RELATED STORY: Elsa R. Flores: Pursuing New Pathways to Foil Cancer
Elsa Flores received her B.S. in chemical engineering from the Massachusetts Institute of Technology and her Ph.D. in cancer biology from the University of Wisconsin-Madison. She did a postdoctoral fellowship, sponsored by the Leukemia & Lymphoma Society of America, in Tyler Jacks’ laboratory at MIT. In his lab, she found that p63 and p73 are required for p53-dependent apoptosis in response to DNA damage, and that p63 and p73 are tumor suppressor genes. Recent work in her laboratory includes deciphering the functions of the TA and ΔN isoforms of p63 and p73 in multiple biological processes using conditional knockout mouse models to target the p53 pathway in cancer therapeutically. Flores is a National Cancer Institute Outstanding Investigator and has received awards from the American Cancer Society and the V Foundation for Cancer Research, in addition to the Rita Allen Foundation. In September 2016 she became Co-Leader of the Cancer Biology and Evolution Program and Chair of Molecular Oncology Department at the Moffitt Cancer Center in Tampa, Florida.
Many genes with driver mutations in cancer are members of gene families. The existence of redundant functions in gene families has made diseases like cancer challenging to treat and cure due to limited knowledge about the functions of each gene within the family. The p53 family is one such gene family. Despite long-standing knowledge that p53 function is frequently altered in cancer, p53 has persisted as an “undruggable” target because of its function as a transcription factor and because it lacks an enzymatic activity that can be readily inhibited. In an effort to identify novel ways of targeting p53 in cancer, the Flores laboratory has been focused on understanding the interrelated biological functions of the p53 family, which includes the p63 and p73 genes. They have identified novel functions for p63 and p73 in metastasis, miRNA biogenesis, long noncoding RNA regulation, stem cell maintenance and metabolism using novel mouse models. These mouse models have also revealed novel functions of p63 and p73 in tumor metabolism and have allowed the manipulation of particular isoforms of p63 and p73 to therapeutically target p53-deficient and mutant tumors.