Light cast on a darkling gene - retinoblastoma

35,000 Americans a year. John Minna of the National Institutes of Health and Susan Naylor of the University of Texas have indications that the oat-cell gene sits in a particular region on chromosome 3. Says

Naylor, ''I'd like to get hold of that gene be- fore the competition in this business becomes

unbearable.'' In Utah, White and his co-workers are pursuing a recessive gene tied to co- lon cancer -- the second most common malignant killer (after lung cancer).

As the field of recessive cancer genes grows, biologists are confident that the genes they uncover will reveal much about the quirks of specific malignancies -- and about the tissues in which they arise. Every cell in the body contains the same repertory of genes, yet the loss of the retinoblas toma gene appears to endanger only eye or bone cells. Scientists know precious little about which genes dictate the formation and activity of various organs; they believe that recessive cancer genes are among the ''tissue specific'' genes they've been waiting for. Says Cliff Tabin, a developmental biologist at Massachusetts General Hospital in Boston, ''These genes will say a

lot about how God or evolution, or what- ever, designed the architecture of the human body.''

Despite the contagious optimism the retinoblastoma breakthrough has fanned, scientists aren't so foolhardy as to claim they have the Answer to Cancer. Childhood malignancies may indeed be the consequence of two, or very few, mutational hits. Most cancers, however, take twenty years or more to develop, which suggests that a series of mutations is needed. ''Recessive oncogenes are an important part of the story of cancer,'' says Weinberg, ''but only a part.'' Tracing the sequence of mutations in the most prevalent cancers and learning which ones can be corrected to stem a tumor's growth will take years, if not decades.

Still, there's hope that the retinoblasto ma discovery may have significant effects far sooner than that. Dryja, who has had to remove the clouded eyes of infants more times than he cares to recall, hopes that the gene he helped clone will rapidly lead to better treatment for the disease. ''If we're right and the loss of this gene is one of the keys to forming the cancer,'' he says, ''some day we might be able to design a treatment by making a drug that mimics what the protein of the gene is doing.''

This may sound naive and Mary Poppins-ish,'' adds Cavenee,

''but when all's said and done, regardless of who's getting credit, who's not getting credit, and who's fighting with whom, the people this work is really for are the kids. Retinoblastoma is a terrible disease. It's not fair. Those kids don't deserve it. They don't do things like this.'' He lifts his pack of cigarettes from the table. ''Forget about scientists' careers or scientific glory. I think anybody who's worked with these kids, or met one of these kids, would feel exactly the same way. Whatever we do, whatever advancements we make, are for them.''

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COPYRIGHT 2004 Gale Group