Cancer Biology
Contact Information
Faculty and their Research Interests
Clockwise from upper left: Postnatal day-14 cerebellum; Osteosarcoma cell undergoing aberrant mitosis; Tube formation of endothelial cells in response to angiogenic factor; Predicting expression program of liver cancer from computed tomography scans.
Established in 1978, the Cancer Biology Program at Stanford University is an interdisciplinary program leading to the Ph.D. degree. During the past 30 years, our understanding of cancer has increased dramatically with the discovery of oncogenes, tumor suppressor genes, pathways of DNA damage and repair, cell cycle regulation, angiogenesis and responses to hypoxia, and recent glimpses into the molecular basis of metastasis and cancer stem cells. In addition, methods of parallel analysis including gene expression arrays, protein arrays, and tissue arrays have begun to refine and redefine the taxonomy of cancer diagnosis. This explosion of basic and clinical science has in turn resulted in the first successful cancer chemotherapies and immunotherapies based on a knowledge of specific molecular targets. With the newly established NCI designated Cancer Center, Stanford presents an excellent environment to pursue interdisciplinary cancer research.
The goal of the Cancer Biology Ph.D. Program is to provide our students with education and training that will enable them to make significant contributions to this remarkable field. Coursework during the first year is designed to provide a broad understanding of the molecular, genetic, cell biological, and pathobiological aspects of cancer. Students also learn about the current state of clinical diagnosis and treatment of human cancers. Each student is required to conduct a series of three laboratory rotations in the first year. By the beginning of the second year, each student will have chosen his/her research advisor and will have begun work on his/her dissertation project. A qualifying examination must be completed by the end of the second year. An annual Cancer Biology Conference at Asilomar on the Pacific Ocean provides our students with an opportunity to present their research to one another and to the faculty. The expected time to degree is four to five years.
For more information contact:
Grace Kolar
Program Administrator
Stanford Cancer Institute
265 Campus Drive, G2103F
Stanford, CA 94305-5456
(650) 723-6198
(650) 736-0607 (fax)
gracebk@stanford.edu
http://cancerbio.stanford.edu/
Faculty and their Research Interests
Ash Alizadeh. Systems immunology & oncogenomics of B-cell lymphomas.Steven Artandi. Cellular and genetic responses to telomere dysfunction and the biochemical role of telomerase, with the goal of better understanding human breast cancer.
Steven Artandi. Telomerase regulation of telomeres and chromatin in stem cells and cancer.
Laura Attardi. p53-mediated apoptosis and tumor suppression, using biochemical, cell biological, and mouse genetic approaches.
Jeffrey D. Axelrod. Genetic, molecular and cell biological analyses of signals controlling cell polarity. Signaling mechanisms regulating cytoskeletal organization and morphogenesis in normal and disease states.
Lab website: http://www.stanford.edu/group/axelrodlab/lab/
Philip Beachy. Biology and mechanism of Hedgehog signaling; tissue regeneration and neoplasia.
Nidhi Bhutani. DNA demethylation, Mechanisms of reprogramming, Musculoskeletal regeneration.
Helen M. Blau. Stem cell biology. Cancer stem cells. Microenvironmental control of cell proliferation rates. Human lymphoma. Embryonic stem cells. Adult stem cells including muscle, blood and pancreas. In vivo imaging. Bioengineered cellular microenvironments. Nuclear reprogramming.
Matthew Bogyo. Functional studies of protease networks using chemical tools; design and synthesis of small molecules probes of proteases; dissection of proteases pathways involved in host cell invasion by the human parasites, Plasmodium falciprum and Toxoplasma gondii; imaging of protease activity during tumorigenesis.
Linda Boxer. Mechanisms of activation of oncogenes in B cell malignancies.
Martin Brown. Role of vasculogenesis (de novo creation of blood vessels from circulating cells) in the response of solid tumors to therapy. Anaerobic bacteria to deliver genes to solid tumors.
More information: http://med.stanford.edu/profiles/Martin_Brown/
Anne Brunet. Our lab studies aging and age-related diseases. We explore the genetic and epigenetic mechanisms of longevity in a range of organisms (worms, short-lived fish, and mammals). We are also interested in brain aging, focusing on aging neural stem cells.
Website:http://www.stanford.edu/group/brunet/
Michele P. Calos. Development of novel vectors and strategies for gene therapy. Both extrachromosomal vectors and vectors that integrate in a site-specific manner are being developed.
Christine A. Cartwright. Molecular mechanisms of oncogene activation in colon cancer.
Chingpin Chang. We focus on understanding the mechanisms of cardiovascular development, particularly how the interactions among the major types of cardiac cells and neural crest cells generate heart tissues. We study the transcriptional and signaling events that coordinate such interactions and assembly into heart tissues.
Howard Y. Chang. Genomic studies of a wound response program in human cancers. Mechanisms of stromal cell specialization in normal and disease states.
James Chen. Understanding embryonic development and oncogenesis at the molecular level, including biochemical events within the Hedgehog and Wnt pathways. Chemical approaches to the study of embryonic patterning.
Yoon-Jae Cho. My laboratory focuses on the study of childhood brain tumors and in particular, medulloblastoma, the most common malignant brain tumor in children. We utilize computational and cell biological approaches to 1) understand the molecular and cellular basis of medulloblastoma, 2) generate new treatment strategies for patients diagnosed with this disease and 3) inform the current and next generation of medulloblastoma clinical trials. We are currently combining genome-wide RNAi with chemical biology and chemical genomic screens to systematically define the functional consequence of genes and biological pathways enriched in the most clinically aggressive subtypes of this disease.
Gilbert Chu. Studies responses of human cells to DNA damage. One focus is the molecular basis for non-homologous end joining, the pathway that repairs double-strand breaks created by ionizing radiation and V(D)J recombination; a second focus is methods for analyzing microarray data to understand the damage response.
http://cmgm.stanford.edu/~chu/
Katrin F. Chua. Mammalian Sir2 proteins in cancer and aging; cellular senescence responses to genotoxic stress; chromatin regulation of genomic instability.
Karlene A. Cimprich. Mechanisms underlying the maintenance of genome stability, with an emphasis on the DNA damage response and DNA damage checkpoints, replication associated DNA damage, mutagenesis and DNA repair processes. We are also interested in understanding the sources of RNA and transcription-associated DNA damage.
http://cimprich.stanford.edu/
Michael Clarke. Dr. Michael F. Clarke is the Associate Director of the Stanford Institute for Stem Cell and Regenerative Medicine. In addition to his clinical duties in the division of Oncology, 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 L. Cleary. The role of onco-proteins in cancer and development. Molecular and cellular biology of lymphoid malignancies; role of lymphoid oncogenes in development.
Jennifer Cochran. The Cochran laboratory uses interdisciplinary approaches in chemistry, engineering, and biophysics to study complex biological systems. Our main goals are to develop new technologies for basic science and biomedical applications. Clinical applications of our research involve bone and wound healing, biomimetic corneas, neural cell regeneration, and cancer imaging and therapy. Our research is driven by the philosophy that in order to control physiological processes it is necessary to understand the molecular mechanisms that drive these processes. We are interested in elucidating molecular details of receptor-mediated cell signaling events; at the same time developing protein and polymer-based tools that will allow us to manipulate cellular processes on a molecular level. For biomedical applications, we are combining rational design and combinatorial methods to create designer protein therapeutics and diagnostic agents.
One such example is highlighted in a recent press release:
http://news-service.stanford.edu/news/2006/may24/cochran-052406.html.
Stanley N. Cohen. Regulation of gene expression in prokaryotes and eukaryotes; cell cycle studies; RNA decay; plasmid biology.
Christopher Contag. Refining immunotherapy through imaging and combination biotherapies.
Gerald R. Crabtree. Regulation in cell proliferation and differentiation. Genetic regulatory mechanisms in T-lymphocyte activation; lymphoid development.
Martha S. Cyert. Mechanisms of Ca2+ dependent signal transduction and role of the conserved protein phosphatase, calcineurin. Genetic, genomic, biochemical and cell biological are applied to study the response of yeast to environmental stress.
Maximilian Diehn. My lab focuses on cancer stem cell biology and its implications for cancer therapy. We are interested in developing a deeper molecular understanding of cancer stem cells, including identifying pathways and genes important for proliferation, survival, and self renewal. We also study these processes in normal adult stem cells in order to identify differences that could be exploited therapeutically. Additionally, we are interested in analyzing and overcoming resistance mechanisms to radiotherapy and chemotherapy in cancer stem cells. The overarching goal of our studies is the development of novel therapeutic strategies for eliminating cancer stem cells in the clinical setting.
Edgar Engleman. Immune mechanisms in pathogenesis and treatment of cancer and autoimmune disease.
Brian Feldman. My laboratory studies the effect of steroid hormones on stem cell fate decisions and the impact of these hormonal signals on body composition and metabolism. We are especially involved in studies of the regulation of the cell fate decision of mesenchymal stem cells to differentiate into adipose cells or muscle and the potential impact this has on the development of insulin resistance and metabolic syndrome. Further, we are exploring the hypothesis that these physiologic signals are important in the pathogenesis of certain cancers via impacting cancer stem cells or metabolic signals of obesity and insulin resistance.
Dean Felsher. How oncogenes induce and sustain tumorigenesis, in particular how MYC proto-oncogene can contribute to tumorigenesis by causing genomic destabilization.
James Ferrell, Jr. Regulation of entry into and progression through mitosis and meiosis; understanding the basic logic of signaling cascades and loops.
Andrew Z. Fire. Cellular responses to foreign nucleic acids; RNA interference; roles of RNA-guided gene silencing in normal development and in disease.
James M. Ford. Mammalian DNA repair and DNA damage inducible responses; p53 tumor suppressor gene; transcription in nucleotide excision repair and mutagenesis; genetic determinants of cancer cell sensitivity to DNA damage.
Judith Frydman. Mechanism of protein folding and protein degradation in eukaryotic cells. Mechanism and function of molecular chaperones. Role of folding defects in cancer and other diseases.
Margaret Fuller. Regulation of self-renewal and differentiation in adult stem cell lineages.
Amato J. Giaccia. Targeting the pathways involved in oxygen sensing in tumors and normal tissue for anticancer therapy and normal tissue repair. Developing new therapeutics to inhibit invasion and metastasis.
Or Gozani. We study the molecular mechanisms by which chromatin-signaling networks effect nuclear and epigenetic programs, and how dysregulation of these pathways leads to cancer.
Lab website: http://www.stanford.edu/group/gozani/
Isabella Graef. We study neuronal development and function using a combination of genetic, cell biological, biochemical, and chemical approaches. The two main foci of our lab are: (1) the interface of signaling and gene regulation in neuronal development, specifically calcineurin-NFAT signaling; and (2) the development of small molecules to modulate protein-protein interactions.
Edward Graves. My laboratory is focused on development and application of molecular imaging techniques towards understanding radiation and cancer biology and improving treatment of human disease. We use modalities including PET, MRI, CT, optical imaging, and small animal conformal radiotherapy to study tumor radiobiology and develop translational imaging and therapeutic approaches.
Andrew Hoffman. Our lab is interested in the epigenetic regulation of gene expression in cancer and in stem cells. We are especially interested in understanding long range chromatin interactions.
Paul A. Khavari. The Khavari laboratory studies stem cell differentiation and cancer. The focus is on genomic reprogramming via epigenetic and genetic regulatory mechanisms as well as on the development of new molecular therapies that target these processes.
Seung Kim. Pancreas developmental biology and disease mechanisms.
Stuart Kim. Mechanisms of aging.
Susan J. Knox. Bcl-2, apoptotic signaling pathways (membrane and mitochondrial-mediated events), development of novel therapeutic strategies to sensitize tumor cells to cytotoxic therapies.
Albert Koong. My laboratory is focused on understanding the role of the unfolded protein response (UPR) in cancer and developing therapies based upon modulating this pathway.
Calvin Jay Kuo. Anti-angiogenic gene therapy, mechanisms of arterial endothelial specification, characterization of a novel mitogen encoded trimerized collagen XVIII endostatin domain.
Quynh Le. Identification and validation of secreted and tissue biomarkers for hypoxia and head and neck cancers; evaluate the relationship between tumor hypoxia and tumor immune privilege, develop novel targeted therapies for head and neck cancer, identify mechanisms of restoring salivary gland function after radiation injury.
Ronald Levy. Immunology and molecular biology of lymphoid malignancy; molecular vaccines for cancer.
Shoshana Levy. Role of the tetraspanin CD81 in the immune system and disease pathogenesis.
Joseph S. Lipsick. Biochemical and genetic interactions of the MYB oncogene and E2F-RB tumor suppressor protein families. Evolution of transcriptional regulation and cell cycle regulation.
Website: http://www.stanford.edu/group/lipsick/
Anson W. Lowe. Regulated secretion and epithelial polarity in exocrine pancreatic cells; cellular precursors of pancreatic cancer.
Bingwei Lu. Neural stem cell biology and neurodegeneration.
Ravindra Majeti. Our lab focuses on the molecular/genomic characterization and therapeutic targeting of leukemia stem cells (LSC) in human hematologic disorders, particularly acute myeloid leukemia. A major focus is the identification of cell surface molecules preferentially expressed on LSC and the development of therapeutic monoclonal antibodies targeting these proteins.
M. Peter Marinkovich. Our lab is focused on studying how interactions among a number of basement-membrane-associated molecules drive tumorigenesis through activation of PI3-kinase, GTPases, and other signaling pathways. In turn, we are studying how these extracellular-derived signals are promoting changes in cell polarity, matrix deposition, proteinase expression, tumor invasion, and protection from cell death. Many of these interactions are proving amenable to antibody-mediated tumor inhibition and hold promise as future cancer therapies.
Tobias Meyer. Systems biology of cell signaling and decision processes.
Beverly Mitchell. The Mitchell lab is focused on the role of nucleolar proteins as therapeutic targets in hematologic malignancies. The specific roles of nucleophosmin and nucleostemin are the major topics of current investigation.
Daria Mochly-Rosen. Protein-protein interactions in cell signaling; PKCs/ALDHs; rational drug design.
Ashby Morrison. We utilize an integrated approach of genetic, biochemical, and molecular techniques to examine the involvement of chromatin in processes that prevent genome instability and the pathogenesis of disease.
http://www.stanford.edu/group/morrison
Robert Negrin. Hematopoietic cell transplantation, immune regulation and cellular immunotherapy.
W. James Nelson. We study molecular mechanisms linking cell-cell adhesion to the development of structural and functional polarity of epithelial cells in tissue development in a wide variety of organisms (zebrafish to slime molds). Our work spans in vitro studies of proteins, ex vivo analysis of cells in tissue culture, and in vivo analysis of early development.
Garry Nolan. High parameter single cell analysis of signaling proteins, cell types, epigenetic states, and mRNA expression patters to delineate and understand cancer lineage and stem cell structures using mass cytometry—a new technology that allows detailed readouts at thousands of cells per second. Use of these technologies to motivate drug screening, immune evasion by cancer, understanding of mechanism, and placement of this understanding against a Systems Biology of Cancer framework in primary human cancer samples.
Roeland Nusse. Role of the Wnt gene family in intercellular signaling during embryogenesis and tumorigenesis. We work on two Drosophila Wnt genes: wingless and DWnt-2.
Anthony E. Oro. Role of Sonic hedgehog (Shh) signaling system in the pathogenesis of basal cell carcinoma (BCCs) of the skin.
Donna Peehl. Development and characterization of realistic and representative preclinical models of prostate and renal cancer.
Sylvia Plevritis. Cancer systems biology. Development of biocomputational and experimental methods that integrate genomic, proteomic and imaging data. Analysis of tumor microenvironment on phenotypic cell state switching. Analysis of early detection strategies for cancer.
Webpage: plevritis.stanford.edu
Jonathan R. Pollack. Application of genomic approaches, including DNA microarrays and next-generation DNA sequencing, to characterize alterations in cancer genomes, with emphasis on common epithelial tumor types. Broad goals include the discovery and characterization of new cancer genes and biomarkers, and the mechanisms underlying genomic instability and the shaping of cancer genomes.
Lab website: http://pollacklab.stanford.edu
Matthew Porteus. Genome Editing and Population Dynamics for Gene Therapy and Cancer Research.
Marlene Rabinovitch. Regulation of genes associated both with tumor cell proliferation and metastasis and with cardiovascular disease. How alterations in matrix-cell interactions, mRNA translation, and co-dependence of receptor signaling pathways cause malignant behavior of cancer and vascular cells.
Thomas Rando.
Associate Professor, Neurology & Neurological Sciences: Member, Bio-X
Our laboratory studies the basic molecular mechanisms of muscle stem cell activation, the effects of aging on skeletal muscle, and gene therapy for hereditary muscle diseases.
Jianghong Rao. We are interested in developing novel molecular probes for specific tumor imaging and cancer diagnostics. Our current focuses are to 1) synthesize nanoparticle-based biosensors, and 2) engineer trans-splicing ribozymes for tumor targeting and imaging.
Renee A. Reijo Pera. Our laboratory studies human embryonic development and pluripotent stem cells as a model of normal development and disease. We focus on innate human reprogramming that encompasses nuclear fusion, epigenetic remodeling, degradation of maternal programs and activation of the embryonic genome. We use human induced pluripotent stem cells to model differentiation of specific lineages, especially the germ line and neural lineages. Projects encompass identification and characterization of embryonic genes, differentiation and programs that are altered in neurodegeneration.
Rajat Rohatgi. Temporal and spatial regulation of signal transduction at primary cilia.
Glenn D. Rosen. Characterization of apoptotic and growth stimulatory pathways in tumor cells. Regulation of the jun kinase pathway in tumor cells.
Julien Sage. Molecular and cellular mechanisms of tumorigenesis and regeneration, with a focus on stem cell biology.
Kathleen Sakamoto. Normal and aberrant hematopoiesis, including leukemia and bone marrow failure.
Matthew Scott. Molecular genetics of pattern formation and gene regulation in animal development and disease, focusing on Hedgehog pathway signal transduction and gene regulation in development and cancer. Intracellular trafficking of sterols and its relation to neurodegeneration.
http://scottlab.stanford.edu/
Lucy Shapiro. Systems architecture regulating asymmetric cell division.
Arend Sidow. Genomics of gene regulation and cancer.
Branimir Sikic. Cancer drug resistance, predictive therapeutic biomarkers, new therapies.
Tim Stearns. We study the organization and regulation of the microtubule cytoskeleton, and the relationship between the cell cycle and the cytoskeleton.
Zijie Sun. Work in our lab is focused on investigating transcriptional regulation that governs the transformation of normal mammalian cells to neoplastic state. Specifically we use biochemical and molecular biological approaches and mouse models to study roles of the nuclear hormone receptors and their interactions with Wnt and TGF-beta signaling pathways in tumorigenesis.
John Sunwoo. Natural killer cells, cancer stem cells.
Alejandro Sweet-Cordero. Our laboratory is devoted to the analysis of pathways involved in the initiation, progression, and maintenance of cancer. Utilizing both human and mouse model systems, we study aberrant oncogenic signaling, the role of the tumor microenvironment, and the mechanisms involved in chemotherapy response and resistance at the molecular, cellular, and organismal levels. We use functional-genomic approaches to identify genes that are relevant to cancer pathogenesis and treatment. Currently, our research focuses on the biology of sarcomas as well as on lung cancer pathogenesis and treatment.
Mary N. Teruel. Systems biology of cell differentiation and cell signaling networks controlling metabolism, obesity, and cancer.
http://med.stanford.edu/labs/mary-teruel/
Virginia Walbot. Developmental regulation of Mutator transposons just before meiosis and the development of anthers in maize, particularly specification of meiotically competent cells and their neighboring somatic support cells.
Learn more about us at: http://www.stanford.edu/%7Ewalbot/
William Weis. Molecular mechanisms controlling the development and maintenance of eukaryotic cell and tissue structure, focusing on cell-cell adhesion, cell polarity, and Wnt signaling.
Irving L. Weissman. Development of T and B lymphocytes; cell-surface receptors for oncornaviruses in leukemia. Hematopoietic stem cells; lymphocyte homing, lymphoma invasiveness and metastasis.
Marius Wernig. We study epigenetic reprogramming, in particular the induction of neuronal (iN) cells and pluripotent stem (iPS) cells from skin fibroblasts, the underlying molecular mechanism, disease modeling and therapeutic applications of reprogramming methods in mouse and human.
http://stemcell.stanford.edu/about/Laboratories/wernig/index.html
Monte Winslow. Our laboratory uses genome-wide methods to uncover alterations that drive cancer progression and metastasis in genetically-engineered mouse models of human cancers. We combine cell-culture based mechanistic studies with our ability to alter pathways of interest during tumor progression in vivo to better understand each step of metastatic spread and to uncover the therapeutic vulnerabilities of advanced cancer cells.
Albert Wong. The goal of our laboratory is to define targets for cancer therapeutics by identifying alterations in signal-transduction proteins. Our lab first identified a spontaneously occurring mutant epidermal-growth-factor receptor (EGFRvIII) in glioblastoma. Basic studies on the signal-transduction pathways initiated by EGFRvIII have uncovered two other critical targets, the c-Jun N-terminal kinase (JNK) and Gab1. Our translational work has created diagnostic tools for EGFRvIII and a vaccine therapy currently in Phase II clinical trials.