talk about what high-risk B-ALL is. When we talk about risk we’re going to talk about residual disease or measurable residual disease following induction chemotherapy. We recognize that those individuals have very, very poor outcomes in the long term. It turns out that we can actually build onto that platform of measurable residual disease, high-risk genotypes...
I think the current role of CAR T-cell therapy in high-risk B-ALL is increasing and I want to talk about what high-risk B-ALL is. When we talk about risk we’re going to talk about residual disease or measurable residual disease following induction chemotherapy. We recognize that those individuals have very, very poor outcomes in the long term. It turns out that we can actually build onto that platform of measurable residual disease, high-risk genotypes. And I think we’re still learning about who benefits and who doesn’t within that high-risk genotype category. So, for example, TP53, which we know in the relapsed refractory setting may be prone to CD19 antigen loss. We’re learning as we bring CAR T-cell into earlier lines of therapy whether we’re going to see the same phenomenon occur. There are others. ZNF384, which is a B-myeloid subtype, Ph-like, which thankfully less often loses CD19 expression, but still very proliferative. And when we talk about risks in general, that is something that we have to account for. So a lot that we’re still learning as we now build the genomics onto that measurable residual disease footprint.
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