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KRAS mutation in primary ovarian serous borderline tumors correlates with tumor recurrence
Austin McHenry1, Douglas A Rottmann2, Natalia Buza1
1Department of Pathology, Yale University School of Medicine, New Haven, CT, USA.
Abstract:
Oncogenic activation of the mitogen-activated protein kinase (MAPK) pathway due to KRAS or BRAF gain-of-function mutation is frequently found in ovarian serous borderline tumor (SBT) and their extraovarian implants. We investigated mutational status of KRAS and BRAF of the primary ovarian SBTs that had a high stage presentation in correlation with clinical outcome. Among 39 consecutive primary SBTs with either invasive implants (20 cases) or non-invasive implants (19 cases), KRAS and BRAF mutational analysis was informative in 34 cases. Sixteen cases (47%) harbored a KRAS mutation, while 5 cases (15%) had a BRAF V600E mutation. High-stage disease (IIIC) was seen in 31% (5/16) of patients with a KRAS mutation and 39% (7/18) of patients without a KRAS mutation (p = 0.64). KRAS mutations were present in 9/16 (56%) tumors with invasive implants/LGSC versus 7/18 (39%) tumors with non-invasive implants (p = 0.31). BRAF mutation was seen in 5 cases with non-invasive implants. Tumor recurrence was seen in 31% (5/16) of patients with a KRAS mutation, compared to 6% (1/18) of patients without a KRAS mutation (p = 0.04). A KRAS mutation predicted an adverse disease-free survival (31% survival at 160 months) compared to those with wild-type KRAS (94% at 160 months; log-rank test, p = 0.037; HR 4.47). In conclusion, KRAS mutation in primary ovarian SBTs is significantly associated with a worse disease-free survival, independent of the high tumor stage or histological subtypes of extraovarian implant. KRAS mutation testing of primary ovarian SBT may servce as a useful biomarker for tumor recurrence.
Insights
KRAS mutations in ovarian serous borderline tumors (SBTs) are linked to a higher risk of recurrence. Testing for KRAS mutations may help predict disease-free survival in ovarian SBT patients.
Area of Science:
- Oncology
- Genetics
- Gynecologic Pathology
Background:
- Mitogen-activated protein kinase (MAPK) pathway activation by KRAS or BRAF mutations is common in ovarian serous borderline tumors (SBTs) and their implants.
- Understanding the correlation between these mutations and clinical outcomes is crucial for patient management.
Purpose of the Study:
- To investigate the association between KRAS and BRAF mutational status in primary ovarian SBTs and their clinical outcomes, particularly focusing on high-stage disease.
- To determine if KRAS or BRAF mutations correlate with tumor recurrence and disease-free survival.
Main Methods:
- Analysis of KRAS and BRAF mutational status in 39 primary ovarian SBTs with invasive or non-invasive extraovarian implants.
- Correlation of mutation status with clinical presentation (high stage), implant type, and patient outcomes (recurrence, disease-free survival).
Main Results:
- KRAS mutations were found in 47% of informative cases, while BRAF V600E mutations were present in 15%.
- KRAS mutations were not significantly associated with high-stage disease or invasive vs. non-invasive implants.
- A significant association was observed between KRAS mutations and tumor recurrence (31% vs. 6%, p=0.04), predicting adverse disease-free survival (31% at 160 months vs. 94% for wild-type, p=0.037).
Conclusions:
- KRAS mutation in primary ovarian SBTs is a significant predictor of worse disease-free survival.
- KRAS mutation status is an independent prognostic biomarker for tumor recurrence in ovarian SBTs, irrespective of stage or implant histology.
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