Cells lining the mouth reflect the molecular damages that is caused by smoking to the lining of the lungs, researchers at The University of Texas M.D Anderson Cancer Center reported today at the annual meeting of the American Association for Cancer Research.
Senior Researcher Li Mao, M.D., professor in M.D. Anderson's Department of Thoracic / Head and Neck Medical Oncology said, that, by examining the oral tissues lining the mouth to gauge the cancer inducing molecular alterations in the lungs could spare patients and those at risk of lung cancer from more invasive, uncomfortable procedures used now.
"We are taking about just a brush in side of the cheek to get the same information we would get from lung brushing obtained through bronchoscopy," said the 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 tissues - called the eepithelium - in 125 chronic smokers enrolled in a large, prospective lung cancer chemo prevention 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 twice, one at the beginning of the study and another 3 months later. The researchers tracked whether either p16, or 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 in the lungs tissues showed methylation of p16 is 23 percent, FHIT is 17 percent and either of the two genes were 35 percent of the study participants. These percentages were similar in the oral tissues, with p16 methylated is19 percents, FHIT is15 percent and one of the two is 31 percent.
A strong correlation were observed between methylation patterns in both the lung and oral 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 is at least one matched brochial sample. Thus compared with only 59 of the 86 (69 percent) individuals without the promoter methylation in the oral samples. Similar correlations were seen on the sample analysis obtained three months later.
"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 bio monitoring method to provide insight into the molecular events that take place in the lungs of chronic smokers."
"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 were also associated with tobacco use."
Senior Researcher Li Mao, M.D., professor in M.D. Anderson's Department of Thoracic / Head and Neck Medical Oncology said, that, by examining the oral tissues lining the mouth to gauge the cancer inducing molecular alterations in the lungs could spare patients and those at risk of lung cancer from more invasive, uncomfortable procedures used now.
"We are taking about just a brush in side of the cheek to get the same information we would get from lung brushing obtained through bronchoscopy," said the 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 tissues - called the eepithelium - in 125 chronic smokers enrolled in a large, prospective lung cancer chemo prevention 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 twice, one at the beginning of the study and another 3 months later. The researchers tracked whether either p16, or 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 in the lungs tissues showed methylation of p16 is 23 percent, FHIT is 17 percent and either of the two genes were 35 percent of the study participants. These percentages were similar in the oral tissues, with p16 methylated is19 percents, FHIT is15 percent and one of the two is 31 percent.
A strong correlation were observed between methylation patterns in both the lung and oral 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 is at least one matched brochial sample. Thus compared with only 59 of the 86 (69 percent) individuals without the promoter methylation in the oral samples. Similar correlations were seen on the sample analysis obtained three months later.
"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 bio monitoring method to provide insight into the molecular events that take place in the lungs of chronic smokers."
"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 were also associated with tobacco use."
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