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SELECTBIO Conferences Flow Cytometry

Richard Hardy's Biography

Richard Hardy, Professor, Fox Chase Cancer Center

Dr. Richard R. “Randy” Hardy is a senior member of Fox Chase Cancer Center’s scientific staff. In addition to his role as Co-Leader of the Keystone Program in Blood Cell Development and Disease, he is also a member of the Keystone Program in Epigenetics and Progenitor Cells. Additionally, Hardy is director of the Research Flow Cytometry Facility and the DNA Sequencing Facility at Fox Chase. His research interests include development of the immune system’s B lymphocytes from stem cells in fetal liver and bone marrow; regulation of this process by pre-B-cell receptors; and the development and function of B-cell subsets, including the early-generated B1 B-cells and their role in autoimmunity, leukemia and chronic B-cell lymphoma. This unusual cell type holds special interest because of its tendency toward self-reactivity and its association with hematologic cancers. Hardy’s research includes study of B1 cell genes and antibody targets to help reveal the genetic origin of related cancers and to increase understanding of their role in malignancies. Hardy earned his B.S. in chemistry from the Illinois Institute of Technology and his Ph.D., in biochemistry from the California Institute of Technology, where he received the Herbert Newby McCoy Award for outstanding achievement in research. He completed his postdoctoral training at Stanford University where he was a fellow of the California Division of the American Cancer Society. He was a visiting scientist at Osaka University’s Institute for Cellular and Molecular Biology in Japan for two years, before joining Fox Chase in 1987.

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Using Multicolor Flow Cytometry to Dissect B Cell Development

Wednesday, 23 January 2013 at 09:30

Add to Calendar ▼2013-01-23 09:30:002013-01-23 10:30:00Europe/LondonUsing Multicolor Flow Cytometry to Dissect B Cell

We used multicolor FACS to show that mouse autoreactive CD5+ B1 B-cells arise by a distinctive developmental pathway, from precursors present in fetal liver. Now we show that retroviral provision of Lin28b/Let7 redirects development, switching fetal to adult and vice-versa.

Add to Calendar ▼2013-01-22 00:00:002013-01-23 00:00:00Europe/LondonFlow