We are studying the novel, RNA-based pathways and virus-host interactions underlying replication, gene expression and evolution by positive-strand RNA viruses, the largest class of viruses.
The focus of our research is on understanding the molecular mechanisms governing the activity of estrogen receptor (ER), a member of the nuclear receptor transcription factor family that is critical in normal reproduction and is implicated in the pathogenesis of breast cancer.
We are studying aspects of mammary gland biology and neoplasia using transgenic mouse models. Particularly, we have found that Wnt signaling dysregulates mammary stem cells, and that this precedes the formation of differentiated, bilineal tumors.
Our laboratory is interested in a family of transcriptional regulators known as PAS proteins. Members of this emerging family of proteins control a number of processes, including xenobiotic metabolism (Ah-receptor and Arnt), circadian rhythms (Per), angiogenesis (HIF1a and Arnt), and neurogenesis (Sim).
Dr. Burkard is a chemical biologist and medical oncologist who specializes the treatment of breast cancer. His research laboratory is focused on using chemical biology to identify and validate mitotic protein kinases as breast cancer drug targets. The laboratory seeks to advance cancer therapy by two approaches-candidate evaluation (“bottom-up”) and therapeutic strategy (“top-down”).
My laboratory is investigating kinase modulation of cellular signaling pathways driven by oncogenic mutant proteins. To screen combinations of targeted agents in the setting of specific genetic alterations, novel mouse models of colorectal cancer including tumors driven by a constitutively active PI3K [Cancer Research, 2012; PLoSOne, 2013; Oncogene, 2013].
The research in our laboratory is designed to enable cells to protect their genomes against toxic molecules, whether the toxins are formed during normal oxidative life, cancer therapy, metabolism of environmental toxicants or exposure to ionizing radiation.
Our research focuses on the molecular biology of Epstein-Barr virus (EBV) nuclear proteins, their role in the virus lifecycle and the pathogenesis of EBV associated malignancies.
Our lab focuses on determining the mechanisms of human cytomegalovirus (HCMV) replication and pathogenesis, and also uses the virus as a tool to probe the pathways that lead to cell cycle progression and oncogenesis.
Our lab’s research is focused on understanding the role of human papillomavirus (HPV) in cancer. HPVs cause 5% of all human cancers. These include cervical cancer, other anogenital cancers and a growing proportion of head and neck cancers.
We are studying the mechanisms of RNA encapsidation, initiation and synthesis of minus-strand DNA, initiation and synthesis of plus-strand DNA, and genome circularization during plus-strand DNA synthesis.
Over the last two decades, the Miyamoto lab has pursued a variety of research interests centered around cell signaling and asked "what happens when cells are no longer able to communicate effectively?" Most of the current research is focused on understanding the NF-κB signaling pathway as a model. Our lab, and others, have shown that NF-κB is key in promoting cell survival (anti-apoptotic), normal immune system development, stress response, early embryonic development, cell adhesion, and tumor metastasis.
Retroviruses cause a variety of cancers and immunodeficiencies throughout the animal kingdom. Our group is interested in the cell biology underlying the assembly and spread of the human immunodeficiency virus type 1 (HIV-1), the etiological agent causing the acquired immunodeficiency syndrome (AIDS), as well as oncoretroviruses such as the murine leukaemia virus (MLV).
Estrogens are inextricably implicated in the etiology of breast cancer. The primary goals of our research group are to utilize the ACI rat model of 17β-estradiol (E2)-induced mammary cancer to identify novel genetic determinants of breast cancer susceptibility and to define the molecular mechanisms through which estrogens contribute to development of breast cancer.
Our research focuses on two facets of EBV pivotal to its inducing and maintaining human tumors. One gene product of EBV, LMP1, mimics cellular signaling pathways but in a ligand-independent manner. Its signaling drives proliferation of EBV-infected B-cells, but at high levels inhibits that proliferation.
Our lab focuses on discovering the molecular mechanisms underlying force production, mitotic checkpoint control, and error correction in accurate cell division, with a focus on the role of the highly conserved Ndc80 complex and the kinetochore structural integirty. We recently developed a FRET (fluorescent resonance energy transfer)-based Ndc80 tension biosensor, which allows us to measure cellular tension using light microscopy.
My lab is interested in elucidation of signaling pathways related to cancer using multi-disciplinary biophysics and biochemical approaches, including structural biology and proteomics, in combination with cell biology. We focus on signaling pathways that affect cancer cell metabolism and cancer cell genome integrity.
My laboratory is focused on the transcriptional regulation of estrogen receptor (ER) signaling pathways by nuclear receptor co-factors. Estrogen receptors regulate cell proliferation, differentiation and cell cycle control in a cell- and tissue-specific manner.
Emeritus Faculty Profiles
As an Emeritus faculty member, Dr. Burgess no longer accepts students or postdocs.
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As an Emeritus faculty member, Dr. Dove no longer accepts students or postdocs. He continues in McArdle to study the research literature and to discuss ways to detect early neoplastic stages that are likely to progress to cancer.
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As an Emeritus faculty member, Dr. Gould no longer accepts students or postdocs.
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As an Emeritus faculty member, Dr. Hoffmann no longer accepts students or postdocs.
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As an Emeritus faculty member, Dr. Pitot no longer accepts students or postdocs.
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As an Emeritus faculty member, Dr. Ross no longer accepts students or postdocs. Dr. Ross continues to teach ONC 735.
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