Damon Runyon News

There are two key types of cancerous mutations: one that turns on growth signals too strongly, like a car with a stuck accelerator, and the other that turns off safety mechanisms, like a car with broken brakes. While some cancers can be treated with drugs that block overactive growth signals—such as Gleevec for chronic myeloid leukemia—there are currently no effective treatments for cancers caused by the loss of these safety mechanisms, also known as tumor suppressor genes.

Dr. Thawani studies how so-called “selfish DNA” elements copy and paste themselves within the human genome. Using advanced methods such as cryo-electron microscopy to reveal the atomic structures of various molecules associated with these selfish elements, she aims to delineate their mechanism of mobility. She is also interested in understanding how selfish DNA elements are recognized and silenced within the human genome. Dr.

Dr. Liu’s research focuses on discovering new drug candidates to treat pancreatic, colorectal, breast, and prostate cancers. Using advanced computational techniques to screen billions of chemical compounds, she aims to identify and develop highly specific molecules that target critical pathways in cancer cells while sparing healthy tissues. For example, she has uncovered compounds that modulate calcium-sensing receptors, which play a role in certain cancers, with reduced side effects compared to the current standard-of-care.

Dr. Gu’s lab studies how cells regulate the destruction of proteins without using the typical "ubiquitin" tag, which signals that a protein should be transported to the proteasome for digestion and recycling of amino acids. The lab has discovered a new pathway, the midnolin-proteasome pathway, that helps degrade key proteins involved in cancer, including several linked to blood cancers like multiple myeloma.

Cells must communicate with each other to maintain homeostasis and respond to external stimuli. This communication typically occurs through chemical signals or via direct physical contact. Dr. Fang plans to develop genomic tools to understand how different types of cells communicate with each other in the healthy brain and how communication goes awry in brain tumors.

Dr. Chen’s research aims to harness a common skin-colonizing bacterium, present on all our skin, to train the immune system to attack cancer without causing infection or inflammation. This process is known to occur—notably, across an intact skin barrier—but its mechanism is not well understood. Dr. Chen is investigating which skin cells sense these bacteria and transmit the signal to immune cells, and why the immune cells that respond are so effective at killing cancer.

Cancer cachexia, characterized by progressive muscle wasting and weight loss in cancer patients, is a common and multifaceted syndrome that negatively impacts patient quality of life. Cachexia has no available treatments to date, due to insufficient knowledge about the underlying mechanisms. Cachexia is particularly prominent in pancreatic cancer patients.

Emerging evidence underscores the profound impact of the gut microbiome, a collection of microorganisms within our digestive system, on cancer. These microorganisms collectively generate various metabolites that can significantly influence cancer progression and treatment outcomes. Dr. Zeng is employing synthetic communities and mouse cancer models to delve into the intricate connections between cancer and the microbiome.

Ependymomas (EPN) are aggressive brain and spinal cord tumors that are especially difficult to treat in children and often come back after treatment. Recent research has shown that interactions between tumor cells and healthy neurons play a key role in EPN growth. It is not well understood, however, how exactly neurons contribute to this process. By mapping the neuronal environment and exploring the different types of neurons involved, Dr. Zheng hopes to uncover the mechanisms that drive EPN growth and find new ways to treat these tumors. Dr.

Hematopoietic stem cells, which are found in the bone marrow and give rise to all other blood cells, maintain lifelong blood production and immune function. Due to their remarkable ability to regenerate the entire blood system, medical uses of HSCs have provided cures for many previously incurable diseases, including blood cancers. However, several unanswered questions limit our ability to full harness their therapeutic potential for cancer treatment. What regulates HSC regeneration? Why does their function decline with age? How does HSC behavior vary in healthy individuals?