University of Arizona Cancer Center research-scientist Gregory C. Rogers, PhD, recently was awarded a five-year, $1.4 million R01 National Institutes of Health (NIH) grant that will support his efforts to reveal new insights into genomic instability, which could lead to new drug targets to combat tumor formation.
His project, “Identifying molecular mechanisms that suppress centriole amplification,” will receive funding on May 1 and will last through 2020.
For the past seven years, Dr. Rogers’ lab has established itself at the forefront of the study of centrosome duplication and the role of the Polo-like kinase 4 (Plk4) pathway in chromosomal instability. When this particular protein is over-expressed, that instability often leads to tumor formation.
“This grant funds a project focused on basic science, where we explore how normal cells work to maintain the integrity of their genomes,” Dr. Rogers said. “Without a fundamental understanding of how normal cells grow, divide and build and organize their organelles, then it is impossible to understand the changes that occur during disease and treat them.”
This is Dr. Rogers’ first R01 grant, and it serves as the culmination of many years of work, publishing a variety of papers in high-impact journals, as well as some well-timed pilot-project funding from the Phoenix Friends of the Arizona Cancer Center.
Dr. Rogers is an associate professor in the UA Department of Cellular and Molecular Medicine and has been a member of the UA Cancer Center Cancer Biology Program since 2008. He is also an associate professor with the UA BIO5 Institute.
Dr. Rogers’ research gained momentum in 2011 with the publication of his article in the Journal of Cell Biology, titled, “The Protein Phosphatase 2A regulatory subunit Twins stabilizes Plk4 to induce centriole amplification,” the first research paper Dr. Rogers published since establishing his own lab at the UA Cancer Center more than six years ago. This paper helped Dr. Rogers land his first major grant in April 2012, from the National Science Foundation, to further his research on the assembly of the centrosome and its influence genomic instability and tumor formation.
In April 2013, Dr. Rogers published another paper in the Journal of Cell Biology, highlighting his laboratory’s groundbreaking work in the field of chromosome territories. His paper, titled, “SCFSlimb ubiquitin ligase suppresses condensin II–mediated nuclear reorganization by degrading Cap-H2,” found that a mutation in the SCFSlimb gene caused cells to have too much condensin II activity, leading to a set of circumstances that may leave a cell vulnerable to diseases such as Progeria (a rare genetic condition that produces rapid aging in children).
Earlier this year, groundbreaking work originating from his laboratory was featured in the Journal of Cell Biology and the Proceedings of the National Academy of Sciences. These papers explored the link between Plk4 and Asterless—two proteins whose mis-regulation drives centriole amplification and potential tumor formation.
This study is supported by grant number 1R01GM110166-01A1 from the National Institutes of Health.
About the University of Arizona Cancer Center
The University of Arizona Cancer Center is the only National Cancer Institute-designated Comprehensive Cancer Center headquartered in Arizona. The UACC is supported by NCI Cancer Center Support Grant No. CA023074. With primary locations at the University of Arizona in Tucson and at St. Joseph’s Hospital and Medical Center in Phoenix, the UA Cancer Center has more than a dozen research and education offices in Phoenix and throughout the state and 300 physician and scientist members work together to prevent and cure cancer. For more information, please go to www.arizonacancercenter.org