title: Relationship between p53 pathway and estrogen receptor status in endometrioid-type endometrial cancer.
abstract: We analyzed the mechanism of estrogen receptor (ER) loss and status of the p53 pathway in 64 cases of endometrial cancer. 26.6% (17 of 64) of endometrial cancers lost ER. Methylation of the ER CpG island was significantly related to ER status (P = 0.0074). However, the methylation site of the ER CpG island differed between breast and endometrial cancers. The abnormal expression rate of p14ARF, MDM2, p53, and the p53 pathway were 7.8% (5 of 64), 32.8% (21 of 64), 25.0% (16 of 64) and 53.1% (34 of 64), respectively. There was no significant difference in the overexpression of MDM2 between p53-positive cases (43.8%: 7 of 16) and p53-negative cases (29.2%; 14 of 48) (P = 0.3595). Abnormal p53 was higher in grade 3 tumors (55.6%; 5 of 9) than in grade 1 and 2 tumors (20.0%; 11 of 55) (P = 0.0364). The abnormality of the p53 pathway was higher in grade 3 tumors (88.9%; 8 of 9) than in grade 1 and 2 tumors (47.3%; 26 of 55) (P = 0.0294). However, there was no significant difference in abnormal p53 pathway between ER-negative and ER-positive cases. In endometrial cancer, ER CpG island methylation was the important mechanism of ER loss. However, there was no significant relationship between the p53 pathway and ER status.
authors.affiliation: Department of Obstetrics and Gynecology, Osaka City University Graduate School of Medicine, Japan.
authors.forename: Kyoko
authors.initials: K
authors.lastname: Maeda
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Tsuda
authors.forename: Yasunori
authors.initials: Y
authors.lastname: Hashiguchi
authors.forename: Kumio
authors.initials: K
authors.lastname: Yamamoto
authors.forename: Takeshi
authors.initials: T
authors.lastname: Inoue
authors.forename: Osamu
authors.initials: O
authors.lastname: Ishiko
authors.forename: Sachio
authors.initials: S
authors.lastname: Ogita
mesh_terms: D018269:Carcinoma, Endometrioid / Q000737:chemistry / Q000235:genetics* / Q000378:metabolism; D019175:DNA Methylation; D004273:DNA, Neoplasm / Q000032:analysis; D016889:Endometrial Neoplasms / Q000737:chemistry / Q000235:genetics / Q000378:metabolism*; D005260:Female; D017353:Gene Deletion; D015870:Gene Expression; D006801:Humans; D007150:Immunohistochemistry; D009154:Mutation; D009687:Nuclear Proteins; D016133:Polymerase Chain Reaction; D018807:Polymorphism, Single-Stranded Conformational; D011518:Proto-Oncogene Proteins / Q000235:genetics; D051736:Proto-Oncogene Proteins c-mdm2; D011960:Receptors, Estrogen / Q000032:analysis* / Q000235:genetics / Q000378:metabolism; D025803:Tumor Suppressor Protein p14ARF / Q000235:genetics; D016159:Tumor Suppressor Protein p53 / Q000235:genetics* / Q000378:metabolism
chemical_list: D004273:DNA, Neoplasm; D009687:Nuclear Proteins; D011518:Proto-Oncogene Proteins; D011960:Receptors, Estrogen; D025803:Tumor Suppressor Protein p14ARF; D016159:Tumor Suppressor Protein p53; C497206:MDM2 protein, human; D051736:Proto-Oncogene Proteins c-mdm2