The Borriello Lab studies how disseminated tumor cells (DTCs) – single cells that have spread from a primary tumor to new locations - survive in a dormant state and what causes them to “awaken” and form metastases. Since most cancer deaths result from metastatic relapse, and there are no drugs to eliminate dormant cells, our goal is to uncover how the tumor microenvironment controls dormancy and awakening. 

We use advanced imaging, organotypic cultures, and in vivo models to identify the signals and cell types that regulate these processes. Our research focuses on two key questions: how the primary tumor environment programs cells to become dormant, and how stromal factors—especially those from fibroblasts—reactivate them in distant organs. 

By revealing these mechanisms, we aim to develop therapies that prevent metastatic recurrence by eradicating or permanently silencing dormant tumor cells. 

The Golemis laboratory focuses on understanding factors contributing to the basis for aggressive tumor growth, and on evaluation of protein-targeted drugs, frequently collaborating with medical and radiation oncologists. To address these topics, the group uses bioinformatic analysis of very large genomic datasets to identify specific genetic features associated with specific patterns of therapeutic response in head and neck, lung, pancreatic and colorectal cancers. We integrate this work with use of animal models and cell-based strategies to elucidate the activity of signaling proteins and targeted therapies. We are particularly interested in investigating the Aurora-A kinase signaling axis in cancer and other pathological conditions.

Peripheral neuropathy and chronic pain are a common side effect of chemotherapy treatment for which there are no available treatments. 

Our group aims to understand how neurons are damaged in response to chemotherapy. However, our research is widely applicable to other neurodegenerative conditions such as glaucoma, traumatic brain injury (TBI) or Amyotrophic Lateral Sclerosis (ALS). 

To do this, we employ a wide range of molecular and biochemical techniques, including differentiation of induced pluripotent stem cells (iPSCs) into human neurons, whole genome CRISPR interference screens, RNAseq, CRISPR knock-ins/ knock-outs, and advanced microscopy. 

The lab has a strong clinical focus. We are deeply interested in uncovering new molecular mechanisms that drive axon degeneration and neuron death to develop novel therapeutic strategies.  

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. We are exploring the cellular function of approved drugs that target these processes, to potentially allow repurposing of existing agents for use in cancer.  

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.  

Our goal is to generate new clinical trials using these insights.

Our laboratory studies how cancer cells keep their DNA stable when it is under stress—either from within the cell, or from outside sources such as radiation or chemotherapy. 

We investigate how the packaging of DNA inside the nucleus and certain chemical changes on proteins help cancer cells manage DNA damage and continue growing at the same time. By using powerful tools like quantitative imaging, genomics, and protein analysis, we aim to find new players, mechanisms, and pathways that protect the genome. 

Our long-term goal is to use these discoveries to guide the development of better treatments for cancers marked by inherently high DNA damage and replication stress. 

Our laboratory studies non-small cell lung cancer (NSCLC), and head and neck squamous cell carcinoma.  Standard treatments for these two cancers include chemoradiotherapy, often combined with immunotherapy.  A subset of patients also benefits from targeted therapies, which specifically “target” cancer cells and are generally less toxic than conventional chemotherapy.  However, despite advances in these treatments, long-term benefit remains poor due to limited treatment efficacy or the emergence of therapy resistance. 

Our research focuses on protein kinases, which represent one of the most promising avenues for targeted therapy development.  We investigate how specific protein kinases drive cancer cell growth and survival.  We also study the role of these protein kinases in cellular state changes (plasticity) and the interactions of cancer cells with their surrounding microenvironment, which enable cancer cells to adapt and resist treatment. 

Our goal is to identify new molecular targets that support cancer cell survival and plasticity to aid in the development of targeted therapy strategies to improve outcomes and quality of life for patients with lung and head and neck cancers.