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...more modest expectations. Rituximab was the first, but just a year later, the same approach led to trastuzumab, a drug that keeps growth factors from feeding certain kinds of breast-cancer cells. Such targeted treatments are effective only when the appropriate target exists. Trastuzumab latches onto a receptor known as HER2, which is abnormally abundant in only about 30% of breast-cancer tumors. A biopsy can tell doctors whether a patient is likely to respond to trastuzumab, but they'd hoped to find a molecule that would plug into a growth-factor receptor more prevalent in cancer cells...

Author: /time Magazine | Title: New Hope For Cancer | 5/28/2001 | See Source »

...Sure enough, they found one. Dr. John Mendelsohn, then at the University of California, San Diego, and now president of the M.D. Anderson Cancer Center in Houston, had been focusing since 1981 on a receptor called EGFR, which is host to a protein called epidermal growth factor (EGF). It's a close cousin to HER2, and Mendelsohn and his team know that it is present in a huge variety of tumors; two-thirds of all cancer types, in fact, are blanketed with EGF receptors. In 1984 Mendelsohn and his team showed in mice that blocking the EGF receptor with...

Author: /time Magazine | Title: New Hope For Cancer | 5/28/2001 | See Source »

...Making a drug out of that decoy would prove tricky, since the receptor, like HER2, also shows up on noncancerous cells. Researchers are now learning, however, that normal cells are more adept than cancer cells at finding other growth factors on which to rely when EGFR is blocked. But when Mendelsohn applied for his first grant from the National Cancer Institute in 1983, he was rejected. "Nobody thought it would work," he says. The following year he turned to philanthropic sources for research dollars. Last year he wowed colleagues with a compound called IMC-C225, which proved effective in treating...

Author: /time Magazine | Title: New Hope For Cancer | 5/28/2001 | See Source »

...There are three sub-classes of entry inhibitors: Fusion inhibitors, attachment inhibitors and co-receptor inhibitors. And while each works in a slightly different way, all entry inhibitors work on the same principle: The longer the cells can deflect attacks from HIV, the longer other drugs will have to work on destroying the existing virus already inside the cell...

Author: /time Magazine | Title: New Class of HIV Drugs Spark Much-Needed Hope | 5/17/2001 | See Source »

...Some day, scientists might even be able to switch that receptor gene to an "off" position - a development that could help diabetics and people with weight problems modulate their responses to sugar. It might also mean that people like me (who tend to eat perhaps a bit too much sugar) will have a great new excuse around major holidays. Indulgence, in other words, without guilt: "Oooh, pass the candy dish. Don't give me that look, Mom. I can't help it. My genes are crying out for modified white sugars...

Author: /time Magazine | Title: Is Sweetness in the Genes of the Beholder? | 4/23/2001 | See Source »

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