In the field of Molecular and Cellular Oncology (MCO), cells often arrive frozen to the lab and must be thawed quickly by diluting with culture medium. And so it’s fitting that, on a macro level, molecular oncology researchers themselves arrived frozen to the 2019 MCO Retreat, held Monday at 9:00am and 4 degrees Fahrenheit on the CU Boulder campus, where they were immediately thawed with coffee.

Then things got positively heated.

Throughout the day, researchers from the University of Colorado Cancer Center Molecular and Cellular Oncology Program presented their research to colleagues from Boulder, Anschutz and Colorado State University campuses, detailing advances in the genetic, genomic and epigenetic intricacies that drive cancer.

Andrew Thorburn, PhD, described how inhibiting the cellular process called autophagy may make anti-cancer drugs from chemotherapies to targeted-agents work more efficiently. Ding Xue, PhD, detailed his lab’s work with “bystander effects” due to radiation treatments, explaining the cellular mechanisms by which, “Non-irradiated cells are affected by factors released from irradiated cells.”

Presenting for the Sabrina Spencer Lab, Mingwei Min, PhD, described how mitogen signaling regulates the cell cycle, and how cancer alters the MAPK signaling pathway to increase mitogen signaling that tells cells to proliferate.

Josh Black, PhD, explained his lab’s work with “copy number heterogeneity,” the idea that instead of adjusting a cell’s DNA sequence, some cancers may adjust the pace at which some genes are manufactured into proteins. Rajeev Vibhakar, MD, PhD, talked about the heartbreaking diagnosis of diffuse intrinsic pontine glioma (DIPG), saying that despite decades of work, “DIPG is almost uniformly fatal 11 months after diagnosis.” Being a pediatric tumor, the disease tends to have fewer overall mutations, leaving doctors and researchers fewer drug targets; however, Vibhakar’s work, like Josh Black’s work, shows that “epigenetic” changes may drive the condition, especially molecules that pull apart DNA to make certain, interior genes more readable and thus more replicated.

Karolin Luger, PhD, described the movement of an enzyme called PARP1 that swings through DNA like a child on monkey bars, grabbing onto chromosomes in search of DNA damage, at which point it helps to mark cells with damaged DNA for destruction (unless cancer adjusts its effect).

After lunch, keynote speaker Jan Karlseder, PhD, described the “ticking clock” of telomeres — protective caps at the ends of chromosomes — that shorten as cells replicate, eventually degrading to a point at which cells stop replicating and become senescent…unless cancers rebuilds these telomeres to help cells become immortal. Then Nobel Laureate, Tom Cech, PhD, described the epigenetic changes that induce stem cells to differentiate into tissues; Dylan Taatjes, PhD, spoke at the intersection of stem cells, the immune system, and cancer, describing how CDK8 and CDK19 regulate cells’ use of interferon, which can create a heightened state of immune awareness; and Tatiana Kutateladze, PhD, spoke about how cells read adjustments to the genome that can control the degree to which genes are expressed.

As important as it was to learn updates from the various MCO labs across campuses, equally exciting was discovering how work from these labs overlaps. Questions during presentations became conversations during lunch, which by the end of the day became research collaborations, with researchers sharing ideas, expertise, technology and cell models.

As researchers, it’s easy to stay in silos, head down working to track down the next grant, leading to the next discovery in the line of a lab’s continuing work. Retreats like MCO 2019 explode these silos, injecting these lines of reasoning with new ideas that promise to lead to new understanding and new treatments against the many, complex conditions known as cancer.