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Moving at the speed of science

Moving at the speed of science

Owen Witte, MD, has been a California resident for nearly 35 years, but there’s nothing laid-back about him. The director of the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research retains the rapid fire speech of a native New Yorker. Although it was getting toward late afternoon when Dr. Witte met with Oncology News International, he ushered a steady stream of visitors into and out of his office at the University of California, Los Angeles. When he spoke about his work, it was with the same energy that no doubt drew him to science in the first place.

“I had wonderful science teachers in elementary school. In sixth grade, my teacher recommended a book called Microbe Hunters,” Dr. Witte explained. “It’s a story of the great discoveries of microbiology. It was like the CSI of its day. I got turned on to microbiology.”

What followed was a career with many milestones in hematology and cancer care, including breakthroughs in the treatment of chronic myelogenous leukemia (CML). Now as the director of one of the country’s premier stem cell research institutes, Dr. Witte is working in an area that is rapidly advancing and, no surprise, he has no qualms about keeping up.

“This is an exciting area of science,” he said. “There is no field of medicine that can’t somehow involve the study of stem cells.”

Great mentors, great friends
Dr. Witte graduated from Cornell University in New York with a bachelor of science in microbiology, and he went on to earn his medical degree at Stanford University in Stanford, Calif., in 1976. He completed postdoctoral fellowships under the tutelage of Irving L. Weissman, MD, at Stanford and David Baltimore, PhD, at the Massachusetts Institute of Technology in Boston. Dr. Weissman is the director of the Institute of Stem Cell Biology and Regenerative Medicine. Dr. Baltimore won the 1975 Nobel Prize in Physiology or Medicine for his research in virology.

“Both of them made a huge impact in my life, personally and scientifically,” Dr. Witte said. “They are phenomenally successful scientists. They are very different people, but they both have a relentless drive to answer the question. Whatever they are confronting, they will stop at no obstacles, recruit the best people, never hesitate to use new technology, and go after the answer. That’s what I’ve learned from them.”

During his postdoctoral fellowships, Dr. Witte had what he considers one of the seminal moments in his career: Discovering that phosphotyrosine is the end product of a kinase reaction. “That was a major lightbulb moment,” he said.

The road to Gleevec
Dr. Witte joined UCLA’s department of microbiology and molecular genetics in 1980. Like many young people at a first job, he assumed that he’d only stay a few years. While UCLA offered him the opportunity to handle heady matters in the lab, something a little more earthly kept him around.

“I met my wife, Jami McLaughin Witte, about the fifth day I was in L.A.,” he said. “Jami has worked with me for 20-plus years and is actually responsible for some of the really important work that I receive a lot of credit for!” Ms. McLaughin Witte is a research assistant in the UCLA department of microbiology, immunology, and molecular genetics.

Two of the important discoveries were the BCR-ABL oncogene and the Philadelphia chromosome abnormality, both associated with CML. Then there was the “big one” that led to the development of imatinib (Gleevec). “With that particular discovery, it was very clear that we were on to something major,” Dr. Witte said.

“At the time, my graduate student, James Konopka, was working on a different question: He was looking at human leukemia cell lines. He observed that in human CML, we consistently saw this unexpectedly large and highly active tyrosine kinase. We already knew from our studies on a related mouse gene that that was sufficient to cause transformation. We had a unique molecular signature and a consistent pattern associated with a specific disease. It was clear as a bell: That was the cause of CML.”


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