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dc.contributor.authorStarzynska, T
dc.contributor.authorBromley, M
dc.contributor.authorLane, D
dc.contributor.authorStern, Peter L
dc.date.accessioned2015-01-15T09:54:36Z
dc.date.available2015-01-15T09:54:36Z
dc.date.issued1995-06
dc.identifier.citationThe expression of p53 tumor-suppressor protein during progression of gastric and colorectal carcinomas. 1995, 6 (6):1319-23 Int J Oncolen
dc.identifier.issn1019-6439
dc.identifier.pmid21556675
dc.identifier.urihttp://hdl.handle.net/10541/338268
dc.description.abstractThe expression of p53 was immunohistochemically determined in sets of biopsies from primary and recurrent colorectal (12) and gastric (17) tumours that had progressed to more advanged stages in the following 6-54 months. At presentation 7 carcinomas overexpressed p53 protein in the cell nucleus and 22 tumours had normal, undetectable levels of p53. In most patients, the p53 phenotype was maintained during the process of tumour progression. In two gastric and two colorectal carcinomas p53 overexpression was subsequently detected in recurrent tumour growth at the primary site and was also associated with the development of metastases. These results suggests that in some cases p53 alterations may contribute to the conversion to malignancy and in others to tumour progression and metastatic capacity.
dc.language.isoenen
dc.rightsArchived with thanks to International journal of oncologyen
dc.titleThe expression of p53 tumor-suppressor protein during progression of gastric and colorectal carcinomas.en
dc.typeArticleen
dc.contributor.departmentPaterson Laboratories, Christie Hospital and Holt Radium Institute, Manchesteren
dc.identifier.journalInternational Journal of Oncologyen
html.description.abstractThe expression of p53 was immunohistochemically determined in sets of biopsies from primary and recurrent colorectal (12) and gastric (17) tumours that had progressed to more advanged stages in the following 6-54 months. At presentation 7 carcinomas overexpressed p53 protein in the cell nucleus and 22 tumours had normal, undetectable levels of p53. In most patients, the p53 phenotype was maintained during the process of tumour progression. In two gastric and two colorectal carcinomas p53 overexpression was subsequently detected in recurrent tumour growth at the primary site and was also associated with the development of metastases. These results suggests that in some cases p53 alterations may contribute to the conversion to malignancy and in others to tumour progression and metastatic capacity.


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