The Cancer Genetics Program is focused on revealing the structure and landscape of cancer genomes. Such information provides insight into how cancer develops, progresses, and responds to therapy. The Program includes a diverse collection of faculty who are developing new technology that is changing how researchers across the globe study cancer. The Program currently has three main focus areas: experimental technology, bioinformatics, and cancer progression.
In the Cancer Genetics Program, research is driven by the desire to innovate, developing new strategies that will allow researchers to rapidly interrogate, analyze, or model cancer risk, tumor development and progression, or cancer therapies. This innovative spirit is bolstered by an interactive environment, with numerous partnerships both within the CSHL Cancer Center and with other collaborators around the world. Research in the Cancer Genetics Program has had a broad impact on the cancer community, providing tools and strategies that facilitate bench research while offering new technologies to better diagnose, monitor, and treat cancer in the clinic.
The Cancer Genetics Program continues to make discoveries that have an impact on our understanding of cancer and on the lives of patients. Members of this program are focused on both the genetics and epigenetics of cancer—studying changes in bulk tissue and, increasingly, in single cells. The Program is also expanding their preclinical and clinical research, taking advantage of the close partnership between CSHL and Northwell Health to explore the genomics of patient samples. In addition, this Program benefits from significant strengths in computational research that have a broad impact on research, from helping to identify driver mutations in cancer population to improving cancer diagnostics in the clinic.
The biological landscape is made up of millions of variables that interact in complex and often seemingly random ways. I am applying principles from physical and computational sciences to the study of biology to find patterns in these interactions, to obtain insight into population genetics, human evolution, and diseases including cancer.
Currently the Director of the Functional Genomics Shared Resource at CSHL. His studies focus on shRNA, microRNA, RNA interference, and siRNA. The lab has studied cancer proliferation gene discovery through functional genomics.
Next generation sequencing technologies revolutionized many areas of genetics and molecular biology, enabling quantitative analyses of the entire genomes and paving the way for Personalized Medicine. We develop novel statistical methods and computational algorithms for multi-omics processing and integration, and leverage Big Genomic Data to elucidate various problems in precision health, such as genetic and epigenetic mechanisms of cancer development and progression, and clinical impact of functional variants.
Of the tens of thousand of protein-coding genes in the human genome, only a small portion have an experimentally defined function. For the rest, how can we determine what they do? My lab develops computational predictions based on co-expression networks. We are applying our predictions to understand neuropsychiatric disorders.
As organisms develop, genes turn on and off with a precise order and timing, much like the order and duration of notes in a song. My group uses model organisms to understand the molecules that control the tempo of development. We also study how changes in the timing of gene expression contribute to diseases like cancer.
Many types of cancer display bewildering intra-tumor heterogeneity on a cellular and molecular level, with aggressive malignant cell populations found alongside normal tissue and infiltrating immune cells. I am developing mathematical and statistical tools to disentangle tumor cell population structure, enabling an earlier and more accurate diagnosis of the disease and better-informed clinical decisions.
Cells are amazingly complex, with the ability to sense, and remember timing, location and history. I am exploring how cells store this information, and how their surroundings influence their communication with other cells. I am also developing various imaging and molecular sequencing methods for tracking genes, molecules, and cells to understand how cancer cells arise and evolve.
We have recently come to appreciate that many unrelated diseases, such as autism, congenital heart disease and cancer, are derived from rare and unique mutations, many of which are not inherited but instead occur spontaneously. I am generating algorithms to analyze massive datasets comprising thousands of affected families to identify disease-causing mutations.
Applies non-invasive imaging methods and develops new imaging reagents to facilitate the use of genetically engineered mouse models of cancer in pre-clinical and basic cancer research. As Director of Animal Imaging, he provides collaborative research support to investigators at both CSHL and neighboring institutions and will an important role in the pre-clinical research facility at CSHL.
Over the last two decades, revolutionary improvements in DNA sequencing technology have made it faster, more accurate, and much cheaper. We are now able to sequence up to 10 trillion DNA letters in just one month. I harness these technological advancements to assemble genomes for a variety of organisms and probe the genetic basis of neurological disorders, including autism and schizophrenia, better understand cancer progression and understand the complex structures of the genomes of higher plants.
Cells employ stringent controls to ensure that genes are turned on and off at the correct time and place. Accurate gene expression relies on several levels of regulation, including how DNA and its associated molecules are packed together. I study the diseases arising from defects in these control systems, such as aging and cancer.
Developing single-cell genomics technologies for applications related to cancer progression, immune surveillance, and discovery of rare novel cell types and transcriptional programs.
Nearly all tumors exhibit a condition known as aneuploidy – their cells contain the wrong number of chromosomes. We’re working to understand how aneuploidy impacts cancer progression, in hopes of developing therapies that can specifically eliminate aneuploid cancers while leaving normal cells unharmed.
I am a computer scientist who is fascinated by the challenge of making sense of vast quantities of genetic data. My research group focuses in particular on questions involving human evolution and transcriptional regulation.
Devastating diseases like cancer and autism can be caused by spontaneous changes to our DNA—mutations first appearing in the child, or in our tissues as we age. We are developing methods to discover these changes in individuals, tumors, and even single cells, to promote early detection and treatments