Website: http://www.niehs.nih.gov/research/atniehs/labs/lmc/cge/index.cfm
Email: archer1@niehs.nih.gov
Voice: (919) 316-4565
Molecular carcinogenesis: cancer, chromatin, transcription, and epigenetics
]]>Email:aziz_sancar@med.unc.edu
Voice: 919.962.0115
]]>Website: http://www.med.unc.edu/pharm/people/primaryfaculty/channing-der-1
Email: cjder@med.unc.edu
Voice: (919) 966-5634
Our research centers on understanding the molecular basis of human carcinogenesis. In particular, a major focus of our studies is the Ras oncogene and Ras-mediated signal transduction. The goals of our studies include the delineation of the complex components of Ras signaling and the development of anti-Ras inhibitors for cancer treatment. Another major focus of our studies involves our validation of the involvement of Ras-related small GTPases (e.g., Ral, Rho) in cancer. We utilize a broad spectrum of technical approaches that include cell culture and mouse models, C. elegans, protein crystallography, microarray gene expression or proteomics analyses, and clinical trial analyses.
]]>Website: http://www.med.unc.edu/ent/research/cancer-research-1/d-neil-hayes-md-mph
Email: hayes@med.unc.edu
Voice: (919) 966-3786
Molecular carcinogenesis, research translation, biomarkers, computational toxicology
]]>Website: http://www.med.unc.edu/kaufmannlab
Email: william.kaufmann@pathology.unc.edu
Voice: (919) 966-8209
Research in the Kaufmann laboratory is concerned with determining the mechanisms whereby cell cycle checkpoints suppress human cancer development. We are focused on two checkpoints that help to stabilize the genome. The decatenation G2 checkpoint delays mitosis until daughter chromatids are sufficiently disentangled by topoisomerase II. This checkpoint is regulated by the breast cancer susceptibility gene BRCA1. The intra-S checkpoint regulates DNA synthesis by controlling the rates of replicon initiation and DNA chain elongation. This checkpoint is regulated by two proteins, Timeless and Tipin, that mediate signaling at stalled replication forks. A program project is studying how the Timeless-Tipin replication fork protection complex protects against UV-induced chromosomal damage and sunlight-induced melanoma.
]]>Website: http://www.med.unc.edu/biochem/ramsden
Email: dale_ramsden@med.unc.edu
Voice: (919) 966-9839
The end joining pathway is a major means for repairing chromosome breaks in vertebrates. My lab is using cellular and cell-free models to learn how end joining works, and what happens when it doesn't.
]]>Email: rathmell@unc.edu
Voice: (919) 966-3522
The focus of my research group is the tumorigenesis of renal cell carcinoma. Our approach utilizes genetically engineered cells expressing clinically important point mutations in genes identified from renal cancers. Using cellular and animal models we are able to investigate processes integral to tumorigenesis including angiogenesis, hypoxic response signaling, extracellular matrix remodeling, and cell cycle signaling. Using data from the experimental models, I oversee a clinical research program that offers biologically active protocols to patients with renal cell carcinoma and examines correlative radiographic and serum or tumor biomarkers of tumor response to treatment.
]]>Website: http://cancer.med.unc.edu/research/faculty/displayMember.asp?ID=274
Email: norman_sharpless@med.unc.edu
Voice: (919) 966-1185
The lab relies on murine genetic approaches to study the roles of the INK4/ARF tumor suppressor locus in human cancer and aging. At present, the lab has two main focuses: Stem Cell Aging:Cancer and degenerative diseases are much more common in old people than young. Although this has been well-recognized in clinical medicine for decades, scientists do not agree as to why this occurs. Recently, work from several labs including our own has shown that humans age, in part, because important regenerative cells lose their capacity to divide with the passage of time. That is, the tissues and organs from old people are less able to replace and regenerate lost or damaged cells than the corresponding tissues and organs from young people. Our lab has studied mechanisms that underlie this age-dependent failure of cell division; in fact, we have shown the surprising result that cellular programs that function to prevent cancer untowardly also affect aging. Specifically, cellular “senescence” is now believed to be of major importance in the process of aging. Senescence refers to a permanent growth arrest induced in formerly dividing cells by the activation of genes that prevent cancer. The good news in this system is that the normal functioning of these ‘tumor suppressor genes’ prevents cancer; the bad news is that these same genetic events appear to cause aging by activating cellular senescence. Melanoma and Murine Models of Cancer: Because of the important role of p16INK4a in preventing melanoma, the lab has long been interested in this particularly deadly form of skin cancer. Specifically, we are interested in using genetically engineered models of cancer to study melanoma genetics. We have shown a role for the p16INK4a-RB and ARF-p53 tumor suppressor pathways in repressing this important human cancer in response to RAS-RAF activation. We have generated highly faithful models of human melanoma, and have used these to study novel therapeutics. We have also discovered a novel human melanoma sub-type based on expression profiling, and have identified a new therapeutic target (CD200) for treatment of melanoma.
]]>Website: http://www.sph.unc.edu/?option=com_profiles&Itemid;=1891&profileAction;=ProfDetail&pid;=704283985
Email: james_swenberg@unc.edu
Voice: (919) 966-6139
My laboratory focuses on understanding mechanisms of carcinogenesis, with emphasis on the role of DNA damage and repair. During the last few years, we have developed ultra-sensitive and highly specific mass spectrometry methods for measuring the DNA and hemoglobin adducts of vinyl chloride, crotonaldehyde, ethylene oxide, propylene oxide, styrene oxide, butadiene, malondialdehyde, cis-platin and O6-methyldeoxy-guanosine, as well as slotblot methods for AP sites and oxidative DNA damage. These methods have been applied to understanding critical mechanisms in carcinogenesis, as well as undertaking molecular epidemiology studies of workers in the butadiene and reinforced plastics industries. We are also examining changes in gene expression associated with oxidative stress and environmental chemical exposure.
]]>Website: http://www.med.unc.edu/derm/research/dr.-nancy-thomas-lab
Email: nancy_thomas@med.unc.edu
Voice: (919) 966-0785
Molecular carcinogenesis, environmental toxicology, research translation, biomarkers
]]>Website: http://www.med.unc.edu/pathology/faculty/biosketch-of-dr.-vaziri
Email: cyrus_vaziri@med.unc.edu
Voice: (919) 843-9639
Our broad long-term goal is to understand how mammalian cells maintain ordered control of DNA replication during normal passage through an unperturbed cell cycle, and in response to genotoxins (DNA-damaging agents). DNA synthesis is a fundamental process for normal growth and development and accurate replication of DNA is crucial for maintenance of genomic stability. Many cancers display defects in regulation of DNA synthesis and it is important to understand the molecular basis for aberrant DNA replication in tumors. Moreover, since many chemotherapies specifically target cells in S-phase, a more detailed understanding of DNA replication could allow the rational design of novel cancer therapeutics. Our lab focuses on three main aspects of DNA replication control: (1) The S-phase checkpoint, (2) Trans-Lesion Synthesis (TLS) and (3) Re-replication.
]]>Website: http://cancer.med.unc.edu/research/faculty/displayMember.asp?ID=208
Email: weissman@med.unc.edu
Voice: (919) 966-7533
How the loss of different components of the SWI/SNF complex contributes to neoplastic transformation remains an open and important question. My laboratory concentrates on addressing this question by the combined use of biological, biochemical and mouse models for SWI/SNF complex function.
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