A study of aberrations in the genetic code of lung adenocarcinoma has revealed a host of new genes, including one that plays a critical role in spreading the deadly disease, media reported Monday.
The research, conducted by an international team of scientists, provides a comprehensive view of the abnormal genetic landscape in lung cancer cells, revealing more then 50 changes frequently associated with the tumors.
"This view of the lung cancer genome is unprecedented, both in its breadth and depth," said lead author of the study, Mathew Meyerson of Harvard and MIT.
"It lays an essential foundation, and has already pinpointed an important gene that controls the growth of lung cells."
The study, appearing in the Nov. 4 advance online issue of journal Nature, uncovered a total of 57 genomic changes that occur frequently in cancer patients.
Of these, at least 40 are associated with genes not previously known to be involved in lung adenocarcinoma.
The genetic anomaly that turned up the most frequently incriminates a gene called NKX2.1 as an accelerator of cancer cell growth.
NKX2.1 normally acts as a "master regulator" that controls the activity of other genes in cells lining tiny air sacs in lungs called alveoli.
"If you have mice that lack this gene, they don't make alveoli and they can't breathe. They die when they are born," said Meyerson.
The discovery could help scientists design drugs to fight not just lung cancer but a wide range of cancers.
"This information offers crucial inroads to the biology of lung cancer and will help shape new strategies for cancer diagnosis and therapy," Meyerson said.
In addition, the use of powerful tools and technologies to sequence the genomes of lung cancer patients "represents a general approach that can and should be used to analyze all types of cancer," said co-author Eric Lander, director of the Broad Institute of MIT and Harvard.
Lung cancer is the leading cause of cancer deaths worldwide with more than 1 million people dying of the disease each year.
(Agencies via Xinhua News Agency November 5, 2007)
