BACKGROUND: The phosphatase and tensin homolog deleted on chromosome 10 (PTEN) gene, a candidate tumor suppressor, is localized to chromosome 10q23 and shares extensive homology with cytoskeletal proteins auxilin and tensin. It appears to have multifunctional roles involved in cell proliferation, migration, and invasion. The role of PTEN alteration in the lung cancer and its relationship with other suppressor genes are not well established. METHODS: Formalin-fixed, paraffin-embedded tissues from 105 patients with diagnosed with primary lung cancer were evaluated for PTEN and p53 protein expression using immunohistochemical methods. The results of the expression pattern of PTEN were compared with clinicopathological parameters and the expression pattern of p53. RESULTS: Forty-seven (44.8%) of 105 cases had loss of PTEN expression. Loss of PTEN expression was significantly associated with histologic type (p<0.05), but did not correlate with tumor size, lymph node metastasis, and stage. There was no significant relationship between loss of PTEN expression and p53 expression, and no significant difference in clinicopathologic characteristics between particular groups of patterns with the four possible tumor carrying PTEN/p53 phenotypes. CONCLUSION: It is suggested that loss of PTEN expression occurs commonly in primary lung cancers and correlates with histologic type. Our results also support the proposed role of PTEN as a candidate tumor suppressor in lung cancer, and we suggest that there is a need for further study of this gene.
Auxilins ; Cell Proliferation ; Chromosomes, Human, Pair 10 ; Cytoskeletal Proteins ; Genes, Suppressor ; Genes, vif ; Humans ; Immunohistochemistry ; Lung Neoplasms* ; Lung* ; Lymph Nodes ; Neoplasm Metastasis ; Phenotype ; Tumor Suppressor Proteins

OBJECTIVE: Phosphate and tensin homolog deleted on chromosome 10 (PTEN) is a potent tumor suppressor gene, localized to chromosome 10q23, and shows extensive homology with auxilin and tension. PTEN has variety roles involved in cell proliferation, invasion, and migration in tumorigenesis of solid tumors. In this study, the expression of the PTEN in the ovarian epithelial tumors, including benign, borderline malignancy, and adenocarcinomas was investigated. METHODS: Immunohistochemical expression of PTEN were analyzed in formalin fixed tumor tissues of 20 benign cystadenomas, 22 borderline tumors, and 49 malignant ovarian cancer. In the same tissue extracts, single nucleotide polymorphism were studied. RESULTS: Most of benign and borderline ovarian tumors revealed strong positive reaction, but a few cases showed negative reaction or weak positive reaction. In adenocarcinomas, 33% of cases was negative, and 43% was focal weakly staining, grade 1. The remainder of adenocarcinomas showed strong nuclear staining. In SNP assay, A/A allele of rs1234213 shows low frequency, but A/G allele reveals high frequency. C/C allele of rs701848 shows high frequency, and rs9651492 is not detected polymorphism. CONCLUSION: These results suggest that loss of PTEN expression is associated with tumorrigenesis of ovarian epithelial tumors, and is related with single nucleotide polymorphism.
Adenocarcinoma ; Alleles ; Auxilins ; Carcinogenesis ; Cell Proliferation ; Chromosomes, Human, Pair 10 ; Cystadenoma ; Female ; Formaldehyde ; Genes, Tumor Suppressor ; Ovarian Neoplasms ; Ovary* ; Polymorphism, Single Nucleotide* ; Tissue Extracts