Academic Accolade — Dr. Susan Horwitz, distinguished professor and co-chair of molecular pharmacology and the Rose C. Falkenstein Chair in Cancer Research at Einstein, has been inducted into the inaugural class of Fellows of the American Association for Cancer Research (AACR) Academy, comprised of 105 of the world’s leading investigators. The AACR Academy was established to recognize distinguished scientists, selected through a rigorous peer review process, whose scientific contributions have had extraordinary impacts in the field of cancer biology. Dr. Horwitz’ research was instrumental in evaluating and identifying the active properties of Taxol, a revolutionary anti-cancer drug that has saved millions of lives in treating breast, lung and ovarian cancers. Membership in the academy represents the most prestigious honor bestowed by the AACR. In addition to her induction into the academy, Dr. Horwitz has received the 8th AACR Award for Lifetime Achievement in Cancer Research.
Recognizing Excellence — Dr. Britta Will a postdoctoral fellow in the laboratory of Dr. Ulrich Steidl, has been selected as a finalist for the Regeneron Prize for Outstanding Research. On May 6, for the final round, she will describe the “dream project” she designed to the selection committee at the company’s headquarters in Tarrytown, NY. The mission of the competition is to honor excellence in biomedical research done by early-stage scientists. Finalists are awarded $5,000 and winners (one graduate student and one postdoctoral fellow) will receive $50,000 for themselves and an additional $50,000 for their home institutions.
Fateful Regulator — Researchers led by postdoctoral fellow Dr. Britta Will and her mentor, Dr. Ulrich Steidl, have identified a new critical regulator of hematopoietic stem cell (HSC) fate called Satb1, a protein that has been linked to several types of cancer. HSCs are precursor blood cells that have the ability to mature into specialized cell types. They are guided by various factors within the cell to either commit to a particular cell lineage (differentiation commitment) or to maintain their immature form (self-renewal). Although individual molecular mechanisms underlying each of these two opposing cell fates are understood, until recently, how they are coordinated has remained elusive. By studying stem cells lacking Satb1, the research team was able to show that the protein indeed coordinates the two processes: Satb1 regulates self-renewal by simultaneously promoting quiescence (halting cell division) and by repressing differentiation commitment. The findings appear in the April 7 issue of Nature Immunology. Dr. Steidl is assistant professor of cell biology and of medicine (oncology).