Dr. Toru Ouchi is a graduate from the Osaka University School of Medicine. After postdoctoral training at the Rockefeller University, he started his lab at the Mt. Sinai School of Medicine of New York University to study molecular mechanism of mammary tumor development of BRCA1-deficiencet cells. In 2012, he joined Roswell Park Cancer Institute from University of Chicago as Member and Professor of Oncology.
He is involved in Cellular and Molecular Biology Graduate Program and Genetics, Genomics and Bioinformatics Graduate Program of University at Buffalo. He is chairing the Systems Biology Lecture Series.
Our research uses cell culture, animal model and genome dataset. Biological functions of cellular proteins are investigated by overexpression/knockdown/knockout in cell culture and animal model. We are studying how abnormal activation/inactivation of specific signaling pathways results in causing human diseases. We are also performing translational analysis by taking advantage of anti-disease drugs in both models.
Aglipay, J. and Ouchi, T. (2005) ATM activation by ionizing radiation requires BRCA1-associated BAAT1, J. Biol. Chem. 281, 9710-9718.
Martin, S.A. and Ouchi, T. (2005) BRCA1 phosphorylation regulates caspase-3 activation in UV-induced apoptosis, Cancer Res., 65, 10657-10662.
Wang, X., Zhou, Y.-X., Qiao, W., Tominaga, Y., Ouchi, M., Ouchi, T. and Deng, C. (2006) Over expression of Aurora kinase A in mouse mammary epithelium induces genetic instability precedes mammary tumor formation, Oncogene 25, 7148-7158.
Lin S., Du, P., Jafari, N. and Ouchi, T (2009) Using Open-Source Bioconductor Package to Analyze Array Comparative Genomics Hybridization (cCGH) Data, Current Genomics 10, 60-63.
Ouchi, M. and Ouchi, T. (2010) Regulation of ATM/DNA-PKcs phosphorylation by BRCA1-associated BAAT1, Genes & Cancer, 1, 1211-1214.
Ausman, M., So, E.-Y., and Ouchi, T. (2012) DNA damage induces reactive oxygen species generation through the H2AX-Nox1/Rac1 pathway, Cell Death Dis, 3, e249.
Ausman, M. and Ouchi, T. (2012) Deregulation of the DNA response pathway by intercellular contact, J. Bio. Chem., 287, 116246-16255.
So, E.-Y., and Ouchi, T. (2014) Decreased DNA repair activity in bone marrow due to low expression of DNA damage repair proteins, Cancer Biology & Therapy, 15, 906-910.