title: p21WAF1/CIP1 protein expression in primary ovarian cancer.
abstract: p21WAF1/CIP1 protein is a cyclin-dependent kinase inhibitor, able to prevent the CDK2/cyclin E induced retinoblastoma protein (pRB) phosphorylation, thus inhibiting cell cycle progression at G1 phase. p21WAF1/CIP1 protein levels were examined in a series of 102 ovarian tissue samples including normal ovary, primary ovarian tumors, omental metastasis, recurrent disease and residual tumor after chemotherapy exposure, by Western blot analysis. The association of p21WAF1/CIP1 status with clinicopathological parameters and clinical outcome was also investigated. p21WAF1/CIP1 protein was detectable in 76 out of 102 (74%) ovarian tissue samples. We observed a significant trend of p21 levels to gradually increase from normal ovarian tissues (median 0 a.u.) through primary ovarian cancers (median 0.19 a.u.), omental metastases (median 0.33 a.u.) and recurrence of disease (median 0.44 a.u.) (p=0.015). In the group of stage III-IV ovarian cancer patients, p21-positive cases showed a more favourable prognosis with respect to p21-negative cases: the 3-year time to progression (TTP) rate was 58% for p21-positive compared with 33% of p21-negative cases (p=0.036). In conclusion, p21WAF1/CIP1 expression levels seem to be correlated with tumor status at the time of diagnosis and can predict TTP in a selected group of patients.
authors.affiliation: Department of Gynecology and Obstetrics, Catholic University, Rome, Italy.
authors.forename: G
authors.initials: G
authors.lastname: Ferrandina
authors.forename: A
authors.initials: A
authors.lastname: Stoler
authors.forename: A
authors.initials: A
authors.lastname: Fagotti
authors.forename: F
authors.initials: F
authors.lastname: Fanfani
authors.forename: R
authors.initials: R
authors.lastname: Sacco
authors.forename: A
authors.initials: A
authors.lastname: De Pasqua
authors.forename: S
authors.initials: S
authors.lastname: Mancuso
authors.forename: G
authors.initials: G
authors.lastname: Scambia
mesh_terms: D000328:Adult; D000368:Aged; D000971:Antineoplastic Combined Chemotherapy Protocols / Q000627:therapeutic use; D018269:Carcinoma, Endometrioid / Q000188:drug therapy / Q000235:genetics / Q000378:metabolism / Q000473:pathology / Q000556:secondary / Q000601:surgery; D002453:Cell Cycle; D002945:Cisplatin / Q000008:administration & dosage; D050759:Cyclin-Dependent Kinase Inhibitor p21; D016213:Cyclins / Q000096:biosynthesis* / Q000235:genetics; D018282:Cystadenocarcinoma, Mucinous / Q000188:drug therapy / Q000235:genetics / Q000378:metabolism / Q000473:pathology / Q000556:secondary / Q000601:surgery; D018284:Cystadenocarcinoma, Serous / Q000188:drug therapy / Q000235:genetics / Q000378:metabolism* / Q000473:pathology / Q000556:secondary / Q000601:surgery; D018450:Disease Progression; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D016158:Genes, p53; D006801:Humans; D015993:Life Tables; D008875:Middle Aged; D009363:Neoplasm Proteins / Q000096:biosynthesis* / Q000235:genetics; D009364:Neoplasm Recurrence, Local; D009367:Neoplasm Staging; D018365:Neoplasm, Residual; D009852:Omentum; D010051:Ovarian Neoplasms / Q000188:drug therapy / Q000235:genetics / Q000378:metabolism* / Q000473:pathology / Q000601:surgery; D010053:Ovary / Q000378:metabolism; D010534:Peritoneal Neoplasms / Q000378:metabolism / Q000556:secondary; D016019:Survival Analysis; D016896:Treatment Outcome
chemical_list: C493956:CDKN1A protein, human; D050759:Cyclin-Dependent Kinase Inhibitor p21; D016213:Cyclins; D009363:Neoplasm Proteins; D002945:Cisplatin