Expression of the tumor suppressor gene PTEN is not altered in the progression of ovarian carcinomas and does not correlate with p27Kip1 expression.
This study was designed to investigate the role of PTEN in the progression of ovarian cancer. We performed mutation analysis and determined PTEN gene expression in tissue from both primary and relapsed cancers and in the corresponding occult metastases. Furthermore, p27Kip1 staining was conducted in order to explore a putative functional link. The study group comprised 112 tumor tissue specimens from 37 ovarian cancer patients. Expression of both PTEN and p27Kip1 was determined by immunohistochemistry. The PTEN mutational spectrum was determined by PCR-based sequence analysis. Fifty-six per cent of the tumors were positive for PTEN expression and 75% were p27Kip1 positive. For both markers, tumor cells ranged from 0 to 90% positivity. In 55% (20/37) of the cases, PTEN expression in the primary tumor was consistent and in the corresponding advanced cancer tissues, whereas the remainder showed considerable variation. p27Kip1 was consistently expressed in 16 out of 37 cases (43%). No mutations were observed in the coding region of the PTEN gene. No correlation was observed between PTEN and p27Kip1 expression. Our data indicate that expression of PTEN, but not p27Kip1 (one of the major mediators of PTEN function) is unchanged during the progression of ovarian cancer. This study suggests that in ovarian cancer PTEN does not play a major role in disease progression and is not involved in the alteration of p27Kip1 expression.
Schöndorf
Thomas
T
Department of Gynecology and Obstetrics, University of Cologne, 50924 Cologne, Germany.
Hoopmann
Markus
M
Eversheim
Barbara
B
Valter
Markus M
MM
Becker
Martina
M
Wappenschmidt
Barbara
B
Göhring
Uwe-Jochen
UJ
Kübler
Tanja
T
Schmutzler
Rita K
RK
Schäfer
Robert
R
D000328:Adult; D000368:Aged; D014408:Biomarkers, Tumor / Q000096:biosynthesis; D002277:Carcinoma / Q000378:metabolism; D018797:Cell Cycle Proteins / Q000096:biosynthesis*; D050760:Cyclin-Dependent Kinase Inhibitor p27; D004252:DNA Mutational Analysis; D018450:Disease Progression; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D007150:Immunohistochemistry; D008875:Middle Aged; D009154:Mutation; D009362:Neoplasm Metastasis; D010051:Ovarian Neoplasms / Q000378:metabolism*; D051059:PTEN Phosphohydrolase; D010744:Phosphoric Monoester Hydrolases / Q000096:biosynthesis*; D016133:Polymerase Chain Reaction; D012008:Recurrence; D016896:Treatment Outcome; D025521:Tumor Suppressor Proteins / Q000096:biosynthesis*
D014408:Biomarkers, Tumor; D018797:Cell Cycle Proteins; D025521:Tumor Suppressor Proteins; D050760:Cyclin-Dependent Kinase Inhibitor p27; D010744:Phosphoric Monoester Hydrolases; D051059:PTEN Phosphohydrolase; C494929:PTEN protein, human