2001•Chinese Journal of Bases and Clincs In General SurgeryRequires access

THE EXPRESSION OF CYCLIN D_1、Rb AND p16 PROTEIN IN EARLY GASTRIC CARCINOMA

Xiao Chen

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Abstract

Objective To investigate the expression of cell division regulators p16, Rb and cyclin D 1 in human early gasric carcinoma tissues and their role in tumor transformation and the correlation among p16, Rb and cyclin D 1. Methods A comparative study was carried out by using immuno histochemical techniques between the paracarcinomatous intestinal metaplasia of 39 cases of early gatric carcinoma and the non carcinomatous gastric mucosal intestinal metaplasia tissues of 34 cases.Results Over expression of cyclin D 1 was determined in 33/39 carcinomatous samples(84.6%) and also in para carcinomatous intestinal metaplasia tissues. p16 was undetectable in 12 of 39 samples. Interestingly, 15 of 26 Rb positive cancers had no or low p16,while 9 Rb negative cancers showed high levels of p16.Conclusion The over expression of cyclin D 1 may be a common molecular abnormality and an early molecular event in early gastric carcinoma. Cyclin D 1 over expression and Rb inactivation can co exist in early gastric carcinoma. However, there is a reciprocity between Rb inactivation and p16 expression in early gastric carcinoma. Thus, abnormality in the negative feedback regulatory pathway of cyclin D 1,Rb and p16 may be related to the tumorigenesis in early gastric carcinoma.

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Objective To investigate the expression of cell division regulators p16, Rb and cyclin D 1 in human early gasric carcinoma tissues and their role in tumor transformation and the correlation among p16, Rb and cyclin D 1. Methods A comparative study was carried out by using immuno histochemical techniques between the paracarcinomatous intestinal metaplasia of 39 cases of early gatric carcinoma and the non carcinomatous gastric mucosal intestinal metaplasia tissues of 34 cases.Results Over expression of cyclin D 1 was determined in 33/39 carcinomatous samples(84.6%) and also in para carcinomatous intestinal metaplasia tissues. p16 was undetectable in 12 of 39 samples. Interestingly, 15 of 26 Rb positive cancers had no or low p16,while 9 Rb negative cancers showed high levels of p16.Conclusion The over expression of cyclin D 1 may be a common molecular abnormality and an early molecular event in early gastric carcinoma. Cyclin D 1 over expression and Rb inactivation can co exist in early gastric carcinoma. However, there is a reciprocity between Rb inactivation and p16 expression in early gastric carcinoma. Thus, abnormality in the negative feedback regulatory pathway of cyclin D 1,Rb and p16 may be related to the tumorigenesis in early gastric carcinoma.

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Available abstract

Objective To investigate the expression of cell division regulators p16, Rb and cyclin D 1 in human early gasric carcinoma tissues and their role in tumor transformation and the correlation among p16, Rb and cyclin D 1. Methods A comparative study was carried out by using immuno histochemical techniques between the paracarcinomatous intestinal metaplasia of 39 cases of early gatric carcinoma and the non carcinomatous gastric mucosal intestinal metaplasia tissues of 34 cases.Results Over expression of cyclin D 1 was determined in 33/39 carcinomatous samples(84.6%) and also in para carcinomatous intestinal metaplasia tissues. p16 was undetectable in 12 of 39 samples. Interestingly, 15 of 26 Rb positive cancers had no or low p16,while 9 Rb negative cancers showed high levels of p16.Conclusion The over expression of cyclin D 1 may be a common molecular abnormality and an early molecular event in early gastric carcinoma. Cyclin D 1 over expression and Rb inactivation can co exist in early gastric carcinoma. However, there is a reciprocity between Rb inactivation and p16 expression in early gastric carcinoma. Thus, abnormality in the negative feedback regulatory pathway of cyclin D 1,Rb and p16 may be related to the tumorigenesis in early gastric carcinoma.

Key concepts: Intestinal metaplasia, Cyclin D1, Cancer research, Carcinoma, Carcinogenesis, Biology, Metaplasia, Pathology

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