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)
