[Relationship between expression of p57(kip2), cyclin E protein, PCNA, and clinicopathological factors in human pancreatic cancer].

BACKGROUND & OBJECTIVE: The abnormality of mammalian cell cycle regulation is an important cause of cell over-proliferation and oncogenesis. There were few reports about the relationship between p57(kip2) protein as negative factor of cell cycle regulation and pancreatic cancer. This article aims to investigate the effects of p57(kip2), cyclin E and proliferating cell nuclear antigen (PCNA) protein on the occurrence and progression of pancreatic cancer. METHODS: Expression of p57(kip2), cyclin E, and PCNA in tumor tissue and adjacent tissue from 32 patients with pancreatic cancer were detected using SP immunohistochemical technique. RESULTS: The positive-expression rate of p57(kip2) protein in tumor tissue of pancreatic cancer was 46.9%, which was lower than that in adjacent pancreatic tissue (75.0%) (Chi(2)=5.317, P< 0.05); p57(kip2) protein positive-expression was remarkably correlated with tumor cell differentiation (P< 0.05), but was not correlated with lymph node metastasis (P >0.05). The positive-expression rate of cyclin E in tumor tissues was 68.8%, which was higher than that in adjacent pancreatic tissue (43.8%) (Chi(2)=4.063,P< 0.05); Cyclin E positive-expression was remarkably correlated with tumor cell differentiation and lymph node metastasis (P< 0.05). The positive-expression rate of PCNA protein in tumor tissues was 71.9%, which was higher than that in adjacent pancreatic tissue (43.8%) (Chi(2)=5.189,P< 0.05); PCNA positive- expression was remarkably correlated with tumor cell differentiation and lymph node metastasis(P< 0.05). CONCLUSION: The decreased expression of p57(kip2) protein and over-expression of cyclin E and PCNA proteins may significantly related to genesis and progress of pancreatic cancer.