Oncogenes and Cancer Biology
Cancer is one of the leading causes of death worldwide, and it is estimated that approximately one out of every three people will be diagnosed with cancer in their lifetime. The principle goal in cancer biology is to understand more about what makes cancer different than normal, in order to identify strategies to selectively eradicate these abnormal cells. In its basic tenets, cancer is a set of related diseases caused by genetic mutations that dysregulate cell growth and survival. Although every cancer subtype is distinct, these mutations produce a set of “hallmark” traits that are shared by all cancers. For example, cancer cells have unlimited proliferation capability and tend to grow rapidly. They have gained the ability to block immune responses and to evade cell death. And they have changed the rules that regulate growth/survival/movement in normal cells, to facilitate their dissemination and colonization of distant parts of the body. Research by investigators in Molecular Medicine aims to discover genes that regulate tumorigenesis, to understand the basic regulation of biological processes that are altered in cancer cells and to improve our ability to identify, prevent, and treat various forms of cancer.
Bach Lab
Our research investigates molecular and epigenetic mechanisms of gene expression during cell fate specification. We use mouse embryogenesis as model system applying molecular, biochemical and genetic methods. (Bach profile)
Benanti Lab
Our laboratory is interested in the molecular mechanisms that control how cells grow and divide. We are using genetics, biochemistry and cell biology, in both yeast and mammalian cells, to study how protein degradation by the ubiquitin proteasome system controls cell cycle and metabolic transitions. (Benanti profile)
Brehm Lab
Our laboratory studies the biological mechanisms that control human immune responses to infectious agents and transplanted non-self tissues. To investigate these mechanisms we are using humanized mouse models that contain functional human immune systems. The humanized mice are generated using immnodeficient mice, which are engrafted with either human hematopoietic stem cells or with mature human immune cells. These humanized mouse models allow the direct study of human immunity that is not possible with patients. (Brehm profile)
Brodsky Lab
We use Drosophila melanogaster as a model organism to study how cells distinguish between normal and dysfunctional chromosomes. We are particularly interested in how p53-dependent and p53-independent signaling pathways regulate apoptosis in response to DNA damage and unprotected telomeres. (Brodsky profile)
Castilla Lab
Our laboratory studies how leukemia oncogenes alter cellular programs to transform hematopoietic stem and progenitor cells into a leukemia initiating cells. We combine genetic, biochemistry, and molecular biology approaches in transgenic mice and human cells to identify and characterize pathways deregulated by mutations in the members of the CBF gene family that redefine survival, self-renewal, and expansion of pre-leukemic progenitors. Recent efforts use this knowledge to develop high throughput small-molecule screens to identify inhibitors of oncoproteins that may be used as new drugs for improved therapies. (Castilla profile)
Ceol Lab
Our laboratory is interested in the genetic and molecular mechanisms underlying tumor initiation and maintenance. We focus primarily on melanoma, using genetically-engineered zebrafish models and mammalian cultured cells to identify unique features of cancer cells that can potentially be used for diagnostic, prognostic or therapeutic benefit. (Ceol profile)
Davis Lab
The cJun NH2-terminal kinase (JNK) signal transduction pathway is implicated in several stress-related disease processes including cancer, diabetes, inflammation, and stroke. Our hope is that drugs targeting the JNK pathway may be useful for the treatment of these diseases. The goal of this laboratory is to understand the molecular processes that are engaged by JNK in both health and disease. (Davis profile)
Fazzio Lab
Our lab is focused on the identification of regulatory networks controlling gene expression in stem cells. In particular, we are interested in the roles of chromatin regulators in stem cell self-renewal and differentiation, and we take molecular, genomic, and biochemical approaches to understand these processes. (Fazzio profile)
Green Lab
My lab is interested in the mechanisms that regulate gene expression in eukaryotes, and the role of gene expression in various human disease states. A major emphasis is the use of transcription-based approaches and functional screens to identify new genes and regulatory pathways involved in cancer. (Green profile)
Greiner Lab
Our laboratory investigates the pathogenesis of type 1 diabetes, how to prevent it, and how to reverse it through islet transplantation. We use mouse and rat models of type 1 diabetes, and are building mice with human immune systems that permit the direct study of human disease without putting patients at risk. (Greiner profile)
Kaufman Lab
We study several different classes of proteins used by eukaryotic cells to deposit histones onto DNA, as well as enzyme complexes that chemically modify chromosome proteins in order to alter DNA accessibility. We study these processes in yeast and human cells, using biochemical, genetic, genomic, and cell biological techniques. (Kaufman profile)
Lambright Lab
Crystallographic, biophysical, biochemical, and cell biological approaches are used to investigate mechanisms of membrane trafficking and cell signaling. Defects in these fundamental regulatory mechanisms play critical roles in genetically linked disorders and complex disease states including cancer and diabetes. (Lambright profile)
Lee Lab
Treatment of many human diseases, including cancer, typically involves modulation of signal transduction pathways. These pathways are functionally integrated, very plastic, and incredibly sensitive to environmental context. Our group uses a combination of experimental and computational approaches to study the organization and function of signaling networks controlling the growth, survival, and death of cancer cells. We are particularly interested in understanding the adaptive properties that cells engage when faced with anti-cancer drugs, as well as identifying genetic, non-genetic, and contextual factors that contribute to the therapeutic variability seen in cancer patients. (Lee profile)
Lewis Lab
Primary pancreatic and liver cancers are deadly malignancies characterized by the rapid decline of patients after diagnosis. Work in the Lewis lab aims to elucidate the molecules and signaling pathways involved in tumor initiation, tumor progression and metastasis, and response to therapy in these tumors, using genetically engineered mouse models, cultured primary cells, and cancer cell lines. (Lewis profile)
Tissenbaum Lab
Our work in focused on understanding the molecular mechanisms involved in the aging process using a combination of genetics, molecular biology and biochemistry. Our long term goal is to increase the healthspan (the number of active, productive years before the onset of age-associated decline) of individuals; redefining middle age. (Tissenbaum profile)
Torres Lab
Our research interests are focused on understanding how aneuploidy affects cellular physiology and metabolism, and how aneuploidy influences cell evolution leading to further gross genomic alterations. Utilizing Saccharomyces cerevisiae as a model organism, we generated a series of aneuploid strains, each carrying an additional copy of 1 of the 16 yeast chromosomes and characterized their effects on cell physiology. (Torres profile)
Xue Lab
Our lab uses mouse models of cancer to investigate cancer genetics and treatment. We use CRISPR genome editing to functionally dissect cancer mutations in liver and lung cancer. Projects are ongoing to develop CRISPR tools to speed up cancer gene discovery and disease gene repair. (Xue profile)