The research of the McArdle Laboratory for Cancer Research is divided into three broad categories: Biochemical Studies in Chemical Carcinogenesis, Molecular Biology and Genetics of Tumor Viruses, and Regulatory Mechanisms in Tumor Biology. The chemical carcinogenesis program encompasses a broad fundamental approach to the chemistry, biochemistry, and biology of tumor initiation and promotion by chemicals. The overall objective of these studies is a detailed knowledge of chemical carcinogenesis that will facilitate the identification of the stages at which controls can be imposed on the process. The studies in tumor virology have as their overall objective a broad understanding of the molecular biology and genetics of the oncogenic retro-, papova-, and herpes-viruses. The ultimate goal of these studies is the elucidation of the features that determine the oncogenicity of these viruses and the mechanisms by which they cause transformation. Of special interest are the essential features of the DNA genomes of these viruses, genetic factors that influence the expression of the viral oncogenes, and control of transcription of the viral genomes. The tumor biology program is a multidisciplinary approach to regulatory mechanisms that influence the growth, replication, and differentiation of normal and cancer cells. The approaches include studies of DNA and chromatin replication, transcription of DNA, the processing of nuclear RNA, the stability of mRNA and its transport to the cytoplasm, the mechanisms of differentiation of phage and of various cell types, and the immunogenetics of transplantation antigens of the mouse.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Center Core Grants (P30)
Project #
5P30CA007175-22
Application #
3101237
Study Section
(SRC)
Project Start
1978-09-01
Project End
1987-02-28
Budget Start
1985-03-01
Budget End
1986-02-28
Support Year
22
Fiscal Year
1985
Total Cost
Indirect Cost
Name
University of Wisconsin Madison
Department
Type
Schools of Medicine
DUNS #
161202122
City
Madison
State
WI
Country
United States
Zip Code
53715
Thompson, Nancy E; Glaser, Bryan T; Foley, Katherine M et al. (2009) Minimal promoter systems reveal the importance of conserved residues in the B-finger of human transcription factor IIB. J Biol Chem 284:24754-66
Habig, Jeffrey W; Loeb, Daniel D (2006) Sequence identity of the direct repeats, DR1 and DR2, contributes to the discrimination between primer translocation and in situ priming during replication of the duck hepatitis B virus. J Mol Biol 364:32-43
Liu, Ning; Ji, Lin; Maguire, Megan L et al. (2004) cis-Acting sequences that contribute to the synthesis of relaxed-circular DNA of human hepatitis B virus. J Virol 78:642-9
Tessier, Charles R; Doyle, Glenn A; Clark, Brad A et al. (2004) Mammary tumor induction in transgenic mice expressing an RNA-binding protein. Cancer Res 64:209-14
Ostrow, Kristin M; Loeb, Daniel D (2004) Underrepresentation of the 3' region of the capsid pregenomic RNA of duck hepatitis B virus. J Virol 78:2179-86
Habig, Jeffrey W; Loeb, Daniel D (2003) Template switches during plus-strand DNA synthesis of duck hepatitis B virus are influenced by the base composition of the minus-strand terminal redundancy. J Virol 77:12412-20
Habig, Jeffrey W; Loeb, Daniel D (2003) The conformation of the 3' end of the minus-strand DNA makes multiple contributions to template switches during plus-strand DNA synthesis of duck hepatitis B virus. J Virol 77:12401-11
Bunger, Maureen K; Moran, Susan M; Glover, Edward et al. (2003) Resistance to 2,3,7,8-tetrachlorodibenzo-p-dioxin toxicity and abnormal liver development in mice carrying a mutation in the nuclear localization sequence of the aryl hydrocarbon receptor. J Biol Chem 278:17767-74
Liu, Ning; Tian, Ru; Loeb, Daniel D (2003) Base pairing among three cis-acting sequences contributes to template switching during hepadnavirus reverse transcription. Proc Natl Acad Sci U S A 100:1984-9
Mueller-Hill, Karlyn; Loeb, Daniel D (2002) cis-Acting sequences 5E, M, and 3E interact to contribute to primer translocation and circularization during reverse transcription of avian hepadnavirus DNA. J Virol 76:4260-6

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