This webinar, the first in a “Meet the Authors” series sponsored by Mission Bio, will discuss the application of single-cell analysis to decipher clonal evolution across several stages of disease development in myeloid malignancies.
Our invited speaker, Dr. Ross Levine of Memorial Sloan Kettering Cancer Center, will discuss his study published in Nature, “Single-cell mutation analysis of clonal evolution in myeloid malignancies,” which provides insights into the pathogenesis of myeloid transformation and how clonal complexity evolves with disease progression.
As part of this work, Dr. Levine’s lab performed single-cell DNA sequencing on 146 samples from 123 patients with clonal hematopoiesis, myeloproliferative neoplasms, and/or acute myeloid leukemia to delineate mutations at single clone resolution and map out the clonal complexity of each indication. Furthermore, they combined cell-surface protein expression with mutational analysis to correlate genotype and immunophenotype.
Dr. Levine will talk about the benefits of using single-cell analysis to elucidate clonal evolution, including the ability to distinguish which mutations occur in the same clone(s), accurately measure clonal complexity, and definitively determine the order of mutations.
Dr. Ross Levine’s presentation will be followed by a live audience Q&A.
Speaker bio:
Dr. Ross Levine is the Chief of the Molecular Cancer Medicine Service, Laurence Joseph Dineen Chair in Leukemia Research, Member of the Human Oncology and Pathogenesis Program, and Attending Physician at Memorial Sloan Kettering Cancer Center. Dr. Levine’s pioneering research has illuminated the genetic basis of myeloid malignancies, including studies that delineated the role of the JAK-STAT pathway and other oncogenic drivers in the pathogenesis of myeloproliferative neoplasms (MPN) and acute myeloid leukemia (AML). His current efforts focus on the role of mutations in epigenetic modifiers in MPN and AML pathogenesis and therapeutic response, investigation of the role of different signaling pathways in hematopoietic transformation, and mechanisms of resistance to targeted therapies in MPN/AML.
