IMR Press / EJGO / Volume 25 / Issue 4 / pii/2004212

European Journal of Gynaecological Oncology (EJGO) is published by IMR Press from Volume 40 Issue 1 (2019). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with S.O.G.

Original Research

K-ras gene point mutations and p21ras immunostainingin human ovarian tumors

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1 2nd Department of Gynecology, University School of Medicine, Lublin (Poland)
2 Cytogenetic Laboratory, University School of Medicine, Lublin (Poland)
3 Department of Human Genetics, University School of Medicine, Lublin (Poland)
4 Department of Phamiacology , University School of Medicine, Lublin (Poland)
5 Department of Pathology, University School of Medicine, Lublin (Poland)
Eur. J. Gynaecol. Oncol. 2004, 25(4), 484–488;
Published: 10 August 2004

It is well recognized that genetic alterations within oncogenes, tumor suppressor genes, DNA mismatch repair and excision repair genes contribute to tumorigenesis within the human ovary. This study was undertaken to screen for the existence of K-ras gene point mutations in paraffin-embedded slides randomly selected from benign and malignant ovarian tumors applying the PCR-RFLP tech­nique. Expression of p21ras was also assessed in 30 primary ovarian adenocarcinomas immunohistochemically. K-ras codon 12 point mutations occurred in nine of 40 (22.5%) cases. They were not identified in two benign mucinous cystadenomas, but in one out of two (50%) mucinous tumors of LMP (low malignant potential), in five out of 30 (17%) ovarian adenocarcinomas, and in one case of adenocarcinoma metastatic to the ovary. K-ras activation was also detected in one out of four (25%) sex cord-stromal cell tumors (folliculoma), and in one dysgerminoma. None of these tumors exhibited K-ras codon 13 point mutations. Gene alterations were more frequently found in mucinous than in non-mucinous (30% vs 10%) tumors, although the difference did not reach significance (p > 0.05). The frequency of K-ras point mutations was correlated neither with clinical nor with pathological variables of cancer. Cytoplasmic p2 I'" was expressed in all adenocarcinomas negative for K-ras point mutations, whereas one of five (20%) K-ras-pos­itive tumors exhibited lack of immunoreactivity. In conclusion, these findings confirm the role of K-ras activation in mucinous ovarian tumors. p21ras expression is not necessarily associated with K-ras gene alterations in human ovarian adenocarcinomas.

Ovarian cancer
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