| PrefaceSince 1950s, the morbidity and mortality of lung cancer rose obviously. It is a focus of medicine to diagnose and treat lung cancer accurately. Tumor is the result of abnormal proliferation of somatic cells as well as a multiphase process of genes changing involving activation of oncogenes and inactivation of tumor suppressor genes. At present, mutations of p53 and p16/INK4a are commonly seen in many observations. P53 is one of the widely distributed tumor suppressor genes. As a negative regulator of cell cycle, p53 can control cell cycle by target genes and regulate cell apoptosis and maintain genetic stability of genomes.Recently, an alternative reading frame ( ARF) was found in INK4a location. ARF encodes p19 protein. So the location encoding p19 and pi6 proteins is called INK/ARF. INH/ARF is the only location that includes two overlapped genes at present, and each of them has their own independent promoter. The p19 protein increases the level of p53 by neutralizing Mdm2 which destabilize p53, ultimate-ly plays a role in suppressing cancer. As a new tumor suppressor, the relationship of p19 and occurrence, histological type, pathologic grade and lymphatic metastasis of lung cancer is .still waiting to be studied. This study uses immunohistochemical method to explore the relationship of pi9, p53 proteins and lung cancer.MaterialsAll cases were from Department of Pathology, Second Hospital of China Medical University, and from 1999-2000, including 8 normal lung tissue, 27 NSCLC, 5SCLC. Tumor tissue was resected at the same time 4jxm section and S-P method used. Agents in this experiment, p19 monoclonal antibody was from Boster company Wuhan, p53 monoclonal antibody was from Zhongshan company Beijing.MethodesWith sensitive immunohischemistry S-P method, p19 protein and p53 protein were detected in 8 normal lung tissue and 32 lung cancers after defining their pathological type by HE stain.ResultsThe positive rate of p53 protein was 45. 78% in lung cancer, and it was zero in 8 normal lung, there was statistic difference between them(p <0. 05). The positive rate of p53 in NSCLC was 44. 06% and it is 75.0% in SCLC, there was statistic difference between them (p <0.05). The positive rate of p53 protein in different pathologicalgrade was that it was 48. 89% in well differentiated NSCLC, in moderately differentiated NSCLC it was 44. 54% , in poorly differentiated NSCLC it is 48. 57% , there were no statistic difference among them (p >0. 05 ) . It was 56. 67% in lung cancer with lymphatic metastasis , in lung cancer without lymphatic metastasis it was 43.27% , there was no difference between them( p >0. 05) .The positive rate of p19 protein was 1. 91% in lung cancer, and it was 21. 88% in 8 normal lung, there was statistic difference between them(p <0. 05). The positive rate of p19 in NSCLC was 2. 16% and it was 0. 24% in SCLC, there was statistic difference between them(p < 0. 05). The positive rate of p19 protein in different pathological grade was that it was 3. 89% in well differentiated NSCLC, in moderately differentiated NSCLC it was 2. 25% , in poorly differentiated NSCLC it is 1. 25% , there were statistic difference a-mong them( p <0. 05 ) . It was 0. 20% in lung cancer with lymphatic metastasis, in lung cancer without lymphatic metastasis it was 2. 39% , there was difference between them(p <0. 05) .P19 protein and p53 protein accorded with line correlation and regression equation, they are negative correlative. ( Y = -2.983X + 55.497 r =0.366 r2 =0.134 p =0.04 <0.05).DiscussionNormally, the p53 protein is difficult to be detected for its short half life. The conformation of mutated p53 protein come up changing, half life is turned long, 20 -40 hours. It is mutated type p53 protein that is detected clinically. P53 can block cell-cycle in Gl stage, make cell gain opportunity for plerosis injured DNA. If cell can not success-fully recover injured DNA or effectively fight against the interference of out factors, suicide defensive system in cell is activa... |
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