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Dr. Einav is focusing on how the human immune system, with its millions of different antibodies, protects us against a range of assaults from pathogens such as influenza to rapidly evolving cancers. Recently, researchers have designed antibodies to help the body fight cancer, infection and other diseases. These efforts have only begun to tap into the potential of developing antibody mixtures. By understanding the collective action of multiple antibodies, this research will investigate how the immune repertoire can be bolstered to better combat diseases.
Dr. Yin has developed single-cell assays that will be combined with statistical modeling to understand homologous recombination (HR). Cells use the process of HR to accurately repair harmful breaks that occur on both strands of DNA. Failure to correct such DNA damage can play a role in cancer initiation and progression. Dr. Yin aims to understand this critical mechanism to help guide treatment approaches for many cancer types.
Our DNA is constantly subjected to damage, and our cells must repair this damage to ensure survival. Breaks in DNA that completely sever DNA molecules are particularly toxic, and failure to repair these breaks can lead to genetic alterations that drive cancer initiation and progression. Dr. Stinson studies the two main cellular pathways that repair these DNA breaks: non-homologous end joining (NHEJ) and homologous recombination (HR). Defects in these pathways are linked to predisposition to many cancers, including leukemia, breast, ovarian, and prostate cancers.
Dr. Case is investigating the mechanisms that regulate focal adhesion formation, growth, physical properties and subsequent downstream signaling. Focal adhesions are large protein complexes that connect the cell cytoskeleton to the extracellular membrane, which is the connective material holding cells in place. She is using a unique in vitro system in parallel with live cell imaging and cellular perturbations to dissect the specific molecular interactions that contribute to integrin signaling and focal adhesion function. Dr.
Cancer survivors are at a higher risk of developing blood cancers than the general population due to the toxic effects of cancer treatments. Therapy-related blood cancers are often resistant to existing drugs and therefore extremely challenging to treat. Contrary to previous thought, recent studies show that the mutations causing these blood cancers can be identified in patients' blood many years before they receive therapy. Dr.
Oxygen is a double-edged sword in pancreatic cancer biology. Pancreatic cancers require oxygen, but they are amongst the most hypoxic of cancers, with oxygen concentrations as low as 200-fold below atmospheric oxygen concentrations. Pancreatic cancers use oxygen to make molecules critical for their survival and proliferation, but they are also vulnerable to oxidative stress, which is essential for the effectiveness of cancer treatments such as radiation. Dr.
DNA methyltransferase enzymes, responsible for adding methyl groups to DNA strands, are critical for controlling gene expression. These enzymes are often disrupted in cancers, including acute myeloid leukemia (AML), but their regulation is not understood. One form of enzyme regulation, called allostery, involves a regulator molecule binding to an enzyme at a site other than its active site. Dr. Liau is pioneering approaches to explore allostery, specifically focusing on allosteric mechanisms that regulate DNA methyltransferase function.
One of the unique features of liver cancer is the way in which it obtains and uses different forms of energy, especially fats. Drs. Evason and Ducker found that a certain type of fat (phosphatidylcholine lipids) is elevated in both zebrafish and human liver cancer cells. They are using zebrafish, which form tumors similar to the human disease and can be easily manipulated to study liver cancer. The goal of this project is to determine why phosphatidylcholine lipid levels are higher in liver cancer and how they might be targeted with drugs to prevent or cure this disease.
One of the unique features of liver cancer is the way in which it obtains and uses different forms of energy, especially fats. Drs. Evason and Ducker found that a certain type of fat (phosphatidylcholine lipids) is elevated in both zebrafish and human liver cancer cells. They are using zebrafish, which form tumors similar to the human disease and can be easily manipulated to study liver cancer. The goal of this project is to determine why phosphatidylcholine lipid levels are higher in liver cancer and how they might be targeted with drugs to prevent or cure this disease.
Immunotherapies that rely on reinvigorating T cells to patrol the body, detect cancerous cells, and eliminate them have shown the potential for long-lasting cures. Despite their initial success, however, immunotherapies have been effective only for some cancers and for some patients. To improve outcomes, Dr. Birnbaum has developed a new method to match T cells with their antigen targets on cancer cells by engineering viruses to use T cell recognition as a means of cell entry.