Faculty Advisors

Amato Giaccia: The long-term goal is to identify and characterize the molecular and physiological changes induced by the tumor microenvironment that influence the malignant progression of transformed cells.

Steven Artandi:  Our laboratory is investigating the role of mammary stem cells in breast cancer through the creation of novel mouse models that will reproduce the chromosomal instability seen in human breast cancer. We are also actively investigating the effects of TERT on other stem cell populations.  Furthermore, we are dissecting TERT's mechanism of action in molecular detail.

Laura Attardi: The main focus of my laboratory is to understand the p53 tumor suppressor using mouse model systems. We aim to identify and characterize p53 target genes, and under p53 function through in-depth structure-function studies.

Jeffrey Axelrod: My laboratory is investigating how genes orchestrate the amazing processes of development and morphogenesis. We are using genetic, molecular and cell biological analyses in both the fruitfly, Drosophila melanogaster, and in the mouse, to address some specific questions such as when, why and how cells acquire their morphology to carry out their functions.

Helen Blau: Our research is directed at understanding this apparent paradox and elucidating the nature of cell memory and cell plasticity. By perturbing the intracellular or extracellular milieu, we are probing the regulatory network that determines cell fate and how it can be altered. This knowledge is key to our understanding of stem cell quiescence, self-renewal, differentiation, and how cancer arises.

Matthew Bogyo: Our laboratory is interested in developing and applying chemical tools to dissect the functional roles of proteases in a number of human health conditions. We are currently using synthetic chemistry to build new reagents that allow protease activity to be monitored in complex biological samples including cells, tissues and whole animals.

J. Martin Brown: My lab has two main goals, 1)To improve cancer therapy by   
exploiting the low oxygenation and presence of necrosis in solid tumors. 2) To find  
new radiation and cancer susceptibility genes using the power of yeast genomics.

Patrick Brown: Ongoing research in my lab has several intertwining themes:  1.  Development of experimental and computational methodology for systematic profiling of genomes and global gene expression programs.   2. Systematic studies of global gene expression programs in human cells and tissues 3.  Basic investigations of the architecture and molecular mechanisms of post-transcriptional regulation.  4.  Development of novel molecular imaging and molecular profiling methods for early detection of cancer.  5.  Development of high-throughput methods for systematic, quantitative profiling of complex microbial populations and their application to human biology and disease.

Anne Brunet: In my lab, we are interested in understanding the importance of the FOXO family in mammals, with particular focus on the role of these factors in oncogenesis and organismal longevity. By studying FOXO transcription factors, we hope to gain new insights into the molecular mechanisms of oncogenesis and into how organismal lifespan is regulated.

William Burkholder: Our lab is broadly interested in how bacteria monitor the status of DNA replication and repair so as to regulate cell division and development.

Michele Calos: The Calos lab is developing new vectors and approaches for gene therapy.  Our research focuses on use of a novel phage integrase system for obtaining site-specific integration into the chromosomes of mammalian cells.

Christine Cartright: Research in my laboratory focuses on molecular mechanisms of intestinal cell growth control. Areas of active investigation include studies of Src function in cell cycle progression, proliferation, differentiation, adhesion, survival and malignant transformation; discovery of endogenous inhibitors of Src kinases.

Chingpin Chang: My laboratory focuses on the mechanisms of cardiovascular development, particularly how the three major types of cardiac cells (endocardial, myocardial and epicardial cells) and neural crest cells interact with each other to generate heart tissues.

Howard Chang: The Chang group is focused on two fundamental questions in epithelial biology: (1) the basis of positional identities in epidermal structures throughout the body, and (2) how those signals and boundaries may be abrogated to allow cancer metastasis.

James K Chen: Our laboratory studies the molecular mechanisms that regulate the Hedgehog (Hh) signaling pathway We want to identify small molecule modulators of this pathway, vertebrate-specific Hh signaling proteins, and zebrafish models of Hh-dependent embryonic patterning and oncogenesis.

Gilbert Chu: One goal is to elucidate nonhomologous end-joining, a pathway that repairs DNA double-strand breaks created by ionizing radiation and V(D)J recombination. We use Significance Analysis of Microarrays (SAM) and Prediction Analysis of Microarrays (PAM)to predict adverse reactions to radiation therapy from the transcriptional responses of 24 genes.

Katrin Chua: Our lab is interested in understanding molecular processes that underlie aging and age-associated pathologies in mammals. In particular, we are interested in how SIRT factors regulate chromatin, the molecular structure in which the DNA of mammalian genomes is packaged, and how such functions may link genome maintenance to stress resistance and aging.

Karlene Cimprich: My lab is focused on understanding the mechanism that the cell uses to maintain genomic stability, with an emphasis on DNA damage checkpoints. In recent years, our emphasis has been on understanding how the checkpoint is activated following DNA damage and how this pathway is integrated with the processes of DNA replication, cell cycle progression and DNA repair.

Michael F. Clarke: Dr. Clarke maintains a laboratory focused on two areas of research: i) the control of self-renewal of normal stem cells and their malignant counterparts; and ii) the identification and characterization of cancer stem cells. A central issue in stem cell biology is to understand the mechanisms that regulate self-renewal of hematopoietic stem cells, which are required for hematopoiesis to persist for the lifetime of the animal. Until recently, the molecular mechanisms that regulate adult stem cell self-renewal were not known. His laboratory recently found that the proto-oncogene Bmi-1 regulates stem cell self-renewal via an epigenetic mechanism. By investigating the pathways upstream and downstream of Bmi1, the laboratory is actively investigating the molecular pathways that regulate self-renewal.

Michael Cleary: The Cleary lab employs a multifaceted experimental approach to investigate the molecular, biochemical, and cellular biological foundations of hematopoietic malignancies.  We have developed and used a variety of gain- and loss-of-function mouse models to characterize leukemia proto-oncogenes.

Stanley Cohen: Then Cohen lab ‘s primary field of research is molecular genetics, and the research interests focus on understanding important biological processes and events at the molecular level. My lab also develops bioinformatics tools to aid in this understanding.

Marco Conti: Our research program focuses on understanding the regulation of the specialized cell cycle that controls maturation of mouse and frog oocytes. Specifically, we are investigating how the G2/M transition of the first meiotic division is controlled in oocytes.

Gerald Crabtree: The interests of our laboratory have centered about the origin of biologically specific patterns of transcription and information transfer from the cell membrane to the nucleus. A long-term area of investigation in the laboratory has been a signaling pathway in lymphocytes that is also important for development of the mammalian heart and the functioning of specific neurons in the hippocampus.

Martha Cyert: Current research projects in my lab aim to identify all subtrates of the Ca2+/calmodulin-regulated phosphatase, calcineurin, using genetic, genomic and proteomic approaches. Other studies focus on identifying the biological function of these novel calcineurin substrates and elucidating calcineurin's role in regulating their activity.

Nicholas Denko: Our work is focused around the central hypothesis that hypoxia-dependent physiologic changes that we see at the cellular and tumoral levels are at least in part due to gene expression changes induced by the hypoxic environment.  We therefore started by taking a genetic approach and identified gene expression changes that occur during hypoxia. We are now trying to identify specific hypoxia-regulated genes that can then explain some of the physiologic changes that occur in hypoxia.

Dean Felsher: The Felsher laboratory studies how oncogenes initiate and sustain tumorigenesis. Utilizing novel conditional transgenic mouse models, we address three questions:  How does oncogene activation induce tumorigenesis?  How does inactivation induce tumor regression?  How do tumors escape dependence upon oncogenes?

James Ferrell Jr.: Much of our research centers on the signal transduction pathways that trigger Xenopus oocyte maturation. In addition, the signal transduction networks --the MAPK cascade and the Cdc2-cyclin B system--are of great importance in many biological contexts. We are studying how these networks function as systems.

Andrew Fire: Our lab studies the mechanisms by which cells and organisms respond to genetic change. We study a variety of natural mechanisms that are utilized by cells adapting to genetic change. These include mechanisms activated during normal development and systems for detecting and responding to foreign or unwanted genetic activity.

James Ford: DNA Repair and Genomic Instability. My goals are to understand the role of genetic changes in cancer genes in the risk and development of common cancers. Currently, my lab is developing techniques for high-throughput genomic analyses of cancer to identify molecular signatures for targeted therapies.

Judith Frydman: The focus of our lab is to understand the pathways of chaperone-mediated protein folding in eukaryotic cells and how this folding is regulated. We are also interested in understanding the role of chaperone systems in targeting proteins for degradation and their connection with components of the ubiquitin-proteasome system.

Or Gozani: Our work focuses on understanding at the molecular level the relationship between histone modifications and biological outcomes (such as DNA damage responses), and how disruption in these mechanisms affects tumor biology. Future research aims to (i) investigate ING2 and other PHD domain containing proteins linked to cancer, (ii) identify novel chromatin effector domains, and (iii) develop new tools and methodologies to test how diverse chromatin modifying activities contribute to tumorigenesis.

Edward Graves: I am interested in applications of emerging functional and molecular imaging techniques in radiation therapy of cancer.  In order to integrate these novel imaging procedures with state-of-the-art radiation therapy, a number of issues must be addressed.  First, what are the molecular targets that hold the most promise for targeting and monitoring response to radiation therapy, and how can they best be visualized in vivo?  Second, what are the limitations of novel imaging techniques that may bear on their application in radiation oncology?  Third, how can one display, analyze, and segment multiple three-dimensional datasets to effectively integrate the information contained with therapy planning?  And finally, how will the information contained in imaging results of different modalities be integrated into the selection of a treatment course for a patient and subsequently, where appropriate, the specification of an optimized radiation target?  Projects that address these topics within my laboratory include the development and validation of novel methods for preclinical and clinical imaging of tumor hypoxia and hypoxia-inducible physiology, study of tumor hypoxia and radioresistance in small animal models using a multimodality molecular imaging approach, implementation and evaluation of clinical PET/CT imaging for radiation treatment planning, and development of software for multimodal image analysis.

Isabella Graef: We are interested in addressing questions in neuronal development and function by a combination of genetic, cell biological, biochemical and chemical approaches. The main focus of the our lab is centered around two topics: 1) the interface of signaling and gene regulation in neuronal development, with a focus on calcineurin-NFAT signaling; 2) the development of small molecules, which interfere with pathogenic protein-protein interactions underlying neurodegenerative diseases.

Samira Guccione: The focus of our laboratory is translational research leading to agents for clinical use in detection, diagnosis, treatment, monitoring, and prognosis of clinical pathologies. We take a comprehensive approach in design of agents that can span the “bench to bedside” timeline efficiently with our primary focus in development of novel agents for cancer. The research in our laboratory uses high throughput genomic and proteomic analysis on clinical pediatric and adult tissue samples to identify molecular targets. We are currently performing toxicity studies as the preclinical requirement for clinical trials. Other research areas include tissue engineering applications in revascularization to enhance wound healing and vascularly compromised tissue; localized drug delivery systems; and biomarker development.

Andrew Hoffman: The laboratory is interested in examining the role of insulin-like growth factors (IGF) in normal physiology and in oncogenesis. We are studying the molecular biology and physiology of IGF with an emphasis on the following areas:  1) We have shown that the IGF2 gene is parentally imprinted in most normal tissues, but that in some malignant neoplasms, the gene is biallelically expressed. Our inital work has concentrated on IGF2 gene expression in normal and neoplastic liver, kidney, uterine and breast tissues, where we have shown that the gene is overexpressed. Moreover, in nearly half of these tumors, IGF2 genomic imprinting is relaxed, leading to biallelic expression of the autocrine growth factor. 2) During our investigation of the mechanism for IGF2 imprinting, we have discovered that the imprinting process is promoter-specific, i.e., transcripts derived from promoters P2-P4 are imprinted while transcripts from promoter P1 are not imprinted. We are actively investigating the role of DNA and histone methylation in genomic imprinting. 3) Our group has actively studied the role of GH and IGF-I on body composition and exercise tolerance. We now plan to investigate the efficacy and safety of testosterone replacement in elderly men.

Paul Khavari: The efforts of my laboratory are directed at two complementary areas 1) gene regulatory control of epithelial growth and carcinogenesis 2) new molecular therapeutics for epithelial tissues.

Susan Knox: A primary research interest for my laboratory is the study of systemically targeted radiation therapy and the use of biological response modifiers to enhance the radiosensitivity of tumors and/or radioprotect normal tissues. Another relatively new focus in the laboratory has been the study of Selenium in the form of Selenite as a potential novel chemotherapeutic agent for the treatment of prostate cancer. We also study the redox modulation of apoptosis as well the underlying mechanism of action of Selenite as a cytotoxic agent in prostate cancer.

Albert Koong (SC Director): The UPR is an evolutionarily conserved pathway that functions to reduce protein accumulation in the ER resulting in increased capacity to tolerate ER stress. We hypothesize that since the UPR is also activated during hypoxia, it may be a critical regulator of cell survival during hypoxia and is necessary for tumor growth. The focus of my laboratory is to understand the relationship between hypoxia and ER stress, particularly as it relates to tumorigenesis.

Calvin Kuo: Our research is largely focused on angiogenesis and anti-angiogenic therapy, using a combination of adenoviral, knockout mouse and zebrafish models for target validation. In other lines of inquiry, we are developing adenoviral reagents capable of systemic activation or inhibition of the Wnt, Hh and Notch pathways in adult mice.

Quyhn Le: My research focuses on identification of novel secreted protein markers for hypoxia and prognosis in head and neck cancers (HNSCC). We have recently identified Osteopontin (OPN), a secreted protein implicated in the development and progression of several solid tumors as a novel hypoxia marker. Now the major focus in my laboratory is to study the role of OPN on tumor progression in HNSCC.

Ronald Levy:
Our laboratory works at this boundary between immunology and cancer biology. We study normal lymphocyte biology and the biology of malignant lymphomas. We develop immune therapies for lymphomas. We are now developing a vaccine approach for the treatment of lymphoma.

Joseph Lipsick:
Our laboratory studies the Myb oncogene family, with a particular emphasis on Drosophila genetics.  We have recently created the first null mutants of Drosophila Myb.  We used these mutants to show that Myb is required for the maintenance of genomic stability and for the site-specific DNA replication that occurs during chorion gene amplification.

Anson Lowe:
My laboratory is focused on the biology of the pancreas and esophagus and their associated diseases. Using animal models and materials from human subjects, we have used DNA microarrays to characterize the gene expression profile of acute pancreatitis and pancreatic cancer.

M. Peter Marinkovich:
The Marinkovich Lab focuses on discovering how extracellular matrix molecules influence important events in epithelila biology, including carcinoma invasion, epithelial adhesion, embryogenesis and development.

Beverly Mitchell:
Dr. Mitchell's research relates to the development of new therapies for hematologic malignancies. She has a long-standing interest in IMPDH as a therapeutic target and has published extensively on the regulation of this enzyme and the potential role of inhibitors in the treatment of leukemia in preclinical and clinical investigations. Dr. Mitchell is also interested in the role of Pso4 in DNA repair and in nucleolar proteins as a target for cancer treatment.

W. James Nelson:
Our research objectives are to understand cellular mechanisms involved in development and maintenance of cell polarity. We take multi-faceted experimental approaches to these problems.

Roel Nusse:
Our main research efforts are centered around the function of Wnt signaling. A significant recent accomplishment of my group is the first successful purification of active Wnt proteins, showing that they are lipid-modified and act as stem cell growth factors.

Anthony Oro:
Our lab is interested in the role of Sonic hedgehog (Shh) signaling system in the pathogenesis of the most common human tumor, basal cell carcinoma (BCCs) of the skin. Our ultimate goal is to understand the pathogenesis of epithelial cancer in order to develop novel anti-tumor therapeutics.

Donna Peehl:
Dr. Peehl’s research focuses on the molecular and cellular biology of the human prostate and its diseases, benign prostatic hyperplasia (BPH) and cancer.  A major area of interest is the development of in vitro experimental models. Dr. Peehl’s research focuses on the molecular and cellular biology of the human prostate and its diseases, benign prostatic hyperplasia (BPH) and cancer. Determining the role of the stroma in BPH and cancer is another major project in which we are engaged.

Jonathan Pollack:
The Pollack lab uses DNA microarrays to investigate the pathogenesis and biology of human cancer, and to identify strategies for improved cancer diagnosis, prognostication and patient management.

Marlene Rabinovitch:
Our research focuses on the regulation of genes associated with vascular development and disease. Our lab is developing a powerful animal model of severe pulmonary hypertension (PH) using a mouse that constitutively overexpresses the Mts-1 gene, first described in cancer cells. The goal of this study is to understand the global changes in gene expression that accompany the onset and progression of PPH in Mts-1 mice.

Jinghong Rao:
We are interested in developing non-invasive imaging methods for tumor imaging and cancer diagnostics. We are focusing on two strategies in developing such methods to achieve tumor specificity: 1) label cell proliferation markers due to the fast growth rates of tumor cells, and 2) selectively target tumor-specific genetic markers.

Thomas Rando:
A major interest of the lab is the mechanism by which muscle progenitor cells are activated to mediate both postnatal muscle growth and muscle regeneration, in response to injury or disease, and in the setting of neoplastic disorders of skeletal muscle, rhabdomyosarcomas. Our recent studies have focused on the Notch and Wnt signaling pathways in these processes. We have found that activation of the Notch signaling pathway is critical to the transition of satellite cells from a quiescent state to one of active proliferation. The regulation of Notch signaling by its inhibitor Numb appears to determine lineage progression and cell fate determination. We have recently found that activation of the Wnt signaling pathway occurs during muscle injury when satellite cells become activated. There appears to be an antagonistic interaction between Notch and Wnt signaling in activated satellite cells during this process. Furthermore, we have found that the agerelated impairment of muscle regeneration is due to a decline in effective Notch signaling, manifested initially as a failure of injured muscle to upregulate the Notch ligand, Delta. We are currently exploring further the regulation of the Notch and Wnt signaling pathways during satellite cell activation, the mechanisms underlying the transcriptional control of Delta expression, and epigenetic processes that may account for age-related changes in these pathways. Our near term goals are to identify the key signaling processes that control satellite cell activation and lineage progression in order to enhance muscle regeneration

Glenn Rosen:
Our laboratory examines apoptotic and cell cycle pathways in the lung with a focus on fibrotic lung disease and lung cancer. Our laboratory is also collaborating with the laboratory of Dr. Irving Weissman to isolate and characterize lung cancer stem cells, and we are collaborating with a local biotechnology company on a proteomic analysis of lung cancer. We also are involved in trials of novel therapeutics for patients with pulmonary fibrosis.

Julien Sage:
A major focus of the lab is to identify the function(s) of RB that are critical for its tumor suppressor activity and the molecular mechanisms of RB’s tumor suppressor action. Our current goal is to study the role of RB in regulating cell cycle re-entry in somatic cells in vivo using mouse genetics. By determining the consequences of loss of RB in adult somatic cells, we will also identify potential target cells for cancer initiation and the molecular mechanisms of the earlier stages of cancer.

Matthew Scott:
Development and tumorigenesis of the cerebellum; Hedgehog signaling pathway. We study the control of cerebellum development by a number of regulators including Hedgehog signals. Using mouse models of medulloblastoma, we are studying regulators of disease initiation and progression, including growth factors, sterols, and other factors.

John B. Sunwoo:

Tim Stearns: My lab focuses on the molecular mechanisms of transcription factors that govern the transformation of normal mammalian cells to neoplastic state, with a special focus on the androgen receptor and other nuclear hormone receptors.  Our long-term goal is to develop novel diagnostic and therapeutic strategies for prostate cancer and other human malignancies.

Alejandro Sweet-Cordero:
Our laboratory is interested in the discovery and functional analysis of genes involved in the initiation and progression of cancer using mouse models that closely recapitulate human oncogenesis. We are also interested in using mouse models to understand why tumors become resistant to chemotherapy in vivo and to test novel approaches to increase chemotherapy-induced tumor cell kill.

Virginia Walbot:
Our laboratory is interested in how genotypic and phenotypic diversity is created during the life cycle of plants. We are studying the regulation of Mutator transposable elements in response to host developmental signals and environmental cues as an entry point.

Teresa Wang:
Maintenance of Genome Integrity
Our major focus is to understand the molecular mechanisms involved in maintaining genome integrity during chromosome replication. Our current research programs are:
(1). We investigate what types of mutation in genes that play a critical role in DNA replication can cause an early event in tumorigenesis and are a source of the genetic instability observed in cancer cells. 2). We investigate how cells respond to replication stress to maintain genome integrity by checkpoint mechanisms.

William Weis:
Molecular basis of cell adhesion and Wnt signaling.
 Our laboratory uses biochemical reconstitution, x-ray crystallography, and physical biochemistry to understand the molecular mechanisms of 1) cadherin-based cell adhesion and its regulation, 2) the Wnt signaling pathway, including how beta-catenin is degraded in the absence of wnt signal and how it acts as a transcriptional co-activator during wnt signaling.

Irving Weissman:
Irving L. Weissman's research encompasses the phylogeny and developmental biology of the cells that make up the blood-forming and immune systems. His laboratory identified and isolated the blood-forming stem cell from mice, and has defined, by lineage analysis, the stages of development between the stem cells and mature progeny (granulocytes, macrophages, etc.). In addition, the Weissman laboratory has pioneered the study of the genes and proteins involved in cell adhesion events required for lymphocyte homing to lymphoid organs in vivo, either as a normal function or as events involved in malignant leukemic metastases.

Albert J. Wong:
The goal of this laboratory is to define targets for cancer therapeutics by identifying alterations in signal transduction proteins. The major type of cancer that we study is glioblastoma multiforme, the most common and devastating of the human brain tumors. Our work has also had implications for lung, breast, ovarian and prostate cancers.

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