Sponsored by the biology department and the Michael J. Wolk Foundation, Alea Mills, a professor at Cold Spring Harbor Laboratory, presented “A New Epigenetic Fix for Brain Cancer” on Friday, April 11. Mills shared her work in two parts: first, her journey of scientific discovery, and second, the breakthrough her team made in addressing brain cancer.
She began by explaining how she fell in love with science and research. Growing up with four brothers on a farm near Colgate University in Hamilton, she was raised to be adventurous. Mills expressed how her mother and her familial experiences influenced her life trajectory.
“[My mother] instilled the notion of asking questions to challenge the dogma, if you will, from a young age. Growing up, I was encouraged and allowed to explore, and having the freedom and access to nature and the outside was great. These were really great principles growing up,” Mills said.
Mills’ curiosity and drive led her from Hamilton Central School to San Jose State University for her undergraduate studies, and eventually to the University of California, Irvine, where she earned her Ph.D. From there, she pursued postdoctoral research at Baylor College of Medicine, diving into chromosome engineering — manipulating genetic structures through deletions, duplications and inversions. This work laid the foundation for some of her most important contributions to cancer biology and developmental genetics.
One of her early breakthroughs came with the discovery of the gene p63, a cousin of the well-known tumor suppressor p53. While p53 is known for its role in protecting cells from becoming cancerous, Mills’ research revealed that p63 is crucial for development, especially in skin and limb formation. In experiments where mice were engineered without p63, they were born without skin, hair or functional limbs, mirroring symptoms in children with a rare genetic disorder known as EEC syndrome.
Mills then shifted her talk to focus on her most recent work — tackling glioblastoma, the most common form of adult brain cancer. Despite the presence of functional p53 in many glioblastoma cases, the tumor still manages to evade its suppressive effects. Mills’ team discovered that a protein called BRD8 plays a key role in locking down chromatin — a form of tightly packed DNA — effectively silencing p53’s tumor-fighting capabilities.
“BRD8 is like glioblastoma’s Achilles’ heel,” Mills explained.
By targeting the BRD8 protein, her team was able to reawaken p53, restoring its ability to control the cell cycle and suppress tumor growth. First-year Magnus Larson shared his thoughts on the lecture.
“These talks are great for learning about the current status of research across the country. Knowing about BRD8 and its connection to p53 is relevant to my current biology work, but I also found the talk personally interesting and informative to keep me knowledgeable about what’s happening in the science world today,” Larson said.
Mills concluded her lecture by emphasizing her lab’s current goals: mapping the atomic structure of BRD8, developing compounds that can disable it, and testing these treatments using patient-derived organoids.
First-year Katie Jabaut found the talk particularly interesting.
“It is huge that some of the genetics behind what causes cancer have been identified and that methods to prevent the mutations that lead to cancer, such as those that occur in the p63 gene, are being explored,” Jabaut said. “It really struck me how modern technology allows us to alter the DNA within cells or to turn the expression of some genes on and off to combat such a deadly disease.”
