[Expression P53 protein and chromosome aberrations in benign tumors and ovarian carcinoma].
OBJECTIVE
The epithelial ovarian tumors arise from the single layer of epithelial cells that line the ovarian surface or from underlying inclusion cysts. One from many theories of oncogenesis has been proposed that benign, borderline and invasive tumors represent sequential stages in the growth of an ovarian cancer, and p53 tumor suppressor gene mutation is the most common molecular genetic alteration. Because locus of p53 gene is located on 17 chromosome we performed the cytogenic analysis of tumor tissues.


METHODS
Analysis of mutated p53 protein expression and chromosomal aberrations in tissues of benign tumors and epithelial ovarian carcinomas.


METHODS
Tissue samples from 19 women with benign and 17 women with invasive epithelial ovarian cancers were obtained for the study at the time of surgical procedures. From among benign tumors 12 were serous cystadenomas, 5 were endometrial cysts and 2 adult teratomas. All cases of invasive epithelial ovarian carcinomas were histologically recognized as serous adenocarcinomas, and were staged on I (9 cases), II (5 cases) and III (3 cases), according to the FIGO guidelines for ovarian cancers. Frozen tissue samples were stained immunohistochemically for mutated p53 protein using commercial monoclonal antibodies and standard detecting system. The fresh tumor samples were prepared for cytogenic analysis according to standard protocol.


RESULTS
Among the all benign ovarian tumors overexpression of mutated form of p53 protein was not seen in any cases, but was noted in 6 cases in I stage and in all cases in II and III stages of advanced ovarian cancers. In 1 case of benign ovarian tumor deletion of X chromosome was observed. Most common numerical changes were observed in ovarian carcinomas e.g. loss of 8, 13, 17, and 22 chromosomes. Other chromosomes were involved at least once in structural rearrangements and several breakpoint cluster regions were identified: 19p13, 11p13-15, 1q21-23, 1p36, 19q13, and 6q21-23.


CONCLUSIONS
The mutated form of p53 protein is often expressed in ovarian epithelial carcinoma tissues. This protein are unable to function effectively to inhibit proliferation and accumulate in the cells because is resistant to degradation. In tissues of ovarian carcinomas many chromosomal nondisjunctions (monosomics) and multiple structural rearrangements were observed, what means of genetically nonstable cell lines of neoplasms and probably it heterogenous origin.
Kamiński
Krzysztof
K
Katedry i Kliniki Połoznictwa i Perinatologii AM w Lublinie.
Putowski
Lechosław
L
Oleszczuk
Jan
J
D000911:Antibodies, Monoclonal; D014408:Biomarkers, Tumor / Q000032:analysis*; D002869:Chromosome Aberrations; D002886:Chromosomes, Human, Pair 17; D018284:Cystadenocarcinoma, Serous / Q000737:chemistry; D004252:DNA Mutational Analysis; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D007150:Immunohistochemistry / Q000379:methods; D009154:Mutation; D009367:Neoplasm Staging; D010048:Ovarian Cysts / Q000737:chemistry*; D010051:Ovarian Neoplasms / Q000737:chemistry* / Q000473:pathology; D013724:Teratoma / Q000737:chemistry; D016159:Tumor Suppressor Protein p53 / Q000032:analysis* / Q000235:genetics
D000911:Antibodies, Monoclonal; D014408:Biomarkers, Tumor; D016159:Tumor Suppressor Protein p53