Richard Bennett, Ph.D., is a research associate professor in the division of hematology & oncology, department of medicine, in the University of Florida College of Medicine.
Dr. Bennett first became interested in molecular and cellular biology as an undergraduate at Kalamazoo College. Later, as a graduate student at Weill Cornell Graduate School of Medical Sciences, he decided to devote his career to researching the molecular basis of cancer. This provided him with the opportunity to study interesting questions that are fundamental to biology and also of significance to our society.
After graduate school, he worked first as a postdoctoral 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, he had the opportunity to join the research group of Jonathan Licht, M.D., director of the Cancer Center, to study the role of chromatin dynamics in cancer.
His projects in the Licht lab include characterizing how histone mutations that disrupt nucleosome structure may cause changes in gene expression that drive the tumorigenic phenotype, analyzing the mechanism by which an activating mutation of the histone methyltransferase NSD2 dysregulates the chromatin landscape to drive myeloma or ALL, and identifying new genetic vulnerabilities in uveal melanoma.
What are your current research interests and/or what is a project you are currently working on?
One of the most common classes of genes mutated in human cancers are those that affect epigenetic regulation of gene expression. Epigenetic mechanisms are those that alter cell fate and function by regulating patterns of gene expression without altering the primary DNA sequence of the gene. One fundamental way that gene expression is regulated centers on how tightly or loosely DNA is packaged around histone proteins. My primary research focus has been to characterize how histone mutations that are frequently found in lung cancer patient samples may disrupt the interaction between histones or DNA, which causes aberrant gene expression and the development of cancer phenotypes. In addition, I am working on another project to characterize the epigenetic mechanisms that are responsible for the growth of uveal (eye) melanoma cells and their resistance to chemotherapy.
Who or what has inspired you to pursue this career?
As an undergraduate, I fell in love with cell biology, molecular biology and biochemistry. I found it fascinating that a cell has this complicated web of protein interactions that depend on one another and govern how the cell grows, divides and develops into other cell types. Figuring out how cells work and how they become cancerous is like working on a giant jigsaw puzzle. Every time something new is discovered, we are adding another piece to the puzzle. Of course, the science jigsaw puzzle does not have a picture on top of the box; we are figuring out what the puzzle looks like as we solve it. While this is challenging, it is also part of the fun since it is very rewarding to add another piece to the puzzle.
Why did you decide to focus on cancer?
Like many cancer researchers, some of my close family members have succumbed to cancer. Working to better understand how cancer develops and hopefully identifying new strategies to cure cancer has provided me with the opportunity to study interesting questions that are both fundamental to biology and also significant to our society.
What do you want to achieve with your work and/or in your career?
I hope to make a few important contributions that forward our understanding of cancer and lead to new anti-cancer therapies.
What excites you about your work? What is exciting to you about your field right now?
There is a particular joy to discovering something new that no has ever known before. I’ve been a cancer researcher for about 20 years, and I think we are at a very exciting point for cancer research where new discoveries are coming more rapidly than ever before. New sequencing technologies have given us the ability to pinpoint how cancer mutations change gene expression, chromatin accessibility, interactions between protein and DNA and the 3D structure of the genome. New therapies are emerging such as those that activate the immune system to recognize and destroy cancerous cells. Also, in the past few years a new global emphasis has been placed on experimental rigor and reproducibility that has improved the quality of cancer research.
What do you like to do outside of work?
Outside of lab I am kept busy by serving as the scoutmaster for Boy Scouts of America Troop 21 for girls and Troop 125 for boys. Through Scouts I have had the opportunity to sail the Florida Keys, canoe the wilderness parks of Canada and backpack the mountains of New Mexico with my Scouts. While I love all the outdoor activities such as camping, hiking, and water sports that we regularly do, the true joy of these positions is watching the youth that I mentor learn to become the self-reliant, problem-solving leaders of tomorrow.