| Gene/Pathway | Type of Alteration | Frequency (%) | Clinical Significance | PMID references |
|---|---|---:|---|---|
| **KRAS** | Activating somatic mutation, most often MAPK-pathway driver | **40–76%** overall; **43.6–64.9%** in recent summaries; **40–50%** in invasive mEOC | Most common molecular event in MOC; supports Type I/MAPK-driven biology; associated with progression from benign/borderline to carcinoma, platinum resistance, poor prognosis, and can aid distinction from other ovarian histotypes (pqac-00000004, pqac-00000006, pqac-00000015) | Not available in retrieved contexts |
| **ERBB2 (HER2)** | Gene amplification / protein overexpression | **15–35%** overall; **18.8%** in one summary; **20–30%** in invasive mEOC; **35.3%** in MOC vs **5.3%** in borderline tumors in one recent report | Actionable target for trastuzumab-based and ADC strategies; may help differential diagnosis and molecular stratification; enriched in some Asian cohorts and relevant to targeted therapy selection (pqac-00000004, pqac-00000006, pqac-00000007, pqac-00000013, pqac-00000015) | Not available in retrieved contexts |
| **TP53** | Pathogenic mutation / p53-abnormal pattern | **52–75%** overall; **~48.9–57%** in one summary; **16–52%** in another review of mEOC | More frequent in frankly malignant/high-grade tumors than benign/borderline lesions; associated with advanced FIGO stage, residual disease, poorer overall survival, and malignancy transition (pqac-00000004, pqac-00000006, pqac-00000015) | Not available in retrieved contexts |
| **CDKN2A** | Copy-number loss, inactivation, homozygous deletion | **33–76%** | Characteristic lesion of mucinous carcinoma; loss increases with progression from benign/borderline to malignant disease and helps define the genomic profile of MOC (pqac-00000002, pqac-00000004, pqac-00000015) | Not available in retrieved contexts |
| **BRAF** | Activating mutation | **~8.7%**; part of combined **KRAS/BRAF/CDKN2A** alteration set totaling **91%** in MOC and **95%** in mucinous borderline tumors in one report | Less common than KRAS but supports MAPK-pathway activation; implicated in progression biology and occasionally co-occurs with other drivers (pqac-00000004, pqac-00000007, pqac-00000015) | Not available in retrieved contexts |
| **PIK3CA** | Activating mutation | Frequency not consistently quantified in retrieved MOC-specific sources | Recurrent but less common alteration; suggests PI3K-AKT pathway involvement and potential therapeutic relevance in selected tumors (pqac-00000006) | Not available in retrieved contexts |
| **PTEN** | Mutation / loss of function | Frequency not consistently quantified in retrieved MOC-specific sources | Indicates PI3K-AKT pathway dysregulation in a subset of MOC; contributes to molecular heterogeneity and possible targeted therapy opportunities (pqac-00000006) | Not available in retrieved contexts |
| **NRAS** | Activating mutation | Not quantified for MOC in retrieved sources | Included among RAS-pathway alterations relevant to ovarian carcinoma biology; highlights broader MAPK activation beyond KRAS (pqac-00000007, pqac-00000008) | Not available in retrieved contexts |
| **AKT1** | Activating mutation | Not quantified | Reported among pathway-activating events in mEOC; supports PI3K/AKT signaling as a secondary oncogenic route (pqac-00000015) | Not available in retrieved contexts |
| **FGFR2** | Mutation / pathway activation | Not quantified | Listed among actionable or potentially actionable alterations in MOC; may inform targeted therapy exploration (pqac-00000006) | Not available in retrieved contexts |
| **STK11** | Mutation | Not quantified | Recurrent but uncommon event in MOC summaries; may contribute to metabolic and growth dysregulation (pqac-00000006) | Not available in retrieved contexts |
| **CTNNB1 (Wnt/β-catenin)** | Activating mutation / pathway alteration | Not quantified | Suggests Wnt-pathway involvement in a subset of MOCs and provides rationale for pathway-directed investigation (pqac-00000006) | Not available in retrieved contexts |
| **SRC** | Mutation / pathway activation | Not quantified | Identified in molecular summaries as a potential contributor to invasive behavior and possible therapeutic target class (pqac-00000006) | Not available in retrieved contexts |
| **SMAD4** | Mutation / loss | Not quantified | Supports overlap with gastrointestinal-like signaling biology and may relate to aggressive behavior in selected cases (pqac-00000006) | Not available in retrieved contexts |
| **GNA11** | Mutation | Not quantified | Rarely reported event contributing to genomic heterogeneity; current clinical significance in MOC remains uncertain (pqac-00000006) | Not available in retrieved contexts |
| **PLK1 pathway** | Functional dependency / overexpression target identified by siRNA screening rather than recurrent mutation | Not a mutation frequency metric | Preclinical vulnerability: PLK1 inhibition suppressed growth, induced apoptosis, and synergized with paclitaxel in mucinous ovarian carcinoma cell lines/xenografts, nominating PLK1 as a therapeutic target despite not being a canonical recurrent genomic alteration (pqac-00000015) | Not available in retrieved contexts |
| **Mucin program (MUC1, MUC2, MUC5AC, MUC6, MUC13, MUC16)** | Differential expression rather than classic driver mutation | Example IHC frequencies in MOC from retrieved review: **MUC13 100% (13/13)**, **MUC5AC 94.8–100%**, **MUC16 66.7% (4/6)**, **MUC2 ~42–70%** across studies | Not primary genomic drivers, but biologically important for diagnosis, progression, chemoresistance, and differential diagnosis of primary vs metastatic mucinous tumors (pqac-00000003, pqac-00000010, pqac-00000011) | Not available in retrieved contexts |


*Table: This table summarizes the major molecular alterations reported for ovarian mucinous carcinoma, including approximate frequencies, clinical relevance, and available evidence from the retrieved sources. It is useful for quickly identifying recurrent drivers, actionable targets, and alterations linked to progression or chemoresistance.*