- Keynote Speakers
- Midwest DNA Program Booklet
Program for Midwest DNA Repair Symposium
Health Science Campus, Mail Stop #1010
3000 Arlington Avenue
Toledo, OH 43614
We will have three keynote speakers and an invited guest speaker during our banquet
|"Random Mutations in Human Cancers: Origins and Consequences"|
|Lawrence A. Loeb, M.D., Ph.D.
Professor of Pathology and Biochemistry
University of Washington School of Medicine
|Larry Loeb, M.D., Ph.D., has been Professor and Director of the Joseph Gottstein Research
Laboratory in the Department of Pathology at the University of Washington since 1978.
Dr. Loeb's research interests are
focused on the association of somatic mutations with human cancers. In 1974, he proposed
the hypothesis that the large
numbers of mutations in human cancers result from the expression of a mutator phenotype.
His laboratory consists of five
postdoctoral fellows, two MD/PhD students, two research scientists, usually a visiting
professor and several undergraduates.
They have extensive experience in measuring the fidelity of DNA synthesis by purified
DNA polymerases and in measuring random
mutations in human tumors. For many years, his laboratory has collaborated with investigators
throughout the world in
studying genetic instability in cancer. He was awarded an NCI Outstanding Investigator
Award from 1985-1999, and has
received numerous meritorious scientific achievement awards from throughout the world.
He is past president of the American
Association for Cancer Research and the Environmental Mutagen Society.
"The Good, the Bad, and the Ugly Related to ERCC1-Deficiency"
|Laura J. Niedernhofer, M.D., Ph.D.
Associate Professor of Microbiology and Molecular Genetics
University of Pittsburgh School of Medicine
|Laura Niedernhofer, M.D., Ph.D. is an Associate Professor in the Department of Microbiology
Molecular Genetics at the University of Pittsburgh School of Medicine and is a member
of the University of Pittsburgh Cancer
Institute. The goal of her research is to understand the health impact of DNA damage.
Inherited diseases caused by defects
in DNA repair mechanisms reveal that DNA damage can drive not only cancer but also
many other age-related diseases such as
neurodegeneration and osteoporosis. Her research team uses mouse models of these
genome instability disorders to test
hypotheses about the underlying mechanism of age-associated degenerative changes including
the contribution of stem cell
dysfunction, mitochondrial dysfunction and signaling pathways. In addition, they
are investigating how DNA repair mechanisms
contribute to resistance to cancer chemotherapy. Their goal is to develop analytical
tests to identify patients most likely
to respond to genotoxic chemotherapeutics and selective inhibitors of DNA repair mechanisms
that will sensitize tumors to these
"Function and Control of Translesion DNA Polymerases"
|Graham C. Walker, Ph.D.
American Cancer Society Research Professor
HHMI Professor of Biology
Massachusetts Institute of Technology
|Graham Walker, Ph.D. is an American Cancer Society Research Professor and HHMI Professor
Department of Biology at the Massachusetts Institute of Technology. He is a senior
co-author of the 1st and 2nd
second editions of DNA Repair and Mutagenesis (ASM Press). For the past 36 years, Graham has worked on how cells respond to
DNA damage, with a particular emphasis on how such DNA damage causes mutations. His
lab was the first to clone and sequence the
mismatch repair genes mutS and mutL, whose human homologs have been implicated in Lynch Syndrome (Hereditary Non
Polyposis Colon Cancer). His recent findings have included the discovery that UmuD2 and RecA regulate DinB (DNA pol IV)
and that NusA, a component of elongating RNA polymerases, has previously unsuspected
roles in DNA repair and damage tolerance.
Graham’s research on bacterial DNA repair is synergistically related to his recent
studies of eukaryotic DNA repair. His
research team has shown that levels of the S. cerevisiae Y Family DNA polymerase Rev1 are strikingly regulated during the
cell cycle and have analyzed various protein-protein interactions necessary for its
function. They have shown that decreasing
levels of the mutagenic translesion DNA polymerases can improve chemotherapy, and
have been working on developing a drug to
inhibit mutagenesis in humans after exposure to a DNA damaging agent by blocking the
Rev1/Rev3/Rev7 pathway of mutagenic
Saturday evening banquet speaker, Dr. Bernard Strauss
|"50 Years of DNA Repair and Mutation Research"
Bernard S. Strauss, Ph.D.
Professor Emeritus, Molecular Genetics and Cell Biology
The University of Chicago