Research Menu

image of cancer cellsThe CSHL Cancer Center is a basic research facility committed to exploring the fundamental biology of human cancer. With support from the National Cancer Institute (NCI) since 1987, our researchers have used a focused, multi-disciplinary approach to break new ground in basic tumor biology and develop innovative, advanced technologies. Research covers a broad range of cancer types, including breast, prostate, leukemia, glioma, pancreatic, sarcoma, lung, and melanoma.

Three Scientific Programs provide focus in Gene Regulation & Cell ProliferationSignal Transduction; and Cancer Genetics. In addition, nine Shared Resources offer essential access to technologies, services, and expertise that enhance productivity. With a strong collaborative environment and open communication, the CSHL Cancer Center is able to make breakthroughs in cancer biology that are translating into real progress in cancer diagnostics and treatment.

Members of the CSHL Cancer Center apply a multi-pronged approach—from genomic biology to animal models to detailed biochemistry—to interrogate the molecular mechanisms that drive tumor growth and metastasis. Building on this basic research, scientists at the Lab are translating their findings into novel therapeutics for many of the most intractable cancers. Much of this research is made possible through numerous collaborations with clinical partners, including a strategic alliance with the nearby Northwell Health System that connects CSHL scientists with clinicians and more than 16,000 cancer patients each year.

Senior Leadership

Deputy Director, Shared Resources

Nicholas Tonks, Ph.D.

Deputy Director, Administration

Denise Roberts, Ph.D.

Program Leaders

Cancer Center External Advisory Board

Stephen Burakoff, M.D.
Director of the Mt. Sinai Cancer Institute, Mount Sinai School of Medicine

Lewis Cantley, Ph.D.
Director, Meyer Cancer Center
Weill Cornell Medical College and New York-Presbyterian Hospital

Walter Eckhart, Ph.D.
Department of Molecular & Cell Biology, The Salk Institute for Biological Studies

Richard Hynes, Ph.D.
Department of Biology, Massachusetts Institute of Technology

Larry Norton, M.D.
Deputy Physician-in-Chief, Breast Cancer Programs
Medical Director, Evelyn H. Lauder Breast Center, Memorial Sloan Kettering Cancer Center

Kornelia Polyak, M.D., Ph.D.
Department of Medicine, Medical Oncology, Harvard Medical School and Dana-Farber Cancer Institute

Cindy Quense, M.P.A.
Assistant Director of Administration, The David H. Koch Institute for Integrative Cancer Research

Martine Roussel, Ph.D.
Professor, Department of Genetics and Tumor Cell Biology, St. Jude Children’s Research Hospital


Cold Spring Harbor Laboratory is an NCI-designated Cancer Center. As a basic research institution, CSHL does not treat patients. Information about individual cancers is available at the NCI CancerNet. Questions about CSHL’s cancer research program should be directed to our Public Affairs Department.

Cancer research at CSHL dates back to 1969, which marked the initiation of the DNA tumor virus research program. At this time, researchers realized that understanding the fundamental molecular and cellular biology of eukaryotic cells would provide powerful insight into the processes of oncogenic transformation.

With early success, the program expanded, and in 1971 the Laboratory was awarded a Program Project Grant from the NCI to fund research on DNA tumor viruses. In the early 1980’s, cancer research at CSHL grew to include the study of cellular oncogenes, yeast genetics, and cell growth and cell cycle control. The program was highly productive, with two researchers independently winning the Nobel Prize in Physiology or Medicine for work that was done during this period. These studies form the foundation of current cancer research at CSHL, which since 1987 has been part of the NCI-designated CSHL Cancer Center.

Past Directors

James Watson
Dr. James Watson
1987 – 1988
Richard Roberts
Dr. Richard Roberts
1988 – 1992
Bruce Stillman
Dr. Bruce Stillman
1992 – 2016

2017

New Method Offers Earlier Detection for Lethal Prostate Cancer
Prostate cancer is common and largely nonlethal. But for some 21,000 men—a small percentage of the total, but a nonetheless substantial number—the disease is fatal. For earlier and more accurate detection, the Krasnitz and Wigler labs have devised a new method to analyze tumor biopsies to identify the most lethal forms of prostate cancer.
            
Crystal Structures Reveal Cancer Enzymes in Action
Tutases are a class of enzymes that regulate the microRNA let-7—a gene that is commonly downregulated in cancers. The Joshua-Tor lab used x-ray crystallography to capture images of the enzyme in action, offering insight into how these potential cancer targets function.
            
Algorithm Finds Novel Recurrent Mutations in Cancer Patients
The Tuveson lab, in collaboration with Dr. Michael Schatz, (now at Johns Hopkins University) has developed an algorithm to identify novel mutations in patient tumor samples. The research team applied the method, called GECCO, to pancreatic cancer samples and discovered multiple mutations, many of which were associated with a significant risk of poor prognosis for patients.
High-Resolution View of the Complex that Initiates DNA Replication
The Stillman and Joshua-Tor labs collaborated to obtain the structure of the active human Origin Recognition Complex (ORC), the proteins that control the initiation of DNA replication. Using both cyro-EM and x-ray crystallography, the labs obtained a high-resolution image of the ORC proteins bound to DNA, providing insights into the most fundamental process in cell proliferation.
            
Novel Insights into the Regulation of PTEN in Prostate Cancer
New research from the Trotman lab has revealed that, in prostate cancer, a protein known as Importin-11 is the ‘Achilles’ heel’ that is required for the stability of the PTEN tumor suppressor. In fact, loss of Importin-11 predicted relapse and metastasis in patients who had had their prostate removed.
            
Extra Chromosome Has Surprising Effect on Cell Growth and Tumorigenesis
Copy number variation is a hallmark of most cancers, and it often serves as a driver of cell proliferation. Surprisingly, new research from the Sheltzer lab suggests that an extra chromosome alone is not enough to initially spur tumor growth. Rather, prolonged changes in chromosome number lead to genetic instability that ultimately causes uncontrolled cell proliferation.
            

2016

Muscle-Wasting Disease Reveals Links Between Metabolism and Immune Evasion
Many cancer patients suffer from extreme weight loss in a condition known as cachexia. The Fearon lab has found that this calorie deprivation can have profound implications for tumor immunology, allowing tumor cells to become resistant to immunotherapy.
            
The Role of RNAi in Quiescence
Cancer forms when quiescent cells begin dividing and proliferating. New research from the Martienssen lab demonstrates that the RNAi machinery—which is often mutated in cancers—plays a key role in this transition, holding cells in quiescence.
            
Tumors Hijack the Immune System to Promote Metastasis
The Egeblad lab made the surprising discovery that tumors take advantage of an immune defense to enhance metastasis. Breast cancer cells can induce the immune system to release webs of DNA and enzymes, known as NETs. These webs directly stimulate the cancer cell’s ability to invade, promoting metastasis.
            
Feedback Loop Controls the Decision to Proliferate
New research from the Stillman lab has revealed that key components of the DNA replication machinery participate in a feedback loop to control cell proliferation. The proteins—which are often mutated in cancer—provide a direct link between replication and proliferation.
            
Research Identifies Signaling Pathway that Drives Metastasis in Ovarian Cancer
The Tonks lab has identified a role for the non-receptor tyrosine kinase, FER, in the invasion and movement of ovarian cancer cells—two traits that are required for metastasis. The work points to a potential drug target that could limit the most aggressive form of the disease.
            
New Method Rapidly Assays Copy Number Variation
Copy number variation is well known as a driver of tumorigenesis and metastasis. The Levy lab has developed a protocol, called SMASH, that combines wet lab techniques with a new computational algorithm to quickly and efficiently analyze copy number variation in cancer cells.

2015

Novel isoform of the tumor suppressor p53 associated with EMTs and metastasis
Camila dos Santos, as a postdoctoral researcher in the Hannon lab, identified the epigenetic changes that occur after pregnancy in the mouse mammary gland. The work offers insight into how pregnancy early in life may protect against breast cancer later.
            
An interactive tool for the analysis of single-cell copy-number variation
The Schatz lab, in collaboration with the Wigler and Atwal labs, has developed a new interactive, open-source analysis program called Gingko that can be used to reduce the uncertainty of single-cell analysis and visualize patterns in copy number mutations across populations of cells.
           
Research reveals how Brd4, known AML drug target, promotes leukemia maintenance
Brd4 is a validated drug target for AML with an inhibitor in clinical trials, yet its precise function has remained unclear. In this study, the Vakoc lab defined how the protein cooperates with hematopoietic transcription factors to create a chromatin signaling cascade that offers additional potential drug targets.
           
Discovery of cancer drug targets using high content CRISPR screening
The Vakoc lab collaborated with Justin Kinney to develop a new screening method using CRISPR-Cas9 technology. The method targets protein domains, rather than the traditional 5’ exon of the gene, to reveal cancer dependencies and identify new drug targets.
           
Tumor cells mimic blood vessels to help cancer spread
The Hannon lab developed a novel mouse model for breast cancer heterogeneity and used it to identify clones that were highly metastatic. The team found that these cells formed tube-like structures that mimic blood vessels, and identified two genes that drive vascular mimicry, which is likely promote growth of the primary tumor as well as metastasis.
            
DOCK4 mediates TGF-β’s pro-metastatic effects in lung cancer
The Van Aelst lab, in collaboration with Molly Hammell and Chris Vakoc, has found that TGF-β promotes metastasis at least in part by inducing the intracellular signaling molecule DOCK4 in lung adenocarcinoma cells. In human patients, elevated DOCK4 levels correlates with poor prognosis, making this pathway an attractive target for future drug discovery.
New signaling pathway in HER2-positive breast cancer cells suggests potential drug targets
The Tonks lab, in collaboration with Senthil Muthuswamy, has identified a novel signaling pathway, including at protein tyrosine phosphatase, that is required for highly aggressive HER2-positive tumor cells to grow. His work suggests two new drug targets for the disease, which might have a dramatic effect on the disease when inhibited in combination.
           
RNA splicing defects spur growth in breast cancer
SRSF1, a splicing factor, is a known oncogene and is overexpressed in many cancers. The Krainer lab has identified hundreds of splicing events that are regulated by SRSF1 and pinpointed at least one of the critical targets that helps to drive breast cancer.
           
New insights into how tumor suppressor PTEN turns off cell growth
The Trotman lab, in collaboration with the Pappin and Joshua-Tor labs, has found that the tumor suppressor PTEN uses microtubules to travel around the cell. The work challenges previous models for how the protein moves and provides new understanding that may be useful for targeted drug development.
           

2014

Novel isoform of the tumor suppressor p53 associated with EMTs and metastasis
The Sordella lab, in collaboration with the Krainer lab, identified a major new isoform of the tumor suppressor p53, called p53Ψ and showed that it induces expression of markers of the epithelial-mesenchymal transition and enhances the motility and invasive capacity of cells.
           
Development of Organoid Models of Pancreatic Cancer
In collaboration with Hans Celvers at the University of Utrecht as well as Darryl Pappin and Molly Hammell, the Tuveson lab established the first organoid models of both normal and cancerous ductal pancreatic cells.
           
Evaluation of Circulating Tumor Cells
James Hicks and Michael Wigler have developed methods to perform copy number analysis and whole genome amplification from circulating tumor cells (CTCs). Their latest data for melanoma and prostate cancer patients demonstrate the potential for this type of analysis to guide personalized therapies, and to monitor tumor evolution in response to therapy.
           
Role of PTP1B in Ras-induced Senescence
The Tonks lab, in collaboration with the Pappin and Hannon labs found that premature senescence in H-RAS(V12)-transformed primary cells is a consequence of oxidative inactivation of PTP1B and inhibition of miRNA-mediated gene silencing.
           
DOCK4 in lung adenocarcinoma metastasis
The Van Aelst lab has identified the atypical Rac1 activator DOCK4 as a novel, key component of the TGF-β/Smad pathway that promotes lung adenocarcinoma cell extravasation and metastasis.
P53 Mutations Change Phosphatidylinositol Acyl Chain Composition
The Trotman, Pappin and Tuveson labs collaborated to develop a high-throughput mass spectrometry method that identifies and quantifies twenty different cellular phosphatidylinositol lipid acyl chains. The method enabled them to discover that the anchoring tails of lipid second messengers form an additional layer of PIP signaling in cancer that is linked to p53.
           
Role of Dicer in Maintaining Genome Stability
The Martienssen lab found that Dicer, a canonical RNAi protein, facilitates the release of transcription machinery from DNA during replication, thereby preventing collisions and protecting the genome from damage.
           
Identification of functional protein domains using CRISPR/Cas-9
The Vakoc lab collaborated with Justin Kinney to develop a high-performance CRISPR strategy for cancer drug target discovery. The method involves targeting CRISPR-Cas9 mutations to functional protein domains rather than 5’ exons of candidate genes.
           
Improved strategy for analysis of large biomedical datasets
Justin Kinney and Gurinder Atwal collaborated to show how a fundamental mathematical quantity called “mutual information” can be used to detect and quantify relationships between variables in large, noisy datasets.
           

2013

Complex interactions between a tumor and nearby normal cells are essential for tumorigenicty.
The Egeblad and Powers labs identified multiple fibroblast-secreted factors that promote tumorigenicity using parallel pathways.
          
Structural characterization of key step in DNA replication
In collaboration with scientists at Brookhaven National Laboratory, the Stillman lab established the architecture of an essential component of eukaryotic DNA replication.
         
High resolution structure of human Argonaute proteins bound to RNA
The Joshua-Tor and Hannon labs collaborated to solve the structure of two human Argonaute proteins in complex with physiologically relevant guide RNAs.
                                    
Clusters of cooperating tumor-suppressor genes are found in large regions deleted in common cancers
Michael Wigler, in collaboration with Alexander Krasnitz, James Hicks and Scott Powers, used a new computational method called CORES to propose an alternative to the “two-hit” hypothesis to explain how cancers arise.
                                    
Identification of a PTP1B inhibitor as potential treatment for breast cancer
Nick Tonks’ lab identified a novel allosteric inhibitor of PTP1B, a small molecule natural product, which is now being investigated as a treatment for HER2-positive breast cancer patients.
         
Novel mechanism for induction of cellular senescence 
Adrian Krainer’s lab identified a novel oncogene-induced senescence mechanism that implicates spliceosomal and ribosomal components in non-canonical roles as regulators of a pathway critical for maintenance of cellular homeostasis.
         
Discovery of potential treatment for AML
The Vakoc lab identified a role for Rnf20 in the pathogenesis of MLL-fusion leukemia.  As other small-molecule drugs targeting other E3 ligase proteins exist, RNF20 could be a new druggable target for AML therapy.
         
The noncoding RNA MALAT1 is a critical regulator of the metastasis phenotype of lung cancer cells
The Spector lab, along with Sven Diederichs lab at the University of Heidelberg, showed that the long noncoding RNA MALAT1 is not only a prognostic biomarker for metastasis but also plays an active role in disease progression.
Characterization of mechanism of the Chd5 Tumor Suppressor
The Mills lab found that the major tumor suppressor Chd5 binds to histone H3, offering insight into how this protein regulates a diverse set of cancers.
          

2012

Tumor suppressor activity for protein tyrosine phosphatase
The Tonks lab collaborated with the Muthuswamy lab to reveal that PTPRO acts as a tumor suppressor and can act as a prognostic marker for HER2-positive breast cancers.
Potential antisense methods for cancer therapy
The Krainer lab has developed antisense oligonucleotides as a potential therapeutic for cancer, targeting the pyruvate kinase M (PK-M2) gene which is crucial for aerobic glycolysis and proliferation in tumor cells.
         
Potential targeted therapy for breast cancer
The Stillman lab demonstrated that the protein DDX5 regulates DNA replication and may be a viable drug target for cancers with the DDX5 gene locus overexpressed or amplified.
Improved assembly method for single molecule sequencing data
Michael Schatz and colleagues devised a method to correct errors in single molecule sequences, by combining long PacBio reads with shorter read sequencing data for > 99.9 percent base-call accuracy.
         
Functional analysis of the protein phosphatase activity of PTEN
The Tonks and Van Aelst labs collaborated on functional analysis of the protein phosphatase activity of the tumor suppressor PTEN, finding that autoregulation is a critical component of PTEN control.
Single cell sequencing demonstrates how tumors progress
Michael Wigler, in collaboration with W. Richard McCombie, Alex Krasnitz and James Hicks, applied single cell sequencing to individual cells from a primary breast tumor, which revealed marked genetic heterogeneity within a single tumor, and shed new light on how a tumor evolves.
Contribution of the tumor environment to resistance to chemotherapy
The Egeblad lab demonstrated that the microenvironment contributes critically to drug response by regulating the permeability of blood vessels around the tumor, and affecting the local recruitment of inflammatory cells.
         

2011

Comprehensive genomic DNA analysis of mast cell leukemia uncovers clues that could improve therapy
Mona Spector, working with Ivan Iossifov, Scott Lowe and collaborators at Northwell Health, identified two novel mutations from a patient with mast cell leukemia, an extremely aggressive subtype of acute myeloid leukemia, offering new possibilities for diagnosis and treatment.
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Novel regulatory role of hydrogen sulfide in cell response to protein misfolding
The Tonks and Pappin labs collaborated to discover how the inactivation and reactivation of PTP1B serves as a novel mechanism to regulate protein synthesis machinery.
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Structure of RITS complex explains its role in heterochromatin assembly and gene silencing
The Joshua-Tor lab and colleagues determined how the three components of the RNA-Induced Initiation of Transcriptional gene Silencing (RITS) interact with each other, offering insight into the establishment of heterochromatin and gene silencing.
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Study reveals details of alternative splicing circuitry that promote cancer’s Warburg effect
The Krainer lab, along with colleagues from Harvard Medical School, showed that the splicing factor SRSF3 is a key determinant in regulating which isoform of pyruvate kinase is expressed in cancer cells, providing mechanistic insights into the complex regulation the Warburg effect.
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New role for RNAi during chromosomal replication
The Martienssen lab found that transcription and replication machinery are coordinated during DNA replication, demonstrating that an RNAi mediated mechanism removes RNA pol II from replicating DNA to allow the replication fork to progress.
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Gene bookmarking accelerates the kinetics of post-mitotic transcriptional re-activation
The Spector lab demonstrated that genes “bookmarked” by an acetylated histone (H4K5Ac) during interphase, which accelerates transcriptional activation after mitosis through recruitment of the bromodomain protein BRD4.
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Discovery of a new prostate tumor suppressor gene
The Trotman lab and colleagues showed that phosphatase PHLPP1 is a prostate tumor suppressor, and loss in combination with PTEN is associated with metastatic disease.
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Discovery of potential treatment for AML
The Vakoc lab, in collaboration with the Lowe lab, found that the protein Brd4 is essential for acute myeloid leukemia. The results establish small-molecule inhibition of Brd4 as a promising therapeutic strategy for the disease.
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Director, David Tuveson, M.D., Ph.D.

Cancer researchers at CSHL are using cutting-edge technology in innovative and collaborative studies to explore the basic biology underlying the disease. Our research can be divided into three main focus areas:

 Cancer Genetics Program
 Gene Regulation & Cell Proliferation Program
 Signal Transduction Program

Cold Spring Harbor Laboratory is an NCI-designated Cancer Center. As a basic research institution, CSHL does not treat patients. Information about individual cancers is available at the NCI CancerNet. Questions about CSHL’s cancer research program should be directed to our Public Affairs Department.

Nick Tonks, Ph.D., Deputy Director, Cancer Center Shared Resources

The CSHL Cancer Center has nine shared resources that facilitate cancer research with state-of-the-art technology and integral services. With the support of world-class staff, these core facilities ensure that Cancer Center researchers have all the necessary tools to make breakthrough discoveries.

Animal Facility Animal and Genetic Engineering  Flow Cytometry
Animal Tissue Imaging Animal & Tissue Imaging   Functional Genomics
  Antibody & Phage Display   Mass Spectrometry
  Bioinformatics   Microscopy
  Next Generation Genomics
Gurinder Atwal

Gurinder Atwal

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.

Semir Beyaz

Semir Beyaz

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.

Kenneth Chang

Kenneth Chang

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.

Camila dos Santos

Camila dos Santos

Among the changes that occur during pregnancy, those affecting the breasts have been found to subsequently modify breast cancer risk. My laboratory investigates how the signals present during pregnancy permanently alter the way gene expression is controlled and how these changes affect normal and malignant mammary development.

Mikala Egeblad

Mikala Egeblad

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.

Douglas Fearon

Douglas Fearon

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.

Thomas Gingeras

Thomas Gingeras

Only a small portion of the RNAs encoded in any genome are used to make proteins. My lab investigates what these noncoding RNAs (ncRNAs) do within and outside of cells, where regulators of their expression are located in the genome, and how perturbations of ncRNAs and their regulators contribute to disease.

Christopher Hammell

Christopher Hammell

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.

Molly Hammell

Molly Hammell

To ensure that cells function normally, tens of thousands of genes must be turned on or off together. To do this, regulatory molecules - transcription factors and non-coding RNAs – simultaneously control hundreds of genes. My group studies how the resulting gene networks function and how they can be compromised in human disease.

Leemor Joshua-Tor

Leemor Joshua-Tor

Our cells depend on thousands of proteins and nucleic acids that function as tiny machines: molecules that build, fold, cut, destroy, and transport all of the molecules essential for life. My group is discovering how these molecular machines work, looking at interactions between individual atoms to understand how they activate gene expression, DNA replication, and small RNA biology.

Justin Kinney

Justin Kinney

From regulating gene expression to fighting off pathogens, biology uses DNA sequence information in many different ways. My research combines theory, computation, and experiment in an effort to better understand the quantitative relationships between DNA sequence and biological function. Much of my work is devoted to developing new methods in statistics and machine learning.

Adrian R. Krainer

Adrian R. Krainer

Our DNA carries the instructions to manufacture all the molecules needed by a cell. After each gene is copied from DNA into RNA, the RNA message is "spliced" - an editing process involving precise cutting and pasting. I am interested in how splicing normally works, how it is altered in genetic diseases and cancer, and how we can correct these defects for therapy.

Alexander Krasnitz

Alexander Krasnitz

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.

Je H. Lee

Je H. Lee

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.

Dan Levy

Dan Levy

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.

Scott Lyons

Scott Lyons

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.

Robert Maki

Robert Maki

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.

Rob Martienssen

Rob Martienssen

Chromosomes are covered with chemical modifications that help control gene expression. I study this secondary genetic code - the epigenome - and how it is guided by small mobile RNAs in plants and fission yeast. Our discoveries impact plant breeding and human health, and we use this and other genomic information to improve aquatic plants as a source of bioenergy.

W. Richard McCombie

W. Richard McCombie

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.

Alea A. Mills

Alea A. Mills

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.

Darryl Pappin

Darryl Pappin

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.

Jon Preall

Jon Preall

Developing single-cell genomics technologies for applications related to cancer progression, immune surveillance, and discovery of rare novel cell types and transcriptional programs.

Jason Sheltzer

Jason Sheltzer

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.

Adam Siepel

Adam Siepel

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.

Raffaella Sordella

Raffaella Sordella

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.

David L. Spector

David L. Spector

The immense amount of DNA, RNA and proteins that contribute to our genetic programs are precisely organized inside the cell¹s nucleus. My group studies how nuclear organization impacts gene regulation, and how misregulation of non-coding RNAs contributes to human diseases such as cancer.

Arne Stenlund

Arne Stenlund

Despite the development of preventive vaccines, human papillomaviruses (HPVs) still infect more than five million women each year, significantly increasing their risk of cervical cancer. I am working to identify how HPV multiplies so that we may develop drugs that can defeat the virus once it has infected an individual.

Bruce Stillman

Bruce Stillman

Every time a cell divides, it must accurately copy its DNA. With 3 billion “letters” in the human genome, this is no small task. My studies reveal the many steps and molecular actors involved, as well as how errors in DNA replication are involved in diseases that range from cancer to rare genetic disorders.

Nicholas Tonks

Nicholas Tonks

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.

Lloyd Trotman

Lloyd Trotman

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.

David Tuveson

David Tuveson

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.

Chris Vakoc

Chris Vakoc

Cancer cells achieve their pathogenicity by changing which genes are on and off. To maintain these changes in gene expression, cancer cells rely on proteins that interact with DNA or modify chromatin. My group investigates how such factors sustain the aberrant capabilities of cancer cells, thereby identifying new therapeutic targets.

Linda Van Aelst

Linda Van Aelst

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.

James D. Watson

James D. Watson

Dr. James D. Watson, co-discoverer of DNA’s double helix, is a Nobel laureate, past president of Cold Spring Harbor Laboratory, and generous philanthropist.

Michael Wigler

Michael Wigler

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

Johannes Yeh

Johannes Yeh

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.

Lingbo Zhang

Lingbo Zhang

The research of my lab focuses on normal and malignant hematopoietic stem and progenitor cells, specifically early erythroid progenitors and leukemic cells. We utilize both CRISPR/Cas functional genomic and forward chemical genomic approaches to uncover critical genes and small chemical compounds regulating the self-renewal of normal and malignant hematopoietic stem and progenitor cells. The ultimate goal of our research is to identify novel therapeutics for treatment-resistant hematopoietic malignancies including myelodysplastic syndrome and acute leukemia through targeting of novel self-renewal pathways and metabolic vulnerabilities.

Hongwu Zheng

Hongwu Zheng

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.