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Objective: To investigate the mutation status of epidermal growth factor receptor (EGFR) and KRAS gene in patients with non-small cell lung cancer (NSCLC) in Xuanwei, Yunnan and to correlate the mutation status with clinicopathologic features., Methods: Mutation status of exons 18, 19, 20 and 21 of EGFR, and codons 12, 13 of KRAS in 63 cases of NSCLC were analyzed by gene sequencing and ARMS-Taqman probe method. Correlation with patients' clinicopathological characteristics was performed., Results: EGFR and KRAS mutations were present in 55.6% (35/63) and 6.3% (4/63), respectively. EGFR gene mutations were present, including exon 18 G719X in 14.3% (5/35), exon 19 in 14.3% (5/35), exon 20 S768I and T790M in 20.0% (7/35), exon 21 L858R in 31.4% (11/35), exon 18 G719X and exon 20 S768I double mutation in 17.1% (6/35), and exon 20 T790M and exon 21 L858R double mutation in 2.9% (1/35). KRAS mutations were seen in codon 12 in 3 of 4 cases, and codon 13 in 1 of 4 cases. EGFR mutations were mutually exclusive with KRAS mutations. According to statistic analysis, EGFR mutations were associated with the histological types of NSCLC(P<0.05), but without correlation with patient's gender, age, smoking status and lymph node metastasis(P>0.05). KRAS mutations in NSCLC had no correlation with the clinical pathologic characteristics of the patients., Conclusions: A higher frequency of EGFR exon 18 G719X and 20 exon S768I mutations are found in the patients in Xuanwei, Yunnan. EGFR mutations are associated with histologic types of NSCLC, but without correlation with patient's gender, age, smoking status and lymph node metastasis. KRAS mutation in NSCLC has no correlation with the clinicopathologic characteristics of the patients.

Lung cancer is the leading cause of cancer mortality in both men and women, with dismal survival rates due to late-stage diagnoses and a lack of efficacious therapies. The new treatment options with completely novel mechanism of therapeutic activity are needed for lung cancer to improve patient outcome. The present study was aimed at testing the efficacy of recombinant adenovirus H101 as an oncolytic agent for killing human lung cancer cell lines in vitro and in vivo. We assessed the coxsackievirus adenovirus receptor (CAR) expression on human lung cancer cell lines by RT-PCR and immunocytochemistry staining. Viral infectivity and viral replication in lung cancer cells was assayed by flow cytometry and real-time fluorescent quantitative PCR. After H101 treatment, cytotoxic effect, cell cycle progression and apoptosis were further examined by lactate dehydrogenase release assay and flow cytometry in vitro, respectively. In vivo, antitumor effects of H101 were assessed on SCID Beige mice xenografted with human lung cancer cells. Receptor characterization confirmed that human lung cancer cell lines expressed CAR receptor for adenovirus type 5. Lung cancer cells were sensitive to infection by the H101 virus. H101 infection and replication resulted in very potent cytotoxicity, G2/M phase arrest and cell lysis. In vivo, we also showed that H101 significantly inhibited tumor growth following intratumoral injection, with virus replication, cell degeneration and necrosis in the tumor tissue. These results have important implications for the treatment of human lung cancer.

This report is to demonstrate the antigen-dependent activity of human lung cancer transfer factor (Sp-TF). Sp-TFM was prepared from spleen of mice immunized with the human lung cancer cell line A549. [3H]-leu leukocyte adherence inhibition assay ([3H]-leu-LAI) was modified to identify activity of Sp-TFM. Leukocytes obtained from non-immunized mice were divided into eight groups as follows: 1. Control without TF or antigen; 2. Sp-TFM and antigen of cell line A549 (A549 Ag); 3. Sp-TFM alone; 4. Sp-TFM and ascitic tumor cell H22 antigen of mice (H22Ag); 5. Sp-TFM and antigen of human gastric cancer cell (HGCCAg); 6. Sp-TFM and antigen of human normal lung tissue (NLTAg); 7. Nor special TF of mice (N-TFM) and A549Ag; 8. A549Ag alone. When normal leukocytes were incubated with Sp-TFM and A549 antigen, the leukocytes adherence inhibition index (LAII) was significantly higher than those of the other groups. The different LAII of Sp-TFM to A549Ag and other experimental groups were highly significant (P less than 0.001). The results demonstrated that Sp-TFM could transfer specific cell mediated immunity to non-immune leukocytes. The TF prepared from spleen of goat immunized with antigen from lung cancer of patients (Sp-TFG) showed antigen specific activity as well as Sp-TFM.