Horvitz Earns Nobel Prize With ‘Cell Death’ ResearchBy Jennifer L. Wong
MIT Professor of Cancer Biology H. Robert Horvitz ’68 was honored as a co-winner of the 2002 Nobel Prize in Physiology and Medicine. The Nobel Assembly at Karlinska Institute in Stockholm, Sweden announced his award early Monday morning. Horvitz is also an Investigator at both the Howard Hughes Medical Institute and McGovern Institute for Brain Research.
He shares this internationally prestigious award with fellow laureates Sydney Brenner, a professor at the Salk Institute for Biological Sciences in La Jolla, California and founder of the Molecular Sciences Institute in Berkeley, California, and John E. Sulston, of Cambridge University’s Sanger Center in England. The $1 million prize will be split equally among the laureates.
The Nobel Prize was awarded jointly to these three men for their discoveries concerning “genetic regulation of organ development and programmed cell death.” These findings have opened up much insight into the development of many illnesses that have continuously troubled the world’s top scientists.
Horvitz heard news of his prize and is celebrating while vacationing in the French Alps. At yesterday’s news conference, he said “I would find nothing more gratifying than to learn that one or more of my discoveries led specifically to pharmaceutical treatments and cures for human diseases. That’s a dream. At this point, I think that dream is still tenable.”
MIT expresses its appreciation
MIT has been supportive and proud to have one of its own recognized as a 2002 Nobel laureate.
President Charles M. Vest said, “A Nobel Prize announcement is the most exciting confirmation of the excellence and importance of what faculty and students do at MIT. This is a great moment for Bob Horvitz, for science, for MIT and for the future of human health.”
He emphasized that “it also reminds us of the critical importance of basic science that is driven by curiosity about the mysteries of life. That is the ultimate source of advances in human health.”
“Bob’s work on programmed cell death, and that of his colleagues, is of a fundamental importance and has long deserved this recognition. It could not have happened to a nicer or higher quality individual,” Vest said.
Horvitz’s laboratory is brimming with pride as well. Ignacio Perez De La Cruz PhD ’02, a postdoctoral researcher in the his lab, said, “Bob encourages independent training and intellectual freedom.”
“He is a very good person who cares about his students and continually tries to train his graduate students to become great in their field,” said Ho-Yon Hwang PhD ’02.
Perez De La Cruz said that “Bob is very non-political and puts science and discovery first. He is not preoccupied with who ultimately will receive the recognition for the work.”
Hillel T. Schwartz G also offered his support for Horvitz by saying their lab was a “community of people driven by their own interests” but motivated and encouraged by Horvitz.
Horvitz has long history at MIT
Howard Robert “Bob” Horvitz was born in 1947 in Chicago. He graduated from MIT in 1968 with degrees in mathematics and economics. He also served as Managing Editor for The Tech. He continued his education by receiving his Master’s Degree in 1972 and his PhD in 1974 in Biology at Harvard University. He then went on to work as a postdoctoral researcher at the Medical Research Council Laboratory of Molecular Biology in Cambridge, England. He came back to MIT in 1978 as an Assistant Professor and became a full Professor of Biology in 1986 and an Investigator at the Howard Hughes Medical Institute in 1988. Since 1989, Horvitz has held appointments in neurology and medicine at the Massachusetts General Hospital.
In addition to joining the ranks of internationally renowned Nobel laureates, Horvitz is a member of the U.S. National Academy of Sciences and a Fellow of the American Academy of Arts and Sciences and the American Academy of Microbiology.
He is also a member of several professional societies, including the Genetics Society of America. He is also a member of the National Advisory Council of the National Human Genome Research Institute and was co-chair of the Working Group on Preclinical Models for Cancer of the National Cancer Institute.
Colleagues lay out foundation
In the early 1960s, Brenner realized that questions about cell differentiation and organ development were difficult to perceive and analyze in high-level organisms. Thus, he selected the nematode Caenorhabditis elegans because this worm was easily viewed under a microscope and had a relatively short generation time.
Brenner broke new ground in 1974 when he showed that specific gene mutations could be induced by ethyl methane sulphonate, proving that various mutations were linked to certain genes and to specific effects on the development of organs.
Sulston continued Brenner’s research by devising techniques to study and examine all of the cell divisions in the C. elegans for all cells in the adult organism. He ultimately discovered and demonstrated how the mutations of certain genes contributed to programmed cell death.
Horvitz extrapolates past work
Horvitz started extrapolating on the work of Brenner and Sulston in the 1970s. In 1986, he identified the first two “death genes”, ced-3 and ced-4, as being the necessary prerequisites for cell death, apoptosis.
Later on, he discovered that ced-9 was another gene that worked to hinder cell death: its product interacts with those of the first two genes. Horvitz also determined certain genes that controlled how dead cells were eliminated from the system and so forth.
By demonstrating that the human genome possesses a gene similar to ced-3, Horvitz’ work provides a great window of opportunity for further research into the possibilities and potential of programmable cell death.
Horvitz has said, “Programmed cell death is a key mechanism for regulating cell numbers and connections and for sculpting tissues. Its misregulation can play a central role in certain cancers, autoimmune diseases and neurodegenerative diseases. We now know many of the molecules that control programmed cell death.”
Programmed cell death has allowed experts to understand the mechanisms at play with viruses and bacteria. Cancers arise because of abnormalities in cells; thus, researchers continually are battling against time to find out more information about this unique system of “cell suicide” in order to attack and induce death in malignant cells.