Targeting DNA damage repair to eradicate leukemia  
The Skorski lab studies how blood cancers like leukemia fix their cells’ damaged DNA. We aim to learn how to stop that repair process to kill cancer cells that are “clones” of each other. 

We start by analyzing an individual patient’s cancer cells using single-cell DNA sequencing. We want to identify cells that have the same specific weak points for repairing their DNA. That lets us develop ways to kill these cancer cells. By taking what we call the “Star Wars against leukemia: attacking the clones” approach, we believe we’ll develop a novel and individualized way to cure this cancer. 

The role of the bone marrow microenvironment in Acute Myeloid Leukemia (AML).  
The Abdul-Aziz lab studies how aging in bone marrow cells affects AML in adults. 

We use patient cancer cells and lab tests to look at how aging — both natural and caused by leukemia — changes bone marrow. These changes can affect important cells that support the immune system and help the body fight disease.  

We also study how targeted leukemia treatments affect these marrow cells. Sometimes these changes help cancer cells survive treatment or come back later. By learning how this happens, our lab hopes to find new ways to stop treatment resistance and prevent the cancer from returning.  

Cancer and Developmental Epigenetics.  
The Ghosh lab studies how genetics and environmental factors help turn genes on or off (“epigenetics”). They look at how these changes can keep us healthy or lead to diseases. 

One focus is Cancer epigenetics. We are working to identify a biomarker that could help doctors find and predict the progress of colorectal cancer. 

Developmental epigenetics is our other focus. We study how fertility treatments (like IVF) and the environment might cause changes in gene control during early embryo development. These changes could lead to long-term health problems.  

Our overall goal is to figure out how both genetics and environmental factors affect cancer and human development and find better ways to prevent or treat diseases. 

Cell cycle control in mammalian cells and its deregulation in cancer.  
The Graña lab focuses on how cells grow and divide and what happens when this process goes wrong in cancer.  

Healthy cells have a “cell cycle” system that tells them when to grow, copy their DNA, and divide. Our researchers study the molecular signaling that controls cell cycle gene expression and checkpoint integrity. Specific proteins that help control this process include key cyclins, cyclin dependent kinases (CDKs), and Ser/Thr protein phosphatases (PP2A). Tumor suppressor genes, such as the retinoblastoma protein family, keep things in check.  

Normal cells carefully regulate this process to prevent damage to their DNA and allow for its repair. However, proteins often function abnormally in cancer. Understanding these processes could lead to novel treatments that target the root causes of cancer at the molecular level. 

Epigenetic therapies for ovarian cancer.  
Epithelial ovarian cancer (EOC) causes more deaths than any other gynecological cancer. The standard treatment is chemotherapy, but survival rates are low. That’s because the cancer rapidly becomes resistant to chemotherapy. 

Epigenetics — how genes are turned on and off — may cause cancer cells to grow and become resistant to treatment. Our goal is to identify new treatments targeting epigenetic factors that help improve survival for EOC patients. 

HIV-mediated dysfunction of the human brain.
Our group studies how HIV-1, the virus that causes AIDS, can harm the brain. One focus is on lysosomes — parts of the cell that break down and recycle waste. When someone is infected with HIV-1, these lysosomes don’t work the way they should. This can lead to nerve cell damage and brain problems, a condition known as neurodegeneration.

We also study how cells control the movement and function of lysosomes. By learning how these systems break down during HIV infection, we hope to discover new ways to treat or prevent brain-related problems caused by the virus.  

Learn more about our lab.

Molecular Mechanisms of Neurodegenerative Diseases and Therapeutic Strategies.
Our lab focuses on two major areas:

Premature brain aging: We investigate how two HIV-encoded viral proteins (Tat and gp120) may cause the brain to age faster. This can lead to memory problems and other thinking issues. We look at how these proteins affect the brain’s energy use, inflammation, and how brain cells talk to each other. Our goal is to link between HIV-related brain changes and other neurodegenerative diseases. 

New cancer treatments: We’re also working on better therapies for hard-to-treat diseases like triple-negative breast, pancreatic, and ovarian cancers. We’ve already found a small molecule that may help shrink these aggressive cancers. We hope our additional research will pave the way for new strategies to help patients in the future. 

Novel therapeutic regimens for small cell lung cancer.  
The Schultz lab focuses on developing better treatments for small cell lung cancer (SCLC), a fast-growing and hard-to-treat form of lung cancer.  
 
Our lab focuses on how these cancer cells grow and survive, how they move through a key phase in the cell cycle (called the G1/S transition) and how they rely on energy from their mitochondria. Our goal is to generate new clinical trials using these insights. 
 
We also test new drug combinations that might work better than alone. One idea we’re studying is “Population Synergy.” That means not just targeting cancer cells but also the nearby healthy cells that they closely interact with. 

Mechanisms of chemoresistance in leukemia.
The Small laboratory studies why chemotherapy stops working in blood cancers, especially in  Acute Myeloid Leukemia (AML).

We focus on a protein called schlafen 11 (SLFN11). This protein helps cancer cells die when they are treated with chemotherapy that damages their DNA. But when cancer cells don’t have SLFN11, they can survive treatment and the cancer keeps growing.

Our goal is to exploit this biology to improve personalized treatment for AML. 

Mechanisms of esophagus homeostasis in health and disease.  

The Whelan lab studies how the esophagus stays healthy and balanced (homeostasis) — and what happens when things go wrong. 

We want to understand how the body keeps the esophagus working properly and what causes it to become damaged or diseased. Problems in the esophagus can lead to pain, trouble swallowing, and more serious health issues.

By learning more about how these problems start, we hope to find new and better ways to treat people with esophageal diseases. Our goal is to help patients feel better and have a better quality of life. 

Novel Molecular Mechanisms of Melanoma Genesis, Progression, and Metastasis.  
We know that too much ultraviolet (UV) radiation from the sun is a major risk factor for melanoma, a serious type of skin cancer. UV rays can damage DNA in skin cells, which may lead to cancer over time. 

But the process isn’t simple. While UV rays cause mutations, new research shows that these changes alone may not fully explain how melanoma starts. Other changes in the body — ones that don’t involve DNA mutations — seem to play a big role.  

Because the answer remains elusive, we are studying which factors play a role and which don’t.  

Our lab’s goal is to clarify what causes skin cancers to start. Our discoveries will help develop new preventative measures, identify biomarkers and create novel melanoma therapies.