Larry Kaiser, M.D.
President

Susan Coulter, J.D.
Vice President, Office
of Institutional Advancement

Wendy K. Mohon
Editor

Michelle Rexroat
Web Developer I

November, 2005
Table of Contents

Take the Risks:

Phillip Carpenter, Ph.D., associate professor of biochemistry and molecular biology,
Medical School and GSBS

 

Research on cell growth and division in response to DNA damage is leading to new knowledge about immunology and some forms of cancer.

Phillip Carpenter, Ph.D.

Phillip Carpenter, Ph.D.

“My research into this problem began by accident but has led us on a great journey into areas I thought I would never be involved in (mouse genetics and immunology),” Carpenter said. “I think that this is the essence of research: to travel into new and challenging areas outside of one’s traditional expertise and to be willing to take the risks associated with this. To find unexpected connections, rather than to incrementally extend existing knowledge, in a timely fashion is a key.”

Carpenter had known since high school biology class that he wanted to study cell division, so he looked for a postdoctoral position in that area. “The decision to go to Caltech as a postdoc was one of the best I have ever made,” he said. “Where we choose to study and who we choose to do it with can make all of the difference in the world.”

Once in Houston, he was originally interested in following up on some key findings he had made about DNA replication while at Caltech. But he was unable to obtain funding for that research.

Luckily, he also had accidentally found a protein called 53BP1 in a genetic screen at Caltech, and his chairman in Houston, Rod Kellems, Ph.D., suggested that he study 53BP1 in mice, “an idea that we took and have been running with ever since,” Carpenter said. An award from the Ellison Medical Foundation supported the transition in his research. “

We learned some very important secrets regarding how cells respond to DNA damage in the context of cell division, an area of research central to the formation of tumors,” he said. “We learned that 53BP1 is intimately involved in the development of the immune system and that animals deficient in the function of the protein were immunodeficient because of their inability to repair broken DNA fragments that are naturally generated during immune development. We also have learned that 53BP1, under certain genetic contexts, prevents the formation of immune cancers (lymphoma).”