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Description:
This scientific session will explore the interaction patterns of disease-associated genetic and epigenetic factors by describing the landscape and order of acquisition of such correlations, including mutation analysis at the single cell level, interplay between gross chromosomal aberrations and gene mutations, and their implications for our understanding of disease pathogenesis, treatment response, and prognosis.
Dr. Seishi Ogawa will discuss the interplay between chromosomal alterations and gene mutations in the pathogenesis of myeloid neoplasms. He will give an overview of genetic studies that have revealed significant correlations between lesions in major subtypes of myeloid neoplasms and clonal hematopoiesis. The interplay is shown to shape clonal evolution during leukemogenesis. Dr. Ogawa will also discuss the functional basis of some of these correlations and their impact on therapeutics.
Dr. Linde Miles will describe clonal evolution at the single cell level and outline its potential clinical implications. She will provide an overview of single cell DNA sequencing and multi-modal technologies used to examine clonal heterogeneity and genotype-immunophenotype relationships in acute myeloid leukemia (AML) patient samples. Dr. Miles will discuss findings that suggest that single cell multi-omics analysis of clonal architecture, mutation order, and immunophenotype of patient samples can help to predict response of patients on treatment regimens used in AML patients.
Dr. Mark Dawson will discuss the role of non-genetic mechanisms that influence cancer cell fitness. Currently, personalized cancer medicine is focused on understanding the genetic mutations in an individual’s cancer and designing targeted therapies. This dogma rests on the premise that differences in cancer cell behavior can only be explained by different genetic mutations. However, emerging work from the Dawson lab and others have challenged this dogma and demonstrated that genetically identical cancer cells can behave very differently in various tissue environments and in response to therapeutic pressure. Dr. Dawson will discuss work from his lab which has shown that non-genetic or “epigenetic” factors are as important as genetic factors in the behavior of myeloid cancers.
Dr. Seishi Ogawa will discuss the interplay between chromosomal alterations and gene mutations in the pathogenesis of myeloid neoplasms. He will give an overview of genetic studies that have revealed significant correlations between lesions in major subtypes of myeloid neoplasms and clonal hematopoiesis. The interplay is shown to shape clonal evolution during leukemogenesis. Dr. Ogawa will also discuss the functional basis of some of these correlations and their impact on therapeutics.
Dr. Linde Miles will describe clonal evolution at the single cell level and outline its potential clinical implications. She will provide an overview of single cell DNA sequencing and multi-modal technologies used to examine clonal heterogeneity and genotype-immunophenotype relationships in acute myeloid leukemia (AML) patient samples. Dr. Miles will discuss findings that suggest that single cell multi-omics analysis of clonal architecture, mutation order, and immunophenotype of patient samples can help to predict response of patients on treatment regimens used in AML patients.
Dr. Mark Dawson will discuss the role of non-genetic mechanisms that influence cancer cell fitness. Currently, personalized cancer medicine is focused on understanding the genetic mutations in an individual’s cancer and designing targeted therapies. This dogma rests on the premise that differences in cancer cell behavior can only be explained by different genetic mutations. However, emerging work from the Dawson lab and others have challenged this dogma and demonstrated that genetically identical cancer cells can behave very differently in various tissue environments and in response to therapeutic pressure. Dr. Dawson will discuss work from his lab which has shown that non-genetic or “epigenetic” factors are as important as genetic factors in the behavior of myeloid cancers.