[Study of gene expression difference in lung carcinogenesis by cDNA microarray].

BACKGROUND & OBJECTIVE: Lung cancer is a kind of disease with high incidence and mortality, however its molecular mechanism is not clear yet. This study was designed to investigate gene expression differences among lung cancer tissues, lung paracancerous tissues,matched peripheral normal lung tissues and the metastases of lymph nodes, and to seek the relatively high expressed genes in lung carcinoma tissues, providing possible theoretical basis for early diagnosis and treatment of pulmonary carcinoma. METHODS: Fresh lung cancer tissue, lung paracancerous tissue, matched normal lung tissue and metastases of lymph nodes were deep-frozen in liquid nitrogen; their total RNA were extracted for reversed transcription cDNA probes, which were labeled and subsequently used to hybridize with cDNA microarray with 588 genes. Different gene expression profiles were obtained by analyzing the integrated density (ID) of spot images on the X-ray. RESULTS: In lung cancer tissues, 40 genes were detected to be differentially expressed, 36 of which such as early growth response protein 1 (EGR1), secreted apoptosis related protein 1 (SARP1) were upregulated while the others such as myeloid cell leukemia protein 1 (MCL1) were downregulated. The upregulated genes were mainly oncogene/suppressor gene, cell cycle regulatory gene, growth factors and apoptosis-related genes. In lung paracancerous tissues, 33 genes had different expression, 20 of which such as matrix metalloproteinase-9 (MMP-9) were upregulated, and the other 13 such as MCL1,endothelin 2 (ET2) were downregulated. In metastases of lymph nodes, there were 21 genes found to be differently expressed, 15 of which such as CD40 receptor-associated factor 1 (CRAF1) were downregulated while the rest were upregulated, and the upregulated genes (6 in 15) were mainly the genes associated with adhesion molecules, matrix metalloproteinases and collagen. CONCLUSION: EGR1, SARP1, NDKA, etc. may be the key genes in pulmonary carcinogenesis course. At the same time, MMP9, thrombospondin 2 (TSP2), etc.may play an important role in pulmonary cancer metastasis and infiltration.

[Clinical value of hypertonic glucose injection in the treatment of recurrent pneumothorax].

OBJECTIVE: To investigate the clinical value of the 50% hypertonic glucose injection in the treatment of recurrent pneumothorax. METHODS: Forty-five patients with recurrent pneumothorax were injected with 60-80 ml of 50% hypertonic glucose into the pleural cavity after air discharge and then were instructed to turn their body to the right and the left quickly. RESULTS: The curative rate was 100% and the curative effect was satisfactory. There was no other complication except for slight stimulative chest pain in 7 patients. The recurrent rate was 4.4% in a 2-7 year follow-up. CONCLUSION: Treating recurrent pneumothorax with the 50% hypertonic glucose injection is safe, effective, and less recurrent.

[Expression of MMP1 and TIMP1 proteins in lung cancer and its biological significance].

OBJECTIVE: To investigate the expression of MMP1 and TIMP1 proteins in lung cancer tissues and its biological significance. METHODS: MMP1 and TIMP1 proteins were detected with the immunohistochemical method of avidin-biotin complex in formalin-fixed and routinely paraffin-embeded specimens of 46 patients. RESULTS: There was no correlation in MMP1 protein expression between normal lung tissues (20%) and lung cancer (52.2%); The positive rate of TIMP1 protein expression was significantly lower in lung cancer (41.3%) than that in normal lung tissues (80%); There was a significant correlation among MMP1 and TIMP1 protein expression and differentiation, TNM stages, and lymph node metastases of lung cancer. There was a significant negative correlation between MMP1 and TIMP1 protein expressions in lung cancer. CONCLUSION: There is a correlation between MMP1 and TIMP1 protein expressions in lung cancer and the invasion and metastasis of lung cancer. The factors may be used as important biological markers in lung cancer.