Table 2. Mutational status and clinical relevance of RAS mutations in OC.
| OC and subtypes | Specimen | Genes mutated | Pathways involved | Outcome | Ref. |
|---|---|---|---|---|---|
| OCCC | Patient specimens | PIK3CA | PIK3CA/AKT/mTOR pathway | PIK3CA could be a potential target | 94 |
| MOC | Patient specimens | KRAS | EGFR signaling | KRAS mutation at codon 12 and high titer of CA125 marker. | 95 |
| MOC | Frozen ovarian tumors |
KRAS
BRAF NRAS |
MAPK pathway | Mutational status of mucinous carcinoma | 90 |
| EnOC | Human tissue specimen |
CTNNB1
KRAS PTEN PIK3CA |
MAPK/RAS, WNT and PI3K pathways | TP53 and CTNNB1 can be potential prognostic markers | 96 |
| OCCC | Ovarian tumor tissue from patients |
ARID1A
PIK3CA KRAS ERBB2 ERBB3 BRAF |
PI3/AKT and RTK/RAS pathways | PI3/AKT and RTK/RAS signaling pathways might be a prognostic marker | 97 |
| OCCC | Serum samples |
ARID1A
PIK3CA KRAS |
PI3K/AKT, TP53, and ERBB2 pathways | Potential therapeutic target | 98 |
| OCCC | Patient sample |
PI3KCA
KRAS |
PI3K/AKT pathway | Carcinogenesis and progression | 99 |
| SBOT | Patient sample |
KRAS
BRAF |
RAS–RAF–MAP–MEK–ERK kinase pathway | Mutations associated with low-grade tumors | 71 , 100 |
| MBOT | Specimens from tumor bank |
KRAS
TP53 CDKN2A PIK3CA PTEN GNA11 ERBB2 |
RAS pathway | Different RAS mutation contributes to unique personality | 89 |
| MBOT | Ovarian tumors |
BRAF
KRAS |
RAS-RAF-MEK-ERK signaling pathway
MAPK pathway |
Better prognostic biomarker in patients undergoing surgery | 101 |
| MOC | Ovarian tumors | KRAS | RAS-RAF-MEK-ERK signaling pathway
MAPK pathway |
borderline tumor progression to carcinomas | 101 |
| MOC | ovarian tissues |
BRAF HRAS KRAS
MET NRAS PIK3CA |
RAS pathway | Better prognosis and low recurrence | 102 |
| MOC, EnOC, OCCC | Patient tumor samples | KRAS | Growth factor signaling
DNA damage response p53 signaling Cell cycle control Apoptosis |
Mutational status differs between distinct histological subtypes | 88 |
| MOC | Patient tissue sample | KRAS | RAS/Raf/MEK/ERK-pathway | Improved survival | 103 |
| LGSOC | Patient tumor tissue |
KRAS
BRAF |
MAPK pathway | Better prognosis
Improved OS |
104 |
| BOT with recurrent LGSOC | Patient tumor tissue |
KRAS G12V
BRAF |
KRAS/RAF/MEK pathway | Shorter survival | 105 |
| MOC | Patient tumor specimen | KRAS | RAS pathway | Without KRAS mutation activation of RAS pathway could not be sustained | 106 |
| SBOT | Patient tumor specimen |
NRAS
BRAF KRAS |
RAS pathway | NRAS may be an oncogenic driver | 107 |
| LGSOC | Patients tissue sample |
KRAS
BRAF HRAS NRAS EIF1AX USP9X |
RAS/RAF/ERBB2-dependent cancer-associated pathways
MAPK/ERBB2 signaling pathways |
USP9X and EIF1AX novel driver of LGSOC | 83 |
| HGSOC | Patients tissue sample |
NRAS
BRAF KRAS TP53 |
RAS/RAF pathway | Co-occurrence of TP53 mutation with mutations in RAS/RAF pathway | 108 |
| LGSOC | Patients tissue sample |
KRAS
NRAS BRAF EIF1AX USP9X |
MAPK pathway | Low mutation rate of NRAS indicates a minor role in LGSOC development | 109 |