iwAL 2019 | Developments in acute leukemias: biology, therapeutics and monitoring
Here, Richard Stone, MD, of the Dana Farber Cancer Institute, Boston, MA, discusses novel therapies and monitoring in acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML). This video was recorded at the International Workshop on Acute Leukemias (iwAL) 2019, held in Barcelona, Spain.
Transcript (edited for clarity):
Richard Stone: There are a lot of interesting developments in the acute leukemias lately, and there are three main areas that were touched upon at the iwAL meeting that we’re lucky enough to be right at now. The three areas are leukemia biology, new therapeutics in the leukemias, and new ways to monitor the disease and assess response.
Richard Stone: So in terms of biology, we’re learning a lot more about leukemia stem cells. The traditional ways of describing leukemia stem cells, it’s been an ability of the inception of the bulk leukemia cells to be able to repopulate in a mouse. But now there’s new technologies, new mice, and new thoughts about how stem cells develop over time and Dr. Majeti from Stanford gave a very exciting lecture about that the other day.
Richard Stone: And so our challenge as clinicians is to be able to take that data and apply it to clinical medicine. A lot of it is the thought about whether we should cover all the potential mutations that might pop up at the beginning, whether we should wait and see what actually occurs in a patient, given with therapy A, and wait to give therapy B until we see the development of those new mutations.
Richard Stone: In terms of therapeutics, in both ALL and AML, it’s an amazing time to be a leukemia doctor because there have been, I think if you add it up, about fourteen new therapies in those two conditions in the last couple of years, or at least new indications. And so, in acute lymphoblastic leukemia we’re beginning to think about application of kinase inhibitors to not only a patient with Philadelphia positive ALL, in which case the ability to give these serial inhibitors has made a huge dent in the disease, and maybe even obviated the need for transplant in what was concerted a very bad risk population, to now that we’re thinking about using kinase inhibitors.
Richard Stone: And another interesting and fairly recently described subset of ALL called Philadelphia-like ALL, where the expression signature in this subtype is similar to what you do see in bonafide Philadelphia positive ALL and whether we should be … it’s this Philadelphia-like ALL, which is seen in all ages, but is usually a marker for disease resistance. Whether we should approach that with specific kinase inhibitors, some patient will respond to JAK inhibitors, others to Abl kinase inhibitors.
Richard Stone: Whether we should be using that, as the pediatricians been doing, whether we should be using so called MRD erasers when the inevitable disease burden is still present after standard chemotherapy.
Richard Stone: In that regard, [Dr. Gakibet 00:02:30] reviewed the data using [inaudible 00:02:33] map, the bio-specific C19-CD3 drug as a MRD eraser as something that can be used after chemotherapy, has done at least a few cycles of chemotherapy, then if you detect MRD by either DNA sequencing, or by flow cytometry, you come up with a [inaudible 00:02:51] and lower the disease burden in that fashion, thereby seeming to making the outcome better. In fact [inaudible 00:02:58] have recently approved for the treatment of minimal residual Zs or measurable residual Zs ALL.
Richard Stone: That’s just one example. We’ll be talking about CAR T-Cells in ALL later today and that’s been a huge new therapeutic option for some, particularly young patients with relapsed ALL.
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