When protein is broken down, one of the by-products is ammonia. Ammonia is toxic, so our bodies have elaborate systems for getting rid of it. Most of the detoxifying work falls to our liver. There, ammonia travels a multistep pathway featuring five enzymes that turn it into urea, to be excreted in urine. People with rare genetic deficits that interfere with the urea cycle often die in childhood. Other mutations, though, may be responsible for some problems in adults, reports the May 2007 issue of the Harvard Health Letter.

One in 8,000 American children has a genetic defect that causes one or more of the enzymes involved in ammonia processing to be defective or scarce. As these children start to consume protein, the ammonia begins to pile up. Treatment includes protein restriction, medications that sop up extra ammonia, dialysis, and possibly liver transplant. The death rate is high.

Urea cycle disorders are viewed as rare and primarily pediatric conditions, but there might be a whole range of unrecognized, genetically determined problems with protein metabolism experienced by adults. Some people may have mild mutations that compromise a gene's function and cause slight symptoms. This may explain why one person eschews meat while another loves nothing more than a steak meal. Defects in protein metabolism may also explain why some people have bad reactions to high-protein diets like the Atkins diet.

The Harvard Health Letter notes that someday genetic tests might be used routinely to diagnose such metabolic disorders, but for now much more research is needed.

Also in this issue:

Open-fit hearing aids Is fructose unhealthy? Standard versus digital mammograms Atkins wins with weight loss By the way doctor: Can exercise and diet cure diabetes? Does asthma go away?

The Harvard Health Letter is available from Harvard Health Publications, the publishing division of Harvard Medical School, for $28 per year. Subscribe at www.health.harvard/health or by calling 1-877-649-9457 (toll free).

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"They're all occurring together on a single chromosome, which results in a greatly increased amount of EGFR, he said. The predicted end result would be a great increase in EGFR protein production in the affected cells, driving them toward cancer.

These findings might explain why East Asians are known to respond better than other ethnic groups to a type of chemotherapy that inhibits EGFR activity, Dr. Gazdar said.

Cancer cells become addicted to EGFR, he said, so these cells are much more susceptible to the cancer-killing effect of EGFR inhibitors.

This type of analysis of cancer genes might be helpful for other types of cancer and other ethnic groups, Dr. Gazdar said, possibly explaining both the different manifestations of the disease seen among ethnic groups and leading the way to matching a specific treatment to the patient.

Other UT Southwestern researchers involved in the study were Dr. Pila Estess, assistant professor of pathology; Dr. Mark Siegelman, associate professor of pathology; Dr. Jerry Shay, professor of cell biology; and Dr. John Minna, professor of internal medicine and director of the Nancy B. and Jake L. Hamon Center for Therapeutic Oncology Research and the W.A. Tex and Deborah Moncrief Jr. Center for Cancer Genetics.

Researchers from Fred Hutchinson Cancer Research Center in Seattle, Tokyo Medical University, the Center of Excellence in Aging in Chieti, Italy, and UT M.D. Anderson Cancer Center also participated, as did visiting researchers from Chiba University Medical School, Okayama University Medical School and Gifu University Medical School, all in Japan.

The work was supported by the National Cancer Institute.

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