Are you really what you eat? Our goal is to uncover the precise mechanisms that link nutrition to organismal health and disease states at the cellular and molecular level. A particular focus in our lab is to understand how dietary perturbations affect the immune system and contribute to the risk of diseases that are associated with immune dysfunction such as cancer.
Cancer cells are surrounded by immune cells, blood vessels, chemical signals and a support matrix – collectively, the tumor microenvironment. Most microenvironments help tumors grow and metastasize, but some can restrict tumors. My lab studies how to target the bad microenvironments and support the good ones to combat cancer.
I’m studying how to harness the power of the immune system to fight cancer. Our underlying premise is that the microenvironment within a tumor suppresses the immune system. We have found a way to eliminate this suppression in the mouse model of pancreatic cancer, which has led to development of a drug for human pancreatic cancer that will enter phase 1 clinical trials in 2015.
With joint appointments at CSHL and Northwell Health, I am working to expand clinical cancer research at our institutions to provide new treatments for patients as well as greater insight into the biology of this complex set of diseases. In my own research, I am collaborating on research in soft-tissue and bone sarcomas to better understand the cancer microenvironment and epigenetics, targeting molecular weaknesses to halt cancer growth.
Our genome can encode hundreds of thousands of different proteins, the molecular machines that do the work that is the basis of life. I use proteomics, a combination of protein chemistry, mass spectrometry and informatics, to identify precisely which proteins are present in cells - cells from different tissues, developmental stages, and disease states.
Two challenges in cancer biology guide my work: first, how do tumors become addicted to certain gene products, and second, how do tumors develop resistance to anti-cancer drugs. I focus on the epidermal growth factor receptor (EGFR), which is both addictive when mutated and a common source of drug resistance. We are also identifying new targets for the treatment of lung cancer.
Cells must constantly react to what is happening around them, adapting to changes in neighboring cells or the environment. I study the signals that cells use to exchange information with their surroundings. Our group is finding drugs that target these signals and thus can treat diabetes, obesity, cancer, and autism spectrum disorders.
We have recently developed the first genetic mouse model for therapy and analysis of metastatic prostate cancer. Now we can test if and how modern concepts of cancer evolution can outperform the 80-year-old standard of care - hormone deprivation therapy - and turn lethal prostate cancer into a curable disease.
Pancreatic cancer is an extremely lethal cancer. On average, patients who are diagnosed with pancreatic cancer succumb to the disease within 6 months. Research is the only way to defeat pancreatic cancer. My lab is making progress toward finding a cure by detecting the disease earlier and designing novel therapeutic approaches.
Normal cell function relies on coordinated communication between all the different parts of the cell. These communication signals control what a cell does, what shape it takes, and how it interacts with other cells. I study these signaling networks to understand how they guard against cancer and neurological disorders.
Studies the creation of engineered biologics such as antibodies, proteins and peptides, for therapeutics and translational medicine. The lab employs protein engineering and chemical biology approaches to develop therapeutic biologics acting on cell signaling machineries in order to abrogate pathological cellular behavior. He is currently the Director of CSHL Cancer Center Antibody Shared Resource- a collaborative resource for high quality antibody development.
I study a type of brain cancer known as malignant glioma, which differs from healthy tissue by a small number of defining characteristics. By forcing glioma cells to adopt these healthy traits, we can stop tumor growth. My group searches for therapeutic ways to force this transition.