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abstract
Highlights
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- The presence of a BRAF mutation in a serous borderline tumour may protect against progression to low-grade serous cancer
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- The presence of a KRAS mutation in a low-grade serous tumour may be a good prognostic factor
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- The most important prognostic factor in patients with low-grade cancer is the amount of residual disease post-surgery
Epithelial
ovarian cancers can be divided into the more common, aggressive type II
cancers and the less common, slow-growing type I cancers. Under this
model, serous ovarian carcinomas can be subdivided into high-grade (type
II) and low-grade (type I) tumours. The two-tier system for grading
serous ovarian carcinomas is superior to more detailed grading systems
in terms of predicting survival. Low-grade serous carcinomas typically
present in young women and have a relatively good prognosis, despite
being resistant to chemotherapy. Low-grade serous cancers have a high
prevalence of KRAS and BRAF mutations, but a low prevalence of TP53
mutations (which are characteristic of high-grade serous cancers). Among
women with low-grade serous ovarian cancer, the presence of a KRAS/BRAF
mutation is a favorable prognostic factor. Studies of the
mitogen-activated protein kinase (MAPK) inhibitor in low-grade serous
ovarian cancer suggest that identifying MAPK mutations might eventually
be useful in guiding treatment.
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MEK stands for the MAPK/ERK kinase, and
it is among the series of regulatory kinases targeting that pathway. It
has a dual role, acting as both a serine/threonine kinase and a tyrosine
kinase.
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