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Mouth may
tell the tale of Lung Damage caused by
smoking
Newswise — Cells lining
the mouth reflect the molecular damage that
smoking does to the lining of the lungs,
researchers at The University of Texas M. D.
Anderson Cancer Center report today at the
annual meeting of the American Association
for Cancer Research.
Examining oral tissue
lining the mouth to gauge cancer-inducing
molecular alterations in the lungs could
spare patients and those at risk of lung
cancer from more invasive, uncomfortable
procedures used now, said senior researcher
Li Mao, M.D., professor in M. D. Anderson's
Department of Thoracic/Head and Neck Medical
Oncology.
"We are talking about
just a brushing inside of the cheek to get
the same information we would from lung
brushings obtained through bronchoscopy,"
said study presenter and first author
Manisha Bhutani, M.D., a post-doctoral
fellow in Thoracic/Head and Neck Medical
Oncology.
The team examined the
oral and lung lining tissue - called the
epithelium - in 125 chronic smokers enrolled
in a large, prospective lung cancer
chemoprevention study.
The status of two
crucial tumor-suppressing genes was
analyzed. The genes, p16 and FHIT, are known
to be damaged or silenced very early in the
process of cancer development. "There is
substantial damage long before there is
cancer," Mao said.
Study participants gave
both an oral and lung sample initially and
then another at three months. The
researchers tracked whether either p16, FHIT
or both had been silenced by methylation -
the attachment of a chemical methyl group to
crucial spots in a gene that shut down its
function. Patterns of methylation were
compared between the tissues.
The baseline tissue
comparison showed methylation of p16 in the
lungs of 23 percent of study participants,
of FHIT in 17 percent and of either of the
two genes in 35 percent.
The percentages were
similar in oral tissue, with p16 methylated
in 19 percent, FHIT in 15 percent and one of
the two in 31 percent.
Strong correlations
were observed between methylation patterns
in both tissues.
When methylation of
either gene was considered positive, 37 of
the 39 individuals (95 percent) with p16
and/or FHIT promoter methylation in the oral
samples had promoter methylation in at least
one matched bronchial sample.
This compared with only
59 of the 86 (69 percent) individuals
without the promoter methylation in the oral
samples. Similar correlations were seen at
the three-month analysis.
"Our study provides the
first systematic evidence that accessible
tissue, the oral epithelium, can be used to
monitor molecular events in less accessible
tissue," Bhutani said.
"This provides a
convenient biomonitoring method to provide
insight into the molecular events that take
place in the lungs of chronic smokers."
One follow-up area of
study is to find additional biomarkers in
oral tissue.
"We hope that our
findings encourage researchers to test an
increasing compendium of biomarkers to
confirm the reliability of oral epithelium
not only in lung cancer chemoprevention but
also in therapeutic settings" said Ashutosh
Kumar Pathak, M.D., another key study author
and a post-doctoral fellow in Surgical
Oncology.
"Our study opens the
door to enhancing our ability to predict who
has higher probability of getting
tobacco-related cancers," Mao said. "Not
only lung cancer, but pancreatic, bladder
and head-and-neck cancers, which also are
associated with tobacco use."
The study was funded as
part of a grant National Cancer Institute to
evaluate celecoxib, known commercially as
Celebrex, as a preventive agent against lung
cancer.
Co-authors with Bhutani,
Mao and Pathak, are You Hong Fan, Jonathan
Kurie, Edward Kim, and M. D. Anderson Chair
of the Division of Cancer Medicine Waun Ki
Hong, all of the Department of Thoracic/Head
and Neck Medical Oncology; Diane Liu, of M.
D. Anderson's Division of Quantitative
Sciences; J. Jack Lee, of the Department of
Biostatistics; Hongli Tang, of the
Department of Molecular Genetics; and
Rodolfo Morice of the Department of
Pulmonary Medicine.
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