GLAND-RELATED PREDICTION OF NON-SMOKERS

The majority of tumors associated with lung cancer and smoking, although a subset of adenocarcinoma
Occur in patients who never smoked. As natural as these mutations
EGFR and HER2 tyrosine kinase receptor ErbB family members.
Reported, it is most likely in a subgroup of patients with lung cancer.
Adenocarcinoma of the race there was no light smokers or never smokers in East Asia
(25, 31 and 36). Understanding the pathogenesis of lung adenocarcinoma] for EGFR mutations
Our team, shows the presence of EGFR mutations in normal bronchial
Mutations adjacent to the tumor, bronchial epithelium. As reported by Tang et al.
Terminal mutations in EGFR (141), appear normal breathing
9 of 21 patients with adenocarcinoma (44%), rather than patients without epithelial
Mutations in the tumor (141). EGFR mutations were more frequently found
Neighborhoods (24%) compared to the volume (43%) indicates the presence of normal epithelium in
Effect of a local phenomenon in this space for more than respiratory
In the lungs. Despite the cell type one of these mutations is unclear, and we assume
Advances of stem cells and the airway epithelium and airway
Types of cells with these mutations. EGFR is included in the relatively rare
Mutant lesions (three of 40 studies) (54,142) found in non-AAH
Mutation (25), relatively low frequency of mutations in lung BACS or for real
Supports the concept of the EGFR gene abnormalities not
Cause of pulmonary alveolar type tumors. These data were recently published by Tang.
(143) of EGFR mutations, indicating that the increase in copy number is preceded
Genetic etiology of lung cancer (143), and increased
EGFR copy number is a phenomenon associated with tumor progression.
And metastasis (Fig. 1).
In summary, we have two different molecular pathways in the pathogenesis
Lung (Figure 1), and activation of tobacco-related
KRAS instead of lanthanum, smoking-related activation indicates EGFR,
Found in normal bronchial epithelium and bronchial histology of the last
(144).
Unlike other organs, lungs, indicating a very broad range of epithelial
Changes in the tumor tissue. These tumors showed a variety
Found exposure to the central relationship between cancer and passive
Max relationships. Molecular lesions found in some tumors that are common
Unique features and changes. Precancerous lesions and different
Some of this knowledge, while the cause is not understood by others
Prior to surgical tumor removal from the list of detected is difficult. In this way
Is not well understood natural history. Emergence of new molecular
Genetic method for testing the amount of lung tissue damage and tumor samples in the past
Will help the molecular abnormalities of the main causes of cancer of the lung to identify
Development and progression of cancer. The number of copies of specific genes to change
Approach has proven to be identified mutations specific to lung cancer.
At the same time, DNA, RNA, and the study of molecular properties and protein levels
Since the molecular classification of lung cancer, while increasing capacity, and
Anticipate, predict response to treatment. Integration of these different
The breaking of the pad and that signature is detected instability. You can combine the molecular characteristics and clinical variables approached.
The best approach for building a new model for lung cancer. The ultimate goal,
And it is possible for all the molecular changes in the volume of each patient
Use this information to predict and detect the early molecular and biological / clinical
Action selection or development of diagnostic and rational treatment.