Biomedical subjects

Daniel J DeAngelo

Publications and source records attributed to Daniel J DeAngelo.

20 records · Page 2Linked to original sources

PubMed2003

Resolution of leukemic retinopathy following treatment with imatinib mesylate for chronic myelogenous leukemia.

PURPOSE: To report a case of leukemic retinopathy before and after treatment with imatinib mesylate (formerly STI-571) for chronic myelogenous leukemia (CML). DESIGN: Interventional case report. METHODS: A 58-year-old man diagnosed with stable phase CML (SP-CML) presented with blurry vision. Fundoscopy revealed several flame-shaped hemorrhages in the macular region in both eyes. One month after this initial visit, imatinib therapy was initiated. RESULTS: : The patient noticed improvement in his visual as well as his medical symptoms; on repeat examination 6 months after the initial visit, the retinal hemorrhages had resolved and remained so after 18 months. CONCLUSIONS: Imatinib appears to be an effective treatment for SP-CML, and the improvement in visual and medical symptoms in our case report correlates with this.

Antineoplastic Agents↗

PubMed2003

PKC412 overcomes resistance to imatinib in a murine model of FIP1L1-PDGFRα-induced myeloproliferative disease.

FIP1L1-PDGFRalpha causes hypereosinophilic syndrome (HES) and is inhibited by the tyrosine kinase inhibitor imatinib (Gleevec). Imatinib is a potent inhibitor of ABL, ARG, PDGFRalpha, PDGFRbeta, and KIT and induces durable hematologic responses in HES patients. However, we observed relapse with resistance to imatinib as consequence of a T674I mutation in FIP1L1-PDGFRalpha, analogous to the imatinib-resistant T315I mutation in BCR-ABL. We developed a murine bone marrow transplant model of FIP1L1-PDGFRalpha-induced myeloproliferative disease to evaluate the efficacy of PKC412, an alternative inhibitor of PDGFRalpha, for the treatment of HES. PKC412 is effective for treatment of FIP1L1-PDGFRalpha-induced disease and of imatinib-induced resistance due to the T674I mutation. Our data establish PKC412 as molecularly targeted therapy for HES and other diseases expressing activated PDGFRalpha and demonstrate the potential of alternative kinase inhibitors to overcome resistance in target tyrosine kinases.

Animals↗