Damon Runyon News

One of the leading causes of death from cancer is metastasis, or when cancer spreads from its original tissue to other parts of the body. A gene that all humans carry, called Apolipoprotein E (APOE), plays a role in how our bodies respond to cancer, including risk of metastasis. The gene comes in one of three forms: APOE2, APOE3, or APOE4. Individuals who carry APOE2 tend to fare worse when diagnosed with melanoma, while those who carry APOE4 tend to have a much lower risk of melanoma metastasis and a much better chance of survival. (Those who carry APOE3 fall somewhere in between.) Dr.

Acute myeloid leukemia (AML) is the most common acute leukemia in adults. Intensive chemotherapy cures only a subset of patients, and immunotherapy has had limited success in AML. One novel approach is chimeric antigen receptor (CAR) T cell therapy, which involves genetically engineering a patient's own immune cells to target cancer cells. The difficulty with this approach is that the majority of available targets present on AML cells also reside on many normal cells. Based on emerging data demonstrating overexpression of the gene CD70 in AML cells compared to normal tissues, Dr.

Acute myeloid leukemia (AML) with rearrangements of the KMT2A gene (KMT2A-r) or NPM1 mutation (NPM1m) affect children and adults and can be difficult to treat even with highly intensive therapy. Targeted, less toxic therapies are urgently needed. Menin inhibitors are novel small molecules that block a critical interaction between the KMT2A protein and another protein called menin. This protein-protein interaction is essential in sustaining both KMT2A-r and NPM1m AML. Menin inhibitors have now entered clinical trials for children and adults have shown promising results.

Every cell contains specialized compartments called organelles that perform distinct functions, and cells employ counting mechanisms to finely tune organelle population. Centrioles are one type of organelle required for proper cell division and mammalian development. Cells normally contain two or four centrioles, depending on cell cycle state, and centriole gains or losses result in cancer. One exception to this rule are the cells that line our airways, brain ventricles, and reproductive tracts.

Many immunotherapy strategies require patient T cells to recognize specific cancer-associated antigens. However, it is unclear what these antigens are and how they contribute to tumor shrinkage during treatment. Dr. Zhu [HHMI Fellow] will use large-scale antigen screening methods to identify cancer-associated antigens recognized by T cells that are activated in breast cancer patients during immunotherapy treatment.

Cells living in aggregates can perform more complex tasks than individual cells, but they also face key challenges as they have less access to space and nutrients. Tumors, like the healthy tissues they disrupt, must balance these physical forces and effectively distribute metabolites to continue to grow. Dr. Klumpe [Merck Fellow] will use yeast as a simplified model of cell aggregation to engineer diverse aggregates and observe their growth and maintenance over many generations.

The astonishing diversity of T cells makes finding ones that specifically target tumor cells but not host cells a major challenge in developing T cell immunotherapies. For this reason, the adoption of T cell immunotherapies in clinical settings has been slow despite their remarkable potential. Dr. Lashkaripour is developing a microfluidic platform capable of screening millions of T cells against millions of tumor antigens per day to identify the stimulatory pairs that drive an efficient immune response.

Extrachromosomal DNA (ecDNA), or DNA not attached to a chromosome, has been found in nearly half of human cancer types, especially in aggressive cancers such as glioblastoma, neuroblastoma, leukemia, lung, and ovarian cancer. Despite being a potent cancer driver, the mechanisms underlying ecDNA regulation remain largely unexplored. Combining both advanced imaging and cutting-edge sequencing technologies, Dr.

Lung cancer remains the leading cause of cancer mortality.

An organism’s life experiences, such as exposure to bacterial pathogens, can cause sustained changes in its physiology and behavior. How these experiences are encoded in heritable RNA and DNA-associated proteins (called chromatin), and how these in turn affect the physiology of the organism itself and its progeny, are not well understood. Previous research has shown that the roundworm C.