The Culprit is Cancer
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1990, Slamon set out to answer the next critical question about
HER-2: Was the defective gene causing the deadly tumors, or was
there something else? To find out, the researchers injected normal
human breast cells with HER-2. "Sure
enough," says Slamon, "the cells grew more rapidly and they behaved
in a more malignant fashion." The experiment was repeated using
mice; the results were identical. Slamon had proved the link between
HER-2 and breast cancer.
was one last piece of the puzzle to solve: Could the researchers
find a way to target HER-2 and mediate its apparently destructive
effect? Slamon developed antibodies, called in others from academic
and commercial pharmaceutical labs and began methodically testing
them on tumor cells. After a dozen or so attempts, he tried Herceptin,
an antibody manufactured by Genentech. It worked.
only did it work on the HER-2 cells," Slamon says, "but when we
tried the antibody on cells that didn't have the alteration, it
had no effect. That was great news: The antibody was specific, unlikely
to affect cells without this alteration. And in mice, exactly the
same thing happened. Herceptin stopped the growth of the tumors."
Now that the antibody had been proven effective in the laboratory,
Slamon and Genentech went to the FDA and received permission to
begin testing the drug in women with advanced breast cancer.
odds against Slamon succeeding were still huge. As the UCLA researchers
entered Phase I of the Herceptin clinical trials, there were plenty
of scientists, many at Genentech even, who remained skeptical. Never
before had an antibody been shown successful in cancer treatment.
Slamon's instinct triumphed again: The early studies proved Herceptin
to be relatively safe. In the summer of 1995, the critical Phase
III trials began. Eventually, 940 very sick, very hopeful women
participated in the breakthrough study at more than 120 institutions
around the world.