ABSTRACT
Most non-small cell lung cancer patients with active epidermal growth factor receptor (EGFR) mutation will eventually acquire drug resistant to EGFR tyrosine kinase inhibitors, such as gefitinib, resulting in disease progression, which involves a variety of complex mechanisms. Up to now, the molecular mechanisms of long non-coding RNAs mediated EGFR-TKIs resistance remains poorly understood. This review aims to outline the current state of information on lncRNAs and progress on its role in EGFR-TKIs resistance in non-small cell lung cancer.
Subject(s)
Humans , Carcinoma, Non-Small-Cell Lung , Drug Therapy , Genetics , Drug Resistance, Neoplasm , Genetics , ErbB Receptors , Lung Neoplasms , Drug Therapy , Genetics , Protein Kinase Inhibitors , Pharmacology , Therapeutic Uses , RNA, Long Noncoding , GeneticsABSTRACT
<p><b>OBJECTIVE</b>To study the link of Helicobacter pylori salive test cassette (HPS) and 13C-urea breath test (13C-UBT) on detecting Helicobacter pylori infection of stomach, and the sensitivity as well as specificity should be determined.</p><p><b>METHODS</b>A screening trial of 13C-UBT and HPS tests was carried out 130 patients included 106 positive and 24 negative results of 13C-UBT. As gold standards of 13C-UBT, a comparison study with HPS was evaluated using Bayes formula.</p><p><b>RESULTS</b>The sensitivity, specificity, accuracy, positive and negative predictive value of HPS was 68.87%, 58.33%, 66.92%, 87.95%, 29.79% respectively. The coincidence was 66.92%.</p><p><b>CONCLUSION</b>There is a correlation between results of 13C-UBT and HPS. Combination of 13C-UBT and HPS may compensate the blind zone of 13C-UBT in detecting oral Helicobacter pylori infection. 13C-UBT could not be used as a gold standard to judge the validation of HPS in detecting Helicobacter pylori oral infection. The methods can be used at the same time in clinic.</p>