Damon Runyon News

Dr. Miller is investigating how cells ensure the correct partitioning of genetic material during cell division. Errors in this process occur in nearly all tumor cells and are the leading cause of miscarriages and congenital birth defects in humans. The vast majority of solid tumors have incorrectly positioned chromosomes, causing high levels of genomic instability and DNA damage. Very little is known about how chromosome segregation becomes so defective during tumorigenesis.

The understanding of the mechanisms by which specific types of immune cells detect and attack tumor cells has enabled the development of promising cancer immunotherapies. Recently, researchers have discovered the important roles of immune cells called macrophages in the surveillance and elimination of tumor cells. Dr. Feng focuses on understanding how cancer cells protect themselves and evade macrophages, and how macrophages recognize cancer cells and target them for elimination.

Dr. Bar-Peled studies how cancer cells adapt to stress environments, focusing on oxidative stress.  His research focuses on understanding how cells sense and respond to specific changes in their environment by activating singling pathways that lead to uncontrolled growth.  He recently studied a particular pathway in non-small cell lung cancer and identified a “druggable” protein that could be targeted with small molecules and disrupt this uncontrolled growth.

Dr. Naik focuses on the fundamentally important interactions between the immune system, microbes, and adult skin tissue stem cells, and the consequences of such interactions for health and disease.  She studies how stem cells in epithelial tissues such as the skin sense and cope with inflammatory stress.  Her goal is to understand how inflammatory signals (either host-generated or microbial) provide adult stem cells with rapid, sensitive, and context-specific information, and how this process can go awry, potentially predisposing stem cells to diseases such as cancer.

The goal of this research is to increase our understanding of the integral membrane protein quality control systems. These systems are involved in regulation of proteins in different cellular organelles. One of these systems, called endoplasmic reticulum associated degradation (ERAD), plays a central role in many cancer processes by regulating the levels of proteins involved in tumor growth and metastasis. A common feature of all types of cancer is survival during unfavorable conditions that would trigger apoptosis in normal cells.

Eukaryotic cells develop sophisticated mechanisms to package and access our genetic information. Recent studies have shown that proteins involved in genome regulation are frequently altered in human cancers. These findings agree with laboratory observations that cancer cells often display abnormal nuclear architecture, and raise the questions of whether, and how, aberrant chromatin organization facilitates tumor development. Collectively, Dr.

The telomerase enzyme adds repetitive DNA sequences to the ends of human chromosomes, assuring genome integrity and providing unlimited proliferative potential to continuously dividing cells. Importantly, 90% of all cancers require telomerase activity for their survival. Mutations that activate the expression of telomerase reverse transcriptase (TERT), the major protein subunit of telomerase, are the most frequent mutations in a number cancers and are strongly correlated with poor clinical outcomes for patients carrying them.

Immunotherapy is revolutionizing the clinical management of a variety of cancers, including hepatocellular carcinoma (HCC), a type of liver cancer that shows little response to conventional therapeutic approaches. Recently, two immune checkpoint inhibitors, nivolumab (Opdivo) and pembrolizumab (Keytruda), have been approved as second line therapy after showing unprecedented complete responses in clinical trials.

Inactivation of the Retinoblastoma 1 (RB) tumor-suppressor gene is a hallmark of cancer. Loss of RB function results in the transcription of genes required for cell growth but surprisingly also cell death. Profiling of RB-deficient cells showed that these cell death mRNAs are induced but not made into protein. Dr. Miles aims to identify the factors that block the production of cell death proteins and determine which of these factors prevent RB-lacking cancer cells from dying.

Targeted cancer therapies that interfere with specific molecules involved in the growth, progression and spread of cancer have been successful in cancer treatment in recent years. However, many known cancer-driving proteins are recalcitrant to the development of traditional small molecule inhibitors.  To address this problem in drug development, researchers are developing "degraders," small molecules that direct cancer-causing proteins to the cellular waste disposal system - the ubiquitin proteasome system - to eliminate them from the cell.