Richard Bennett, PhD
Research Assistant Professor
I first became interested in molecular and cellular biology as an undergraduate at Kalamazoo College, and later, as a graduate student at Weill Cornell Graduate School of Medical Sciences, I decided to devote my career to researching the molecular basis of cancer. This has provided me with the opportunity to study interesting questions that are both fundamental to biology and also of significance to our society. After graduate school, I worked first as a post-doctoral fellow and then as a Research Assistant Professor to determine the role of the interferon-inducible, dsRNA-activated protein kinase PKR in tumorigenesis. In 2016 I had the opportunity to join the Licht laboratory to study the role of chromatin dynamics in cancer. Now I am working on a project to characterize how mutations in the core of histone H2B may disrupt nucleosome structure causing changes in gene expression that drive the tumorigenic phenotype. In addition, I am working to identify how an activating mutation in the histone lysine methyltransferase NSD2, found frequently in relapse of ALL, alters its methyltransferase activity to dysregulate histone marks, chromatin accessibility and gene expression.
Heidi Casellas Roman
I became interested in molecular biology and biochemistry during my undergraduate studies where I also performed biochemical experiments with applications to drug development. I then performed epidemiological research at Johns Hopkins School of Public Health related to aging and age-related diseases. Through my work here, I realized that I wanted to become a physician to work directly with patients and help relieve their ailments and thus I entered medical school. During medical training, I had the privilege to work with pediatric oncology physicians who guided my interest in this rapidly evolving field with the ability to make strong bonds with patients and their families during a challenging period. I joined University of Florida to start my training in pediatric hematology oncology after completing residency in Pediatrics. I am currently completing my fellowship in pediatric hematology oncology with specific interest in improving outcomes of pediatric high-risk leukemia and lymphoma. I was very fortunate to be able to join Dr. Licht’s lab in July, 2020 to learn more about the role of epigenetics in childhood cancers. My current project is to understand the role of activating mutation of histone lysine methyltransferase NSD2 found in relapsed acute lymphoblastic leukemia in modulating signaling cascades. By understanding this relationship between epigenetic and cellular signaling, I hope to be able to contribute to the development of novel therapeutic approaches.
Daphné Dupéré-Richer, PhD
Ashley is Dr. Licht’s administrative assistant.
I joined the Licht Laboratory in July 2017, after a postdoctoral fellowship in the Department of Biochemistry and Molecular Biology, University of Miami Miller School of Medicine during which I worked on epigenetic effects on myeloid malignancies. My current research is focused on studying NSD2 mutations relevant to pediatric ALL and multiple myeloma. I am working to explore how the NSD2-E1099K mutation affects B cell development and the pathogenesis of ALL. Meanwhile, I am also working on the chemoresistance mechanism with NSD2 mutation in this system. Hopefully, these projects will provide more evidence for improving the clinical therapeutic strategies in ALL with NSD2 mutation.
I joined the Licht lab as a graduate student in May of 2018. I received my Bachelor’s Degree from the University of Miami in 2017, where I researched the individual contributions of Retinoic Acid Receptors Alpha & Gamma towards spatial development of the hindbrain in zebrafish embryos. My first project in the Licht lab has been investigating the effects of the H2B E76K mutation, a mutation prevalent in many lung, bladder, and breast cancers. Due to its position, the mutation may be impacting nucleosome structure leading to differences in sensitivity to DNA damage & DNA binding elements. My second project is regarding KMT2C, a histone 3 lysine 4 (H3K4) methyltransferase, and how it can regulate the genome-wide enhancer landscape & higher-order chromatin structure in a hematopoietic background.
Alberto Riva, PhD
I am the Scientific Director of the Bioinformatics Core of the UF Interdisciplinary Center for Biotechnology Research (ICBR). I am a specialist in the development and application of bioinformatics software, in particular in high-performance computing settings. I am responsible for the analysis of Next-Gen Sequencing data produced by the Licht Lab for applications such as RNA-Seq, ChIP-Seq, ATAC-Seq, methylation analysis, and more.
I earned my Ph.D. from the Chinese Academy of Sciences by studying the biochemical and biophysical mechanisms of photosynthesis. I moved in the United States and studied the protein structure and function as a post-doctoral fellow in Kansas State University. Later I joined the Dr. Thomas Yang’s Laboratory in the Dept. of Biochemistry and Molecular Biology (UF College of Medicine), studied the genetic and epigenetic molecular mechanisms of mammalian gene imprinting. To continue my endeavor in the study of the molecular mechanism that control mammalian gene expression I then joined Dr. Michael S. Kilberg’s Laboratory at UF.
I became a member of Dr. Licht’s laboratory on August 1st, 2020. Now I am studying the potential oncogenic functions of histone mutations.
I joined the Licht lab as a postdoctoral associate in May 2018 after I obtained a PhD in Comparative Biochemistry from the University of California, Berkeley. My graduate research focused on the use of functional genomics tools, including genome-wide CRISPR screens, to study cellular mechanisms of toxicant susceptibility as well as nutrient uptake. My current research involves identifying synthetic lethal targets associated with the histone lysine methyltransferase NSD2 overexpression in multiple myeloma (MM) and NSD2 gain-of-function point mutation in B-cell acute lymphoblastic leukemia (B-ALL). I am also investigating NSD2-driven mechanisms of chemotherapy resistance in MM and B-ALL using CRISPR-based genetic screens. The ultimate goal of this work is to identify therapeutic targets in blood malignancies with increased NSD2 activity, where the response to classical chemotherapeutic strategies is minimal.