I think it’s now well-accepted the TKI therapy is critical in the treatment of Philadelphia chromosome-positive ALL. It’s an integral part of therapy for patients of all ages. It has really helped to substantially improve outcomes since this was first started now almost two decades ago.
One of the other recently identified genetic subtypes in ALL is Philadelphia chromosome-like ALL...
I think it’s now well-accepted the TKI therapy is critical in the treatment of Philadelphia chromosome-positive ALL. It’s an integral part of therapy for patients of all ages. It has really helped to substantially improve outcomes since this was first started now almost two decades ago.
One of the other recently identified genetic subtypes in ALL is Philadelphia chromosome-like ALL. A subset of these cases have fusions involving one of about a half a dozen genes we refer to as ABL-class chains. The main ones are ABL-1, ABL-2, CSF1R, and PDGFR-beta. Clinically, these patients are similar to Ph-positive ALL, in that they have high white counts or early response and low cure rates with standard therapies. In vitro, these fusions really behave like BCR-ABL. They can induce growth factor independence. They are inhibited by the same ABL-class tyrosine kinase inhibitors as BCRA. There’s great interest in treating these patients with chemotherapy. Plus, most commonly, imatinib or dasatinib, as in Ph-positive ALL, to see if that improves outcome.