Release date: 2015-09-25
Researchers at Johns Hopkins University used six patients with precancerous lesions to collect lung lesions, blood, and saliva as samples, and found that free DNA can invade surrounding tissues, leading to cancerous lung adenocarcinoma. Opportunities become markers of common and fatal cancer lesions. Relevant research results have been compiled and published in Nature Communications.
Studies have also shown that there are different genetic mutations in different regions of the diseased tissue, and these differences are directly related to benign and malignant lesions.
Precancerous lesions of lung cancer are associated with malignant lesions, and the same mutation may be a "switch" for tumor progression.
At present, the mainstream opinion of lung cancer experts is that the development of lung adenocarcinoma begins with microscopic lesions, which accumulate over time and eventually develop into malignant tumors. But the phenomenon that contradicts the point of view is that many precancerous lesions will disappear after a few years, and some lesions will aggravate the development of cancer.
In order to identify the true determinants of lung adenocarcinoma, the Johns Hopkins University team collected tissue samples from six patients who underwent surgical resection, and unseen observations of the samples to find atypical adenomatous lesions. . Subsequently, the scientists isolated and sequenced the DNA of atypical adenomatous hyperplasia tissue, with other adenocarcinomas, minimally invasive adenocarcinoma, and completely invasive adenocarcinoma (from atypical adenomatous hyperplasia to complete invasion of adenocarcinoma). A series of development stages) for comparison.
Using next-generation sequencing technology, they found a total of 125 mutant genes that are associated with cancer development. By comparing the DNA of the precancerous lesion with the DNA of the primary invasive cancer, three patients were found to have the same lesion in the precancerous lesion and the tumor stage. The study demonstrated for the first time the association between latent premature lesions and invasive tumors, which are likely to be "switches" to tumor progression.
The team also found that different atypical adenomatous hyperplasia lesions from different patients contain different mutation patterns, indicating that lung cancer is caused by different molecular pathways.
Non-invasive liquid biopsy is more accurate than surgical biopsy
When the research team further explored different regions of the same diseased tissue, they found that even the same diseased tissue, there were genetic differences. Mutations associated with benign and malignant are considered to be different regions of the same tumor, which also indicates that there is a limit to the biopsy of a single site when determining the patient's treatment regimen.
Taking the plasma and saliva of two patients as samples, the researchers extracted DNA from the samples and detected a small amount of mutations in the DNA samples by polymerase chain reaction. It was found that the mutations detected in the biopsy could find corresponding mutations in the liquid sample, even if it was Mutations detected in specific parts of the diseased tissue. This means that blood or saliva testing can better replace biopsy for tumor testing.
David Sidransky, MD, professor of oncology and pathology at Johns Hopkins University School of Medicine and director of head and neck cancer research, said the study is important for understanding the molecular biology of lung cancer development and is expected to be extended to clinical applications. At the same time, he also stressed that because of the small sample size, this discovery is still in its infancy.
Source: Bio-Exploration
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