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Background : Recent studies have suggested that loss of p27Kip1 expression correlates with poor prognosis in gastric carcinomas, although the published data is still controversial. However, there are very few reports on the immunohistochemical expression of p27Kip1 in gastric adenomas and its significance in the progression of gastric adenomas to early gastric carcinomas (EGCs) is unclear. We therefore performed an immunohistochemical study for p27Kip1 expression in gastric adenomas with low- and high-grade dysplasia and EGCs to investigate the role of p27Kip1 expression in gastric carcinogenesis. Methods : We collected 45 cases of endoscopic mucosal resection specimens which were diagnosed as gastric adenomas and 20 cases of gastrectomy specimens showing EGCs. Using a monoclonal antibody against p27Kip1, the immunohistochemistry was performed on paraffin-embedded specimens. Results : The loss of p27Kip1 immunoreactivity (<5% of the tumor cells) tended to be observed more frequently in highgrade adenomas than in the low-grade. The loss was found significantly higher in the EGCs than in both high-grade and low-grade adenomas (p=0.000). Gastric adenomas with villous component showed significant loss of p27Kip1 expression (p=0.057). Conclusion : These results suggest that loss of p27Kip1 expression can play a role in the progression of gastric adenomas into adenocarcinomas and the villous component allows reliable estimation of the possibility for malignant transformation.
Two cases of giant cell tumor of bone diagnosed by fine needle aspiration cytology are described. Case 1 was a 28-year-old male who had pain sense for one year at the right distal thigh. His radiologic finding revealed a destructive cortical lesion with soft tissue extension at medial side of epiphysis of the distal femur. Case 2 was a 21-year-old female complaining pain at left distal forearm for eight months and showed a well-demarcated expansile osteolytic lesion with multiseptation, and cortical destruction at epiphysis and metaphysis of the left distal radius on the X-ray. Fine needle aspiration of each lesion was performed. The aspirate of the case 1 revealed moderate cellularity, which was composed of scattered giant cells of osteoclastic type and small round to oval monotonous stromal cells in large areas. Giant cells were evenly distributed in single or small groups and had irregular but abundant cytoplasms with 10 to 20 nuclei in the center. The nuclei showed ovoid shape, fine granular chromatin, and a small but conspicuous nucleolus. Stromal cells were dispersed in isolated pattern or sometimes aggregated in clusters and showed the same nuclei as those of giant cells and scanty cytoplasms. Comparing to case 1, case 2 had a more translucent abundant cytoplasm in the giant cells and more spindled stromal cells. All two cases revealed neither nuclear atypism nor increased abnormal mitoses In both giant and stromal cells, suggesting no evidence of malignancy. Thereafter the lesions were treated with excision and curettage, and histologically confirmed as giant cell tumors of the bone.
Cyclin D1 Overexpression, p16 Loss, and pRb Inactivation Play a Key Role in Pulmonary Carcinogenesis and have a Prognostic Implication for the Long-term Survival in Non-small Cell Lung Carcinoma Patients
Purpose: We investigated the immunoexpressions of cyclin D1, cyclin-dependent kinase inhibitor p16 and phosphorylated retinoblastoma (p-pRb) proteins in nonsmall cell lung carcinoma (NSCLC) to demonstrate their key roles in tumorigenesis, their relationship with the clinicopathologic factors, and their prognostic influences on the long-term survival. Materials and Methods: 115 surgically resected NSCLCs were immunohistochemically stained for the G1/S cell cycle proteins, with using a tissue microarray. The correlation between their immunoexpressions and the clinicopathologic prognostic factors, their inter-relationships and their single or combined effects on the long-term survival (over 5 years) were statistically analyzed by SPSS15.0. Results: Loss of p16 was found in 75% of the cases and cyclin D1 overexpression and phosphorylated pRb (p-pRb) were found in 64% and 46%, respectively. Cyclin D1 overexpression was correlated with the p16 loss and pRb inactivation by phosphorylation. The p16 loss was tightly associated with p-pRb. The Kaplan-Meier survival curves disclosed that the cyclin D1-positive group and the p16-negative group showed a rapid decline of survival at the point of about 5 years after surgery and thereafter. The combined actions of cyclin D1 overexpression, loss of p16 and pRb inactivation tended to have an adverse influence on the prolonged survival. Conclusions: The observation that cyclin D1 overexpression, p16 loss and pRb inactivation were largely found in NSCLCs suggests that they play an important role in pulmonary carcinogenesis. Also, their inverse or positive correlations indicate that the G₁/S cell cycle proteins may act alternatively or synergistically on the mechanisms by which tumor cells escape the G₁ restriction point. Finally, their solitary or combined actions might have a long-term effect on the survival.