Tyler Jacks, Ph.D., is Investigator, Howard Hughes Medical Institute and David H. Koch Professor of
Biology, Massachusetts Institute of Technology, Center for Cancer Research. Dr. Jacks' longstanding
interest in the construction and characterization of mouse models of cancer and his current research on
the use of gene targeting has led to more powerful and accurate models of human cancer.
In 1992 Dr. Jacks joined the faculty at MIT's Department of Biology and the Center for Cancer
Research (CCR). In 2001, he had been named Director for the Center for Cancer Research.
Dr. Jacks' research has focused on the construction and characterization of mouse models of cancer.
His group has produced mice with mutations in several tumor suppressor genes, oncogenes, and genes
involved in cell cycle control and
apoptosis. Dr. Jacks and his colleagues have been able to model various human tumor syndromes and
cancer types. Using both in vivo and cell-based methods, he has
investigated the function of the Rb gene family, functional overlap within
this family, and genetic interactions between the Rb and p53 pathways. In a series of experiments with particular relevance to the
treatment human cancer, Dr. Jacks and colleagues have discovered the requirement for p53 in DNA damage-induced apoptosis in thymocytes and tumor cells and have made
major contributions to the understanding of p53 function and regulation.
Dr. Jacks' current research remains centered on the use of gene targeting to create more powerful and
accurate mouse models of human cancer and to explore the pathways regulated by cancer-associated genes.
He has recently developed novel strategies for cell-specific activation of the K-ras, which has led to important new models of lung cancer. Dr. Jacks and
colleagues are currently using this strategy with a variety of compound-mutant mice to improve the lung
cancer model and to develop new models of cancer of the colon, ovary and breast, among others. These
strains are being evaluated with cutting-edge tools in genetics, genomics and imaging, as well as with
various chemotherapeutic agents. Recent cell-based studies have led to important new insights into the
limitations of functional compensation, the regulation of p53-dependent
apoptosis, and the cellular effects of activation of the K-ras.
Dr. Jacks has served as a member of the National Cancer Institute Board of Scientific Advisors and
the Board of Directors of the American Association for Cancer Research (AACR). He was a long-term member
of the Board of Scientific Advisors of the National Cancer Institute (NCI) and was co-Chair of the
steering committee of the NCI-sponsored Mouse Models of Human Cancer Consortium. Dr. Jacks was a Merck
Fellow of the Helen Hay Whitney Foundation, a Markey and a Searle Scholar and is currently a Daniel K.
Ludwig Scholar in Cancer Research. In recognition of his contributions to the study of cancer genetics,
he received the AACR Cornelius P. Rhoads Memorial Award and the Amgen Award from the American Society of
Biochemistry and Molecular Biology; as well as the 2003 Chestnut Hill Award for Excellence in Medical