I am an Assistant Professor on the tenure track in the Departments of Pediatrics and Oncological Pathology at Rutgers Cancer Institute specializing in the molecular diagnostics of hematological neoplasms and hold American Board of Pathology certifications in anatomic pathology, clinical pathology, hematopathology, and molecular genetic pathology. My genomic pathology research involves investigating the molecular pathogenesis and functional genomics of poorly characterized hematological neoplasms driven by MAP kinase and receptor tyrosine kinase signaling (histiocytic neoplasms and hairy cell leukemia).As a physician-scientist, I applied my expertise in molecular hematopathology to unravel the molecular bases of the BRAFV600E-wild type histiocytoses to identify potential avenues for therapeutic intervention in these poorly characterized neoplasms that have no FDA-approved treatments. During this time, I pursued groundbreaking research on the molecular pathogenesis of the histiocytoses that led to the first published use and dramatic clinical responses of MEK inhibition and sorafenib in refractory histiocytoses patients, as well as the clinical efficacy of RET and ALK inhibition in these neoplasms (Diamond, Durham, Haroche, et al. Cancer Discov. 2016; Zarnegar, Durham, et al. Pediatr. Blood Cancer 2017; Durham, Lopez-Rodrigo, Picarsic, et al. Nature Medicine 2019). This work provided the foundation for a phase II clinical trial using the MEK1/2 inhibitor cobimetinib for adults with histiocytic neoplasms that has led to the FDA granting approval to cobimetinib for the treatment of BRAFV600-negative histiocytic neoplasms in 2022 (Diamond, Durham, et al. Nature 2019). I have also generated and described the first xenotransplantation model of a histiocytic neoplasm, providing the first functional evidence that the cellular origin of a subset of histiocytoses occurs within the hematopoietic stem/progenitor cell compartment (Durham, Roos-Weil, Baillou, et al. Blood 2017). I have also investigated the comprehensive genomic landscape of classical and variant hairy cell leukemia that has led to our initial understanding of the first genetic mechanisms underlying clinical vemurafenib resistance in classical HCL (Durham, et al. Blood 2017). In addition, I have extensively contributed to the development and characterization of genetically engineered murine models of histiocytic neoplasms and other myeloid malignancies for many hematology laboratories internationally, which has provided a wealth of experience in the murine modeling of cancer.