Researchers have identified a gene LKB1 that acts as a tumour suppressor, and mutation in which leads to accelerated lung tumor growth.
The gene is found in almost a quarter of all human lung cancers and in mice its mutation results in aggressive tumors that are more likely to spread throughout the body.
Gene Variation Increases the Risk of Lung Cancer
Scientists from the National Cancer Institute identified Variations in two genes related to inflammation may be a major risk factor for developing lung cancer.
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The study was conducted by a team of researchers led by Dr. Norman Sharpless at the University of North Carolina at Chapel Hill School of Medicine and Harvard Medical School.
As part of the study researchers developed a mouse model with defects in the LKB1 gene that causes one of the most lethal malignancies in man, a form of lung cancer called squamous cell carcinoma.
The researcher demonstrated that cancer developed at a much faster rate in genetically engineered mice as compared to those with defects in other tumor suppressors commonly mutated in lung cancer.
The study found that these mice exhibited not just one, but all three forms of non-small cell lung cancer, adenocarcinomas, squamous cell carcinomas and large cell carcinomas and they were more likely to metastasize, or spread to other organs.
"Clearly mice with lung cancers harboring LKB1 mutations do much worse than those with other types of cancers; however, we still do not know what this gene does," Nature quoted Sharpless, as saying.
Researchers then analyzed DNA from 144 non-small cell lung cancer patients to study whether the mouse model related to genetic events of human lung cancer.
The study noted defects in LKB1 in 34 percent of human lung adenocarcinomas, 19 percent of squamous cell carcinomas and 10 percent of large cell carcinomas.
Dr. Neil Hayes, co-author of the study explained that by studying cancer progression in patients, specific LKB1 mutations can be identified.
"Based on this study and ones like it we should be able to sort patients into groups based on exactly what genetic lesion is causing their cancer," Hayes said.
Source: ANI
LIN/J
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The researcher demonstrated that cancer developed at a much faster rate in genetically engineered mice as compared to those with defects in other tumor suppressors commonly mutated in lung cancer.
The study found that these mice exhibited not just one, but all three forms of non-small cell lung cancer, adenocarcinomas, squamous cell carcinomas and large cell carcinomas and they were more likely to metastasize, or spread to other organs.
"Clearly mice with lung cancers harboring LKB1 mutations do much worse than those with other types of cancers; however, we still do not know what this gene does," Nature quoted Sharpless, as saying.
Researchers then analyzed DNA from 144 non-small cell lung cancer patients to study whether the mouse model related to genetic events of human lung cancer.
The study noted defects in LKB1 in 34 percent of human lung adenocarcinomas, 19 percent of squamous cell carcinomas and 10 percent of large cell carcinomas.
Dr. Neil Hayes, co-author of the study explained that by studying cancer progression in patients, specific LKB1 mutations can be identified.
"Based on this study and ones like it we should be able to sort patients into groups based on exactly what genetic lesion is causing their cancer," Hayes said.
Source: ANI
LIN/J
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