Immunohistochemical analysis of PTEN in endometrial carcinoma: a tissue microarray study with a comparison of four commercial antibodies in correlation with molecular abnormalities

dc.contributor.authorPallares, Judit
dc.contributor.authorBussaglia, Elena
dc.contributor.authorMartínez-Guitarte, Jose Luis
dc.contributor.authorDolcet Roca, Xavier
dc.contributor.authorLlobet Navàs, David
dc.contributor.authorRué i Monné, Montserrat
dc.contributor.authorSanchez-Verde, Lidia
dc.contributor.authorPalacios, José
dc.contributor.authorPrat, Jaime
dc.contributor.authorMatias-Guiu, Xavier
dc.description.abstractThe tumor suppressor gene PTEN/MMAC1 is located on chromosome 10q23.3. Inactivation of PTEN, either by mutations, deletions, or promoter hypermethylation, has been identified in a wide variety of tumors. Inactivation of the two alleles of PTEN is required, because it is a tumor suppressor gene. Immunohistochemical staining may be an effective screening method to demonstrate the absence of the protein in tumors exhibiting PTEN inactivation. We studied a tissue microarray, constructed from paraffin-embedded blocks of 95 endometrial carcinomas, 38 of them previously evaluated for alterations in PTEN. We also studied cell blocks obtained from one PTEN-defective endometrial cancer cell line, after transfection with either a plasmid encoding wild-type PTEN or the empty vector. The tumor samples were tested with four different anti-PTEN commercial antibodies: a polyclonal antibody, the monoclonal antibody 28H6, the monoclonal antibody 10P03, and the monoclonal antibody 6.H2.1. Results were correlated with the presence of abnormalities in PTEN, as well as with the immunohistochemical expression of phosphorylated AKT. Antibody 28H6 produced a predominant nuclear staining, while the other three antibodies produced a predominant cytoplasmic staining. There was no significant correlation between the results obtained with the four antibodies. The monoclonal antibody 6.H2.1 was the only one that exhibited a correlation with the presence of molecular alterations in PTEN, and a statistically significant association with immunostaining for phosphorylated AKT (r ¼ 0.249, P ¼ 0.037). The monoclonal antibody 10P03 exhibited an association with phospho-AKT that did not have statistical significance. Both 6.H2.1 and 10P03 antibodies stained PTEN-transfected cells, and were negative in the PTEN-deficient cell line blocks. The polyclonal antibody and the monoclonal antibody 28H6 produced positive staining in PTEN-deficient cell line blocks, suggesting nonspecific staining. The results indicate that monoclonal antibody 6.H2.1 may be a suitable alternative for tumors with inactivation of PTEN.ca_ES
dc.description.sponsorshipThis work was supported by Grants FISS 01/1656, FISS PI020227, SAF 2004-05250, and 2002XT00115. JP holds a research fellowship from the Fondo de Investigaciones Sanitarias, Ministerio de Sanidad y Consumo (BEFI-02/9007)). JLMG and XD hold a postdoctoral fellowship supported by the Department d’Universitats, Recerca i Societat de la Informació, Generalitat de Catalunya (2002RED005 and, 2003RED0018).ca_ES
dc.publisherNature Publishing Groupca_ES
dc.relation.isformatofReproducció del document publicat a
dc.relation.ispartofModern Pathology, 2005, vol. 18, núm. 5, p. 719-727ca_ES
dc.rights(c) USCAP, Inc., 2005ca_ES
dc.subjectEndometrial carcinomaca_ES
dc.subjectTissue microarrayca_ES
dc.subjectMolecular pathologyca_ES
dc.titleImmunohistochemical analysis of PTEN in endometrial carcinoma: a tissue microarray study with a comparison of four commercial antibodies in correlation with molecular abnormalitiesca_ES
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