SOHO 2023 | Immunotherapeutic approaches in CALR-mutated MPNs
John Mascarenhas, MD, Mount Sinai Medical Center, New York, NY, discusses the development of immunotherapeutic approaches which target mutant CALR, a cell-surface protein which can lead to aberrant JAK/STAT signaling in some patients with myelofibrosis (MF) and essential thrombocythemia (ET). This interview took place at the Eleventh Annual Meeting of the Society of Hematologic Oncology (SOHO 2023) held in Houston, TX.
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Transcript (edited for clarity)
I think the other exciting area in MF and ET right now is mutant CALR, immunotherapeutic approaches. So for example, here at Sinai, we have a mutant CALR vaccine treating patients with high-risk ET who failed hydroxyurea or low-risk myelofibrosis, patients that are CALR mutant positive. And this is an approach that I think is very promising in trying to invigorate an immune response to the mutant CALR protein, which is expressed aberrantly on the surface of the cells in conjunction with the thrombopoietin receptor and leads to aberrant JAK-STAT signaling...
I think the other exciting area in MF and ET right now is mutant CALR, immunotherapeutic approaches. So for example, here at Sinai, we have a mutant CALR vaccine treating patients with high-risk ET who failed hydroxyurea or low-risk myelofibrosis, patients that are CALR mutant positive. And this is an approach that I think is very promising in trying to invigorate an immune response to the mutant CALR protein, which is expressed aberrantly on the surface of the cells in conjunction with the thrombopoietin receptor and leads to aberrant JAK-STAT signaling. So this is an exciting approach, of course, for CALR-mutant patients, not for JAK2-mutant patients. And along the same lines, Incyte has developed an antibody specifically to mutant CALR that has very elegant preclinical data demonstrating the potential to eradicate the disease in murine transplant modeling. And this is now in the clinic in a Phase I dose escalation study, both in Europe, in the US, as a single agent in patients who have CALR-mutant ET or MF.
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