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KRAS mutation analysis in ovarian samples using a high sensitivity biochip assay
Veronika Auner1, Gernot Kriegshäuser, Dan Tong
1Division of Gynaecology, Department of Obstetrics and Gynaecology, Medical University of Vienna, Vienna, Austria. veronika.auner@meduniwien.ac.at
Background:
Mutations in the KRAS gene are one of the most frequent genetic abnormalities in ovarian carcinoma. They are of renewed interest as new epidermal growth factor receptor (EGFR)-targeted therapies are being investigated for use in ovarian carcinoma. As KRAS mutations are associated with poor response and resistance to EGFR-targeting drugs, this study was conducted to obtain more information on the spectrum of KRAS mutations in ovarian carcinoma.
Methods:
The presence of KRAS mutations in codon 12 and 13 was analyzed in frozen and formalin-fixed paraffin-embedded (FFPE) tissue with a low density biochip platform. 381 malignant (29 borderline malignancy, 270 primary carcinomas, and 82 recurrent carcinomas) and 22 benign tissue samples from a total of 394 patients were examined. KRAS mutational status of each sample was correlated with dignity, FIGO stage, grade, histology, and survival.
Results:
KRAS mutations were found in 60 (15%) samples with 58 samples deriving from malignant tissue and 2 samples deriving from benign tissue. In 55 (92%) samples codon 12 was found to be mutated. Frozen and FFPE samples concurred with respect to KRAS mutation status.
Conclusion:
KRAS mutation is a common event in ovarian cancer primarily in carcinomas of lower grade, lower FIGO stage, and mucinous histotype. The KRAS mutational status is no prognostic factor for patients treated with standard therapy. However, in line with experience from colorectal cancer and non-small-cell-lung cancer (NSCLC), it may be important for prediction of response to EGFR-targeted therapies.
Insights
KRAS mutations are common in ovarian cancer, particularly in lower-grade and mucinous types. While not a prognostic factor for standard therapy, KRAS status may predict response to EGFR-targeted treatments.
Area of Science:
- Oncology
- Genetics
- Molecular Biology
Background:
- KRAS gene mutations are frequent in ovarian carcinoma.
- These mutations are relevant due to emerging epidermal growth factor receptor (EGFR)-targeted therapies.
- KRAS mutations are linked to poor response and resistance to EGFR inhibitors.
Purpose of the Study:
- To investigate the spectrum of KRAS mutations in ovarian carcinoma.
- To understand the prevalence and characteristics of KRAS mutations in different ovarian tissue types.
Main Methods:
- Analyzed KRAS mutations in codons 12 and 13 using a biochip platform.
- Examined 394 tissue samples (381 malignant, 22 benign) including frozen and FFPE tissues.
- Correlated KRAS mutational status with clinicopathological factors and survival.
Main Results:
- KRAS mutations were identified in 15% (60/394) of samples, predominantly in malignant tissues (58/60).
- Codon 12 was the most frequently mutated site (92% of mutations).
- Frozen and FFPE samples showed consistent KRAS mutation status.
Conclusions:
- KRAS mutation is common in ovarian cancer, especially in lower grade, lower FIGO stage, and mucinous histotypes.
- KRAS mutational status does not appear to be a prognostic factor for standard therapy.
- KRAS status may be predictive of response to EGFR-targeted therapies, similar to findings in colorectal and non-small-cell lung cancer.
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