"The identification of five genes that are closely associated with the outcomes in patients with non-small-cell lung cancer has clinical implications," said Hsuan-Yu Chen, a research associate at the National Taiwan University College of Public Health in Taipei.

In an article that will be published in Thursday's editions of the New England Journal of Medicine, Chen explained that, for example, patients who have high-risk gene signatures would be candidates for post-surgical treatment with potent cisplatin-based chemotherapy.

On the other hand, Chen suggested that patients who have a low-risk profile could be spared the side effects, costs and time of undergoing chemotherapy treatments that might not be necessary.

"We are moving in the direction of individualized treatment for patients with lung cancer just as we have done in blood cancers or for breast cancer," Roy Herbst, professor of medicine at the University of Texas M.D. Anderson Cancer Center, told United Press International.

He said the Taiwan researchers as well as researchers in the United States have shown that it is possible to find specific differences in lung cancer that will allow doctors to fine tune chemotherapy regimens.

Herbst also said that the work by scientists may also lead to the development of medication that directly impacts certain genes.

The signature was identified after researchers used gene-array technology to isolate more than 600 genes that appear to influence survival. That group of genes was whittled down to 16. Further experimentation found five genes that are significantly related to how well a patient does following surgery.

Chen then compared 125 patients with non-small-cell lung cancer on the basis of how their outcomes compared with the risk signature. He said the signature as well as stage of cancer when diagnosed were critical factors in survival.

The five genes that are included in the signature for non-small-cell lung cancer are:

-- STAT1, which causes arrested growth and programmed cell death, also called apoptosis, in many types of cancer cells.

-- MMD, a gene preferentially expressed in mature macrophages -- cells that promote cancer spread. However, the exact function of the MMD protein is unknown.

-- DUSP6, a gene that inactivates cell signaling, an activity that results in the tumor suppression and apoptosis.

-- ERBB3, a member of the epidermal growth factor receptor family of tyrosine kinases, which can shorten cell survival.

-- LCK, a member of the Src family of protein tyrosine kinases that plays a key role in apoptosis. LCK is expressed in many cancers and regulates the mobility of cancer cells.

Cancer cells do not go through a regular cell life-and-death cycle, somehow avoiding apoptosis. Genes that regulate apoptosis, therefore, are key factors in the growth of cancer.

Herbst, whose editorial in the journal accompanies the article from the Taiwanese scientists, told UPI that the test of whether the gene signature will be useful awaits clinical trials that treat patients upon the basis of the high-risk versus low-risk gene signature.

He said the signature can be developed with off-the-shelf technology, so it will not require exotic protocols for other scientists to replicate the studies or move the studies into clinical trials.

"We are entering an amazingly exciting time in cancer treatment," Herbst said. "Lung cancer is the deadliest cancer in the world. A major effort to improve the control of lung cancer entails the use of molecular profiling to characterize tumors and provide accurate predictions of the outcome after standard or novel treatments."

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