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Mucinous Ovarian Tumors

A plain-English summary of the published research on Mucinous Ovarian Tumors, reviewed and approved by our editors — not a hand-curated clinical overview.

Research summary · reviewed
Educational only: This page is not medical advice. Coordinate decisions with your oncology team.

Reviewed Jun 2026 · OncoForge editorial · How we review →

AI extractedhuman reviewedsources checkedretractions suppressed· last updated Jun 2026

Evidence at a glanceHuman · observationalMixed results⚠ Studies disagree
10 published studies that name Mucinous Ovarian Tumors7 human studies approved & graded (trial, observational, or meta-analysis)3 human clinical studies in the Mucinous Ovarian Tumors corpus188 source documents in the Mucinous Ovarian Tumors corpus

last checked June 19, 2026

Why this grade?

Human · observational — Human observational evidence only — no trials.

Computed deterministically from the studies’ types and reported outcomes — not written by AI, and not a claim that anything works.

What the guidelines say

NCI PDQESMONCCNASCO

We link the authoritative guidelines rather than reproduce them. Below, the treatments on this page are split into standard care, guideline or regulatory options, supportive care, and studied but not standard so established care is not mixed with experimental or supportive items.

Guideline / FDA options - context-specific
  • Mirvetuximab Soravtansine
  • bevacizumab
Studied, not standard - investigational
  • appendicectomy
  • carboplatin + paclitaxel
  • capecitabine + oxaliplatin
  • HER2-targeted therapy
  • PARP inhibitors
  • PD-1/PD-L1 inhibitors
  • primary cytoreductive surgery
  • appendectomy

Read the guidelines

Cancer-specific deep links aren’t curated yet — these search the authoritative sources for Mucinous Ovarian Tumors.

Treatment map: Mucinous Ovarian Tumors

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Standard care plus every compound studied in the literature (each cited) and graded by evidence, organized by clinical readiness. A category, not a verdict that anything works — confirm anything here with your oncology team.

10
Interventions
0
Standard of care
0
Tested in people
0
Lab / animal
8
Named in lit.
5
Classes
Standard of care (0) Guideline option (2) Tested in people (0) Lab / animal only (0) Named in the literature (8)
Clinical evidence
Preclinical evidence
Standard of care
Guideline option
Tested in people
Lab / animal only
Named in the literature
Surgery & procedures
—
—
—
—
3
Chemotherapy
—
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2
Targeted therapy
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2
Immunotherapy
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Supplements & natural agents
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Columns group into clinical evidence (used in, or tested on, people) and preclinical evidence (lab/animal, or only named in the literature). Cell = number of interventions; a dashed cell means none recorded there.

Established care — detail (2)
Targeted therapy
bevacizumab
FDA-approved for this cancer.
—Guideline option
Supplements & natural agents
Mirvetuximab Soravtansinefolate receptor alpha (FRα)
FDA-approved for this cancer.
—Guideline option
Investigational & adjunct compounds — detail (8)
Named in the literature
appendicectomycarboplatin + paclitaxel· Adjuvant (after surgery)capecitabine + oxaliplatinHER2-targeted therapy· biomarker-selectedPARP inhibitorsPD-1/PD-L1 inhibitorsprimary cytoreductive surgeryappendectomy

"Tested in people" rows show the highest trial phase found in that compound's cited human studies (Phase I–IV; "phase not reported" = a human study with no phase tag). "Studied" = named in the cited literature for this cancer. "FDA ✓" = FDA-approved for this cancer; "off-label" = an FDA-approved drug used outside its approved indications (per openFDA). Not a claim that anything works.

Reported figures

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Snapshot

The essentials in ~60 seconds — every line is drawn from the cited sources below.

What it is
Mucinous ovarian carcinoma (MOC) is one of the five main histological types of tubo-ovarian carcinoma and is a rare histologic subtype that is less well characterized than other ovarian cancer types; advanced-stage MOC is reported to have poor chemotherapy response and prognosis. [1][2][3]
Survival
Most patients are diagnosed with stage I disease (about 70%–80% of MOC) and have a good prognosis, while advanced-stage MOC is described as having poor prognosis and poor response to chemotherapy. [2][3]
Standard treatment
For FIGO stage IC–IV MOC, guidelines recommend primary cytoreductive surgery followed by adjuvant chemotherapy with carboplatin and paclitaxel (± bevacizumab). Accurate preoperative diagnosis is described as crucial for guiding surgical strategies and improving outcomes. [2][4][3]
Key test
Clinical practice suggests testing the tumor for somatic mutations during the initial phase of therapy; preoperatively, CA72-4 (especially combined with tumor volume) can help distinguish mucinous carcinoma from mucinous borderline tumor. [4][3]
Biggest challenge
Because MOC is rare and often hard to distinguish from metastatic gastrointestinal tumors, randomized trials and treatment evidence are limited by low accrual and misclassification, and advanced-stage disease has poor chemotherapy response and prognosis. [2][3]

Ask about Mucinous Ovarian Tumors

Answers come only from the cited sources on this page — with the supporting evidence shown. If the sources here don't cover your question, it will say so. Educational information, not medical advice.

Key numbers & factors

Risk factors

  • ▲ increases riskMicroscopic appendiceal disease found at surgery — Can upstage the ovarian tumor and may portend poor survival. [5]
  • ▼ lowers riskInfiltrative pattern of invasion — Classified by linear stromal invasion >5 mm and associated with decreased overall survival within 2 years; may select stage I patients for adjuvant therapy. [2]

Biomarkers

  • CA72-4ActionableHelps preoperatively distinguish mucinous ovarian carcinoma from mucinous borderline tumor (improved discrimination when combined with tumor volume). [3]
  • Folate receptor alpha (FRα) · Absent in all cases of ovarian mucinous carcinoma and mucinous borderline tumor in one series (informing that FRα-targeted approaches are unlikely to apply). [1]
  • FOXA1 · Commonly expressed in mucinous ovarian tumors (seen in cystadenomas, borderline tumors, and carcinomas). [6]
  • THBS2 and TAGLN · Identified as prognostic markers for mucinous ovarian carcinoma. [2]
  • Persistent DNA damage measured by RADD · Reported to correlate with PD-L1 expression, suggesting DNA lesions may be a biomarker to explore for immunotherapy selection. [4]

10 sections — tap any heading to expand its cited detail. Key points are above.

OverviewMucinous ovarian carcinoma (MOC) is one of the five main histological types of tubo-ovarian carcinoma and is a rare histologic subtype that is less well characterized than more common ovarian cancer histotypes. When diagnosed at advanced FIGO stage III/IV, MOC is associated with poor prognosis, very poor survival, and low response to chemotherapy.3 points
  • Mucinous ovarian carcinoma (MOC) is a rare histologic type that is less well characterized compared with more common ovarian cancer histotypes. [2]
  • Sources report that advanced-stage mucinous ovarian carcinoma has poor chemotherapy response and prognosis. [2]
  • Mucinous ovarian carcinoma (MOC) is listed among the five main histological types of tubo-ovarian carcinoma. [1]
EpidemiologyPrimary ovarian mucinous tumors occur across a wide age range: in a large series the mean age at diagnosis was 47.4 years (range 6–94 years). About 70%–80% of mucinous ovarian carcinomas are stage I and prognosis for most patients diagnosed with stage I MOC is good; in one cohort 25 of 187 patients (13%) who had appendicectomy during surgery for mucinous ovarian neoplasms had concomitant appendiceal lesions.3 points
  • For most patients diagnosed with stage I MOC (about 70%–80% of all MOC), prognosis is good. [2]
  • In a large series of primary ovarian mucinous tumors, the mean age at diagnosis was 47.4 years (range 6–94 years). [7]
  • In one cohort of patients undergoing appendicectomy during surgery for mucinous ovarian neoplasms, 25 of 187 patients (13%) who had appendicectomy had concomitant appendiceal lesions. [5]
Key biomarkersReported biomarkers for mucinous ovarian tumors include immunohistochemical markers (for example, FOXA1 and folate receptor alpha), a serum marker (CA72-4) with reported diagnostic AUCs, candidate prognostic genes (THBS2, TAGLN, and HER2 in a small subset), and a reported correlation between persistent DNA damage (RADD) and PD-L1 expression.5 points
  • CA72-4 levels were significantly higher in mucinous ovarian carcinoma (MOC) than in mucinous borderline tumor (MBT), with CA72-4 showing an AUC of 0.834 for discriminating MOC from MBT; combining CA72-4 and tumor volume improved preoperative diagnostic performance for distinguishing MOC from MBT (AUC 0.875). [3]
  • THBS2 and TAGLN were identified as prognostic markers for mucinous ovarian carcinoma (MOC). [2]
  • Folate receptor alpha (FRα) expression was absent in all cases of ovarian mucinous carcinoma (MOC) and mucinous borderline tumor (MBT) in a multi-histotype immunohistochemical series. [1]
  • FOXA1 expression is common in mucinous ovarian tumors, being detected in 73.6% of cystadenomas, 91.4% of borderline tumors, and 87.5% of carcinomas in one series. [6]
  • Persistent DNA damage levels measured by RADD were reported to correlate with PD-L1 expression in ovarian tumors, suggesting DNA lesions may be a biomarker for PD-L1. [4]
Biology & pathwaysMUC2 expression increases from mucinous cystadenomas to borderline tumors and is significantly correlated with FOXA1 expression. Mural nodules in mucinous ovarian tumors commonly show genetic evidence of clonality with the associated mucinous tumor, although no single recurrent genetic alteration was identified for mural nodule development.2 points
  • MUC2 expression progressively increased from mucinous cystadenomas to borderline tumors and significantly correlated with FOXA1 expression in mucinous ovarian tumors. [6]
  • Mural nodules in mucinous ovarian tumors commonly show genetic evidence of clonality with the associated mucinous ovarian tumor, suggesting they represent a morphologic spectrum of clonal neoplasms; no single recurrent genetic alteration was identified as associated with mural nodule development. [8]
Standard managementAccurate preoperative diagnosis is important for guiding surgical strategies and improving outcomes in mucinous ovarian tumors. Standard management for advanced-stage mucinous ovarian carcinoma centers on complete surgical resection (primary cytoreductive surgery) followed by systemic platinum- and taxane-based chemotherapy, although guidelines differ on which early-stage patients should receive adjuvant chemotherapy.5 points
  • For FIGO stage IC–IV mucinous ovarian carcinoma, treatment guidelines recommend primary cytoreductive surgery and adjuvant chemotherapy with carboplatin and paclitaxel (± bevacizumab). [2][4]
  • T2-weighted signal intensity ratio (SIR) of mural nodules with a cut-off of 3.9 was reported as beneficial for differentiating borderline from malignant mucinous ovarian tumors (sensitivity 85%, specificity 83%, AUC 0.943). [9]
  • Accurate preoperative diagnosis is described as crucial for guiding surgical strategies and improving patient outcomes in mucinous ovarian tumors. [3]
  • The US NCCN guidelines recommend adjuvant chemotherapy for MOC FIGO stage IC or higher while European guidelines include consideration of adjuvant chemotherapy for stage IA or IB MOC with an infiltrative growth pattern. [2]
  • Routine appendectomy at primary surgery for suspected or confirmed mucinous ovarian tumors is not supported by the authors' findings unless a specific indication exists. [10]
Treatments & compounds studiedTen therapeutics and procedures are reported across targeted therapy, chemotherapy, immunotherapy and surgical/procedural approaches.10 treatments

Chemotherapy

  • carboplatin and paclitaxel: Adjuvant (after surgery)Carboplatin plus paclitaxel is recommended as adjuvant chemotherapy for FIGO stage IC–IV MOC. [2]
    proportion of HER2+ MOC with poor prognosis 3%
    Source quote
    • “Despite a higher frequency of HER2+ in low-stage and expansile pattern MOC, just 3% of patients with HER2+ MOC have a poor prognosis (advanced stage or infiltrative) and should be considered for anti-HER2 therapy.”
  • capecitabine and oxaliplatin: A gastrointestinal chemotherapy regimen of capecitabine plus oxaliplatin was tested against ovarian regimens in a randomized trial that was closed prematurely due to limited accrual and misclassification issues. [2]
    proportion of HER2+ MOC with poor prognosis 3%
    Source quote
    • “Despite a higher frequency of HER2+ in low-stage and expansile pattern MOC, just 3% of patients with HER2+ MOC have a poor prognosis (advanced stage or infiltrative) and should be considered for anti-HER2 therapy.”

Targeted therapy

  • mirvetuximab soravtansine (MIRV) · Mirvetuximab Soravtansine: folate receptor alpha (FRα)Mirvetuximab soravtansine has been approved for treatment of advanced platinum‑resistant high‑grade serous carcinoma. [1]
  • bevacizumab: Bevacizumab has been used in combination with carboplatin and paclitaxel (as '± bevacizumab') in guideline-recommended regimens for MOC. [2]
    proportion of HER2+ MOC with poor prognosis 3%
    Source quote
    • “Despite a higher frequency of HER2+ in low-stage and expansile pattern MOC, just 3% of patients with HER2+ MOC have a poor prognosis (advanced stage or infiltrative) and should be considered for anti-HER2 therapy.”
  • anti-HER2 therapy · HER2-targeted therapy: biomarker-selectedThe authors state that anti‑HER2 therapy should be investigated in a subset of mucinous ovarian carcinoma patients. [2]
    proportion of HER2+ MOC with poor prognosis 3%
    Source quote
    • “Despite a higher frequency of HER2+ in low-stage and expansile pattern MOC, just 3% of patients with HER2+ MOC have a poor prognosis (advanced stage or infiltrative) and should be considered for anti-HER2 therapy.”
  • PARP inhibitors: Poly(ADP-ribose) polymerase inhibitors and other DNA damage response inhibitors have been discussed for ovarian cancers in the context of targeting DNA repair defects. [4]

Immunotherapy

  • PD-1/PD-L1 inhibitors: PD‑1/PD‑L1 inhibitor immunotherapies are under investigation for ovarian cancer in multiple clinical trials. [4]

Procedures & devices

  • appendicectomy: Appendicectomy is described as a procedure to ascertain or exclude the appendix as the site of primary cancer in patients with ovarian mucinous tumors. [5]
  • primary cytoreductive surgery: Primary cytoreductive surgery (complete surgical resection) is recommended as part of standard treatment for late-stage ovarian cancer and is the surgical approach noted in MOC management. [2]
    proportion of HER2+ MOC with poor prognosis 3%
    Source quote
    • “Despite a higher frequency of HER2+ in low-stage and expansile pattern MOC, just 3% of patients with HER2+ MOC have a poor prognosis (advanced stage or infiltrative) and should be considered for anti-HER2 therapy.”
  • appendectomy: Appendectomy has commonly been performed during primary surgery for mucinous ovarian neoplasms, but a large institutional series concluded appendectomies should not be routine unless there is a specific indication. [10]
Staging & riskMicroscopic appendiceal disease found at surgery for mucinous ovarian neoplasms can upstage the ovarian tumor and has been associated with poorer survival. In one series, an infiltrative pattern of invasion in mucinous ovarian carcinoma was defined as a linear extent of stromal invasion greater than 5 mm.2 points
  • Microscopic disease found in the appendix during surgery for ovarian mucinous neoplasms can upstage the ovarian tumor and thus may portend poor survival. [5]
  • An infiltrative pattern of invasion in MOC was classified in this series by a linear extent of stromal invasion greater than 5 mm. [2]
PrognosisMucinous ovarian cancer (MOC) is a rare epithelial ovarian cancer subtype that is reported to have a poor prognosis, especially in advanced stages. Specific histologic features influence outcome: an infiltrative invasion pattern is associated with worse prognosis and may prompt consideration of adjuvant chemotherapy, while carcinosarcomatous mural nodules have been reported to occur in younger patients, present at an early stage, and in one report were not linked to an adverse prognosis.3 points
  • Mucinous ovarian cancer (MOC) is a rare epithelial ovarian cancer subtype described as having a poor prognosis, particularly in advanced stages. [3]
  • An infiltrative pattern of invasion in mucinous ovarian carcinoma was associated with decreased overall survival within 2 years and may help select stage I patients for adjuvant therapy. [2]
  • Carcinosarcomatous mural nodules associated with ovarian mucinous neoplasms tend to affect younger females, present at an early stage, and in one report were not associated with an adverse prognosis. [11]
Safety & interactionsAppendicectomy performed as part of cytoreductive surgery is reported not to increase morbidity. Clinical practice suggests testing the tumor for somatic mutations during the initial phase of therapy for ovarian cancer.2 points
  • An appendicectomy performed as part of cytoreductive surgery is reported not to increase morbidity in those patients. [5]
  • Clinical practice suggests testing the tumor for somatic mutations during the initial phase of therapy for ovarian cancer. [4]
What we don't know yetKey unanswered questions include whether mesonephric‑like components contribute to histogenesis—one large series found no such association—and how to improve diagnosis and treatment of mucinous ovarian carcinoma. Because MOC is rare and often difficult to distinguish from metastatic gastrointestinal tumors, randomized trials and treatment evidence are limited, creating a need for better molecular markers and treatment strategies; there is also interest in identifying biomarkers to predict response to PD‑1/PD‑L1 blockade because PD‑L1 expression alone has been ineffective for patient stratification.3 points
  • A large series of ovarian mucinous tumors found no associated mesonephric‑like components and concluded that any association is probably too rare to imply a role in histogenesis. [7]
  • Because mucinous ovarian carcinoma (MOC) is rare and often difficult to distinguish from metastatic gastrointestinal tumors, there is a need for better molecular markers and more effective treatment strategies; randomized trials comparing ovarian and gastrointestinal chemotherapy regimens for MOC have been hampered by low accrual and misclassification of metastatic GI tumors as primary MOC, leaving treatment evidence limited. [2]
  • Given variable efficacy of PD‑L1 inhibitors in ovarian cancer, sources explore biomarkers such as persistent DNA damage to aid patient selection for immunotherapy. [4]

Common questions

What is Mucinous Ovarian Tumors?

Mucinous ovarian carcinoma (MOC) is one of the five main histological types of tubo-ovarian carcinoma and is a rare histologic subtype that is less well characterized than more common ovarian cancer histotypes. When diagnosed at advanced FIGO stage III/IV, MOC is associated with poor prognosis, very poor survival, and low response to chemotherapy.

How common is Mucinous Ovarian Tumors?

Primary ovarian mucinous tumors occur across a wide age range: in a large series the mean age at diagnosis was 47.4 years (range 6–94 years). About 70%–80% of mucinous ovarian carcinomas are stage I and prognosis for most patients diagnosed with stage I MOC is good; in one cohort 25 of 187 patients (13%) who had appendicectomy during surgery for mucinous ovarian neoplasms had concomitant appendiceal lesions.

Which biomarkers are important in Mucinous Ovarian Tumors?

Reported biomarkers for mucinous ovarian tumors include immunohistochemical markers (for example, FOXA1 and folate receptor alpha), a serum marker (CA72-4) with reported diagnostic AUCs, candidate prognostic genes (THBS2, TAGLN, and HER2 in a small subset), and a reported correlation between persistent DNA damage (RADD) and PD-L1 expression.

What is the biology of Mucinous Ovarian Tumors?

MUC2 expression increases from mucinous cystadenomas to borderline tumors and is significantly correlated with FOXA1 expression. Mural nodules in mucinous ovarian tumors commonly show genetic evidence of clonality with the associated mucinous tumor, although no single recurrent genetic alteration was identified for mural nodule development.

How is Mucinous Ovarian Tumors treated?

Accurate preoperative diagnosis is important for guiding surgical strategies and improving outcomes in mucinous ovarian tumors. Standard management for advanced-stage mucinous ovarian carcinoma centers on complete surgical resection (primary cytoreductive surgery) followed by systemic platinum- and taxane-based chemotherapy, although guidelines differ on which early-stage patients should receive adjuvant chemotherapy.

What treatments are studied for Mucinous Ovarian Tumors?

Ten therapeutics and procedures are reported across targeted therapy, chemotherapy, immunotherapy and surgical/procedural approaches.

Sources

Every statement above is drawn from these reviewed sources. This page reports what they describe. Sources last checked June 19, 2026.

  1. Review articleFolate receptor alpha (FRα) expression in tubo-ovarian and endometrial tumors: a study of 923 cases · 2026
  2. Review articleGene-Expression Profiling of Mucinous Ovarian Tumors and Comparison with Upper and Lower Gastrointestinal Tumors Identifies Markers Associated with Adverse Outcomes · 2022
  3. Review articleDiagnostic Use of the Combination of CA72-4 and Tumor Volume in Mucinous Ovarian Tumors · 2026
  4. Review articleAssociations between DNA Damage and PD-L1 Expression in Ovarian Cancer, a Potential Biomarker for Clinical Response · 2021
  5. Review articlePrimary Lesions of the Appendix in Patients Undergoing Surgery for Gynecological Tumors · 2025
  6. Review articleFOXA1 expression and its association with mucin expression and KRAS mutation in ovarian mucinous tumors: implications for tumor progression and differentiation · 2025
  7. Review articleOvarian mucinous tumors do not usually harbor a mesonephric-like component · 2025
  8. StudyMural nodules in mucinous ovarian tumors represent a morphologic spectrum of clonal neoplasms: a morphologic, immunohistochemical, and molecular analysis of 13 cases · 2021
  9. Review articleSalient magnetic resonance imaging findings in the differential diagnosis of benign, borderline and malignant ovarian mucinous tumors · 2025
  10. Review articleRevisiting the necessity for routine appendectomies in mucinous neoplasms of the ovary: An evaluation of 460 mucinous ovarian tumors · 2022
  11. Review articleCystic Ovarian Mucinous Carcinoma With Carcinosarcomatous Mural Nodules: An Uncommon Entity · 2022

What supports this page

The kinds of sources behind this page, strongest at the top. Faint rungs show what is not here yet.

Guideline
1
Meta-analysis
1
Systematic review
0
Randomized trial
0
Clinical trial
19
Observational
0
Case report
31
Review
133
Preclinical
0
Other
3

Living document — last change June 19, 2026: Cancer page updated. 2 recent updates logged.

What recent studies report in Mucinous Ovarian Tumors

These are reviewed studies whose abstracts concern Mucinous Ovarian Tumors. Each describes only what that study reported. This is not a claim by OncoForge that any compound helps or harms Mucinous Ovarian Tumors. Most are early lab, animal, or small human studies, and findings often conflict.

10 studies7 human1 animal⚠ Conflicting evidenceMechanism (9)

Tracking 10 published studies of Mucinous Ovarian Tumors: 7 in humans, 1 in animals, 2 reviews/other.

Reported direction across studies: 5 positive, 3 mixed, 2 inconclusive.

Findings conflict — both supportive and negative/mixed results exist (see below). Human evidence is limited.

These counts summarize what the studies reported; they are not a measure of whether anything works for Mucinous Ovarian Tumors.

Human · observationalMechanismMixed resultsLimited evidenceTier 3 · early humann = 923

Folate receptor alpha (FRα) expression in tubo-ovarian and endometrial tumors: a study of 923 cases

The journal of pathology. Clinical research · Mar 2026 · immunohistochemical study on tissue microarrays using the VENTANA FOLR1 CDx assay with standardized scoring criteria

tubo-ovarian tumorsendometrial tumorshigh-grade serous carcinoma (HGSC)low-grade serous carcinoma (LGSC)endometrial serous carcinomaserous borderline tumorendometrioid ovarian carcinomaclear cell ovarian carcinomamucinous ovarian tumorssex cord-stromal tumorsendometrial endometrioid carcinomasundifferentiated carcinomadedifferentiated carcinomaendometrial clear cell carcinoma

The study examined folate receptor alpha (FRα) expression by immunohistochemistry on tissue microarrays of 923 tubo-ovarian and endometrial tumors using the VENTANA FOLR1 CDx assay and standardized scoring. They found FRα expression most commonly in serous carcinomas (45% of HGSC, 25% LGSC) and less commonly in some endometrial serous and serous borderline tumors, while many other ovarian and endometrial tumor types were negative or rarely positive. The work is descriptive and does not report clinical outcomes or functional testing.

Reported effects: HGSC positive cases 45% · Low-grade serous carcinoma positive cases 25% · +4 more

Key findings
  • HGSC (high-grade serous carcinoma): 45% positive cases
  • Low-grade serous carcinoma: 25% positive cases
  • Endometrial serous carcinoma: 11% positive cases
  • Serous borderline tumor: 10% positive cases
  • Endometrioid ovarian carcinoma: 2% positive cases
  • Clear cell ovarian carcinoma: 1% positive cases
  • Mucinous ovarian tumors, sex cord-stromal tumors, endometrial endometrioid carcinomas, undifferentiated and dedifferentiated carcinomas, and endometrial clear cell carcinomas were reported as negative
Limitations: Descriptive immunohistochemistry only — no functional assays or correlation with clinical outcomes reported in the abstract; Use of tissue microarrays may under-represent intratumoral heterogeneity; Cross-sectional/tissue-based study without longitudinal or therapeutic response data.

AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Human · observationalMechanismMixed resultsLimited evidenceTier 3 · early humann = 79

Histological classification of mucinous ovarian tumors: inter-observer reproducibility, clinical relevance, and role of genetic biomarkers

Virchows Archiv : an international journal of pathology · May 2021 · comparative study

mucinous ovarian tumorsmucinous ovarian borderline tumor (MOB)mucinous ovarian carcinoma (MOC)

This observational pathology study had two gynecological pathologists independently review 79 mucinous ovarian tumors (borderline and carcinomas) and performed molecular analysis in 32 cases. They found substantial inter-observer agreement (concordant in 67/79 cases, kappa 0.78). Infiltrative-pattern mucinous carcinomas had worse overall survival and progression-free survival than borderline tumors and expansile carcinomas (OS p < 0.0024; PFS p = 0.0060). KRAS mutations were reported more often in MOB (71%) than in expansile (50%) and infiltrative MOC (14%), while TP53 prevalence was 43% in MOB, 58% in expansile MOC and 71% in infiltrative MOC. No single molecular profile was identified as specific or sensitive for differential diagnosis.

Reported effects: concordant_cases 67, n=79 · kappa 0.78, n=79 · +10 more

Key findings
  • Inter-observer concordance between two pathologists was reached in 67 of 79 cases (kappa: 0.78).
  • Infiltrative mucinous ovarian carcinoma (MOC) had lower overall survival (OS) (p < 0.0024) and progression-free survival (PFS) (p = 0.0060) compared with mucinous borderline tumors (MOB) and expansile MOC.
  • The presence of nuclear grade 3 or microfoci (<5 mm) of infiltrative-type invasion in an otherwise expansile MOC did not alter prognosis compared with expansile MOC without these features (OS p < 0.0028; PFS p = 0.0074).
  • KRAS mutation frequencies: MOB 71%, expansile MOC 50%, infiltrative MOC 14% (molecular analysis in 32 cases).
  • TP53 prevalence: MOB 43%, expansile MOC 58%, infiltrative MOC 71% (molecular analysis in 32 cases).
  • No specific or sensitive molecular profile suitable for differential diagnosis of mucinous ovarian tumors was identified.
Limitations: Observational, retrospective pathology review (not a randomized or prospective study).; Modest total sample size (79 cases) and molecular analysis limited to 32 cases.; Inter-observer reproducibility assessed with only two pathologists.; Follow-up duration not reported in the abstract.; No external validation cohort reported in the abstract..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

Human · observationalMechanismReported positiveLimited evidenceTier 3 · early humann = 13

Mural nodules in mucinous ovarian tumors represent a morphologic spectrum of clonal neoplasms: a morphologic, immunohistochemical, and molecular analysis of 13 cases

Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · Mar 2021 · case series

mucinous ovarian tumors

The authors analyzed morphology, immunohistochemistry, and genetics of 13 mucinous ovarian tumors that contained mural nodules. Twelve of 13 cases showed genetic evidence that the mural nodule(s) and the associated mucinous tumor were clonal, and mural nodules were genetically identical in five cases with multiple nodules. No single recurrent genetic alteration or consistent genetic differences were found among sarcoma-like, anaplastic carcinomatous, and sarcomatous morphologies. Of 11 patients with follow-up, three died of disease at 3, 8, and 9 months after diagnosis.

Reported effects: total_cases_analyzed 13, n=13 · sarcoma-like_mural_nodules 3, n=13 · +4 more

Key findings
  • Analyzed 13 mucinous ovarian tumors with mural nodules.
  • Three tumors harbored sarcoma-like mural nodules; ten contained anaplastic carcinomatous nodules (one tumor had discrete anaplastic carcinomatous and sarcomatous nodules).
  • Twelve of 13 cases showed genetic evidence of clonality between the mural nodule(s) and the associated mucinous ovarian tumor, including all three sarcoma-like cases.
  • Mural nodules were genetically identical in the five cases in which multiple discrete mural nodules were sequenced separately.
  • MTAP and p53 immunohistochemistry confirmed the distribution of neoplastic cells in a subset of sarcoma-like and anaplastic carcinomatous nodules.
  • No single recurrent genetic alteration was associated with mural nodule development and no recurrent genetic differences were identified between the different morphologic types.
  • Of 11 patients with clinical follow-up, three died of disease at 3, 8, and 9 months after diagnosis, and no recurrent genetic events were associated with poor outcome.
Limitations: Small sample size (13 cases).; Retrospective case series without a control group.; Limited clinical follow-up (clinical follow-up reported for 11 patients).; No single recurrent genetic driver identified, which may reflect limited power or scope of sequencing.; No functional validation experiments reported in the abstract to test causality of genetic findings..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

Human · observationalMechanismReported positiveModerate evidenceTier 3 · early humann = 1032

Accuracy of frozen section diagnosis and factors associated with final pathological diagnosis upgrade of mucinous ovarian tumors

Journal of gynecologic oncology · Nov 2019 · retrospective

mucinous ovarian tumors

This retrospective study analyzed 1,032 patients with mucinous ovarian tumors who had intraoperative frozen section diagnosis to assess its accuracy and predictors of upgrade on final pathology. The authors report sensitivities and specificities for benign, borderline, and invasive mucinous tumors, and found that mixed histology, tumor size >12 cm, multilocularity, and a solid component were independently associated with an increased odds of upgrade on final pathology.

Reported effects: sample_size 1032 · sensitivity benign mucinous tumors 99.1% [98–99.6] · +9 more

Key findings
  • Study included 1,032 patients who underwent frozen section diagnosis during surgery.
  • For benign mucinous tumors the sensitivity was 99.1% (95% CI=98%-99.6%) and specificity was 82.2% (95% CI=77.9%-85.7%).
  • For mucinous borderline ovarian tumors the sensitivity was 74.6% (95% CI=69.1%-79.4%) and specificity was 96.7% (95% CI=95.2%-97.8%).
  • For invasive mucinous carcinomas the sensitivity was 72.5% (95% CI=62.9%-80.3%) and specificity was 98.8% (95% CI=97.9%-99.3%).
  • Multivariate analysis identified independent risk factors for final pathological diagnosis upgrade: mixed tumor histology (OR=2.8; 95% CI=1.3-6.3; p=0.012), tumor size >12 cm (OR=2.5; 95% CI=1.5-4.3; p=0.001), multilocular tumor (OR=2.9; 95% CI=1.4-6.0; p=0.006), and presence of a solid component (OR=3.1; 95% CI=1.8-5.1; p<0.001).
Limitations: Retrospective observational design.; Abstract does not report whether findings were validated externally or across multiple centers, so generalizability is unclear.; Abstract provides no information on standardized frozen section procedures or inter-pathologist variability.; No long-term clinical outcomes or prognostic impact reported in the abstract..

AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewMechanismInconclusiveLimited evidenceTier 4 · clinical

Mucinous Ovarian Tumors

Surgical pathology clinics · Jun 2019 · review

mucinous ovarian tumorsmucinous cystadenomamucinous borderline tumormucinous adenocarcinoma

This review summarizes the spectrum of ovarian mucinous tumors from benign cystadenomas through borderline tumors to malignant adenocarcinomas and notes they may show intestinal-type or less commonly endocervical-type differentiation. It highlights controversy about endocervical-type cases because of morphologic and molecular overlap with seromucinous tumors (which relate more to endometrioid tumors) and emphasizes that distinguishing primary intestinal-type ovarian mucinous tumors from gastrointestinal metastases can be difficult.

Key findings
  • Ovarian mucinous tumors range from benign cystadenomas to borderline tumors to malignant adenocarcinomas.
  • Mucinous ovarian tumors may display either intestinal-type morphology or, less frequently, endocervical-type differentiation.
  • Endocervical-type differentiation has been controversial because of morphologic overlap with 'seromucinous' ovarian tumors, which share more molecular features with endometrioid tumors than with serous or mucinous neoplasias.
  • Endocervical-type differentiation in ovarian mucinous tumors may represent an endocervical metastasis.
  • Distinction of primary ovarian mucinous tumors from gastrointestinal metastases can be difficult, as intestinal-type ovarian mucinous primaries sometimes differ only subtly if at all from gastrointestinal metastases.
Limitations: Review article with no original patient-level data reported in the abstract.; Abstract provides descriptive synthesis but no diagnostic criteria, quantitative data, or methods details.; Discussion of molecular features is brief in the abstract and specific biomarkers or testing approaches are not described..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

ReviewMechanismInconclusiveLimited evidenceTier 4 · clinical

Recent Insights into Mucinous Ovarian Carcinoma

International journal of molecular sciences · May 2018

mucinous ovarian carcinomamucinous ovarian tumors

This narrative review summarizes current knowledge about mucinous ovarian tumors, noting an unclear cell of origin and an apparent progression from benign to borderline to carcinoma. It reviews pathogenesis, molecular alterations, differential diagnosis, clinical presentation, and current treatment, and suggests that recent molecular and biological findings might enable more specific clinical management for patients with mucinous ovarian carcinoma.

Key findings
  • Mucinous ovarian tumors are a rare group of neoplasms with an apparent progression from benign to borderline to carcinoma.
  • The cell of origin for these tumors remains undefined.
  • Mucinous tumors are biologically different from other histological subtypes of epithelial ovarian neoplasms.
  • Despite biological differences, mucinous ovarian carcinomas are still commonly treated with a similar chemotherapeutic approach as other epithelial ovarian cancers.
  • Recent molecular and biological information may lead to better and more specific clinical management of patients with mucinous ovarian carcinoma.
Limitations: Review article that does not present new primary data or original experimental results.; Abstract does not provide specific details on the molecular alterations or the strength/level of evidence for those alterations.; Mucinous ovarian tumors are rare, implying limited available data and potential small study sizes in the literature.; Unclear from the abstract whether this is a systematic review or a narrative review (no meta-analytic quantitative synthesis reported)..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Human · observationalMixed resultsLimited evidenceTier 3 · early humann = 365

Clinical and ultrasound features of benign, borderline, and malignant invasive mucinous ovarian tumors

European journal of gynaecological oncology · Jan 2017 · retrospective observational multicenter study

mucinous ovarian tumorsmucinous cystadenomaovarian neoplasms

This retrospective multicenter study reviewed clinical and ultrasound data from 365 women (378 lesions) with histologically confirmed mucinous ovarian tumors and compared benign (n=287), borderline (n=51) and malignant (n=40) lesions. Borderline and malignant tumors more often showed solid components and higher IOTA color scores (p < 0.001) but there was substantial overlap: some borderline/malignant tumors lacked solid components or high color scores and about one-third of benign tumors showed solid components or high color score. The authors conclude that ultrasound features overlap significantly and preoperative discrimination among these lesions is difficult.

Reported effects: n_women 365, n=365 · mean_age 46.1, n=365 · +9 more

Key findings
  • Study cohort comprised 365 women (mean age 46.1 years) with 378 mucinous ovarian tumors; 14 women had bilateral lesions.
  • Histology distribution: 287 benign, 51 borderline, 40 malignant.
  • Borderline and invasive tumors showed solid components and IOTA color score 3 or 4 more frequently than benign lesions (p < 0.001).
  • However, 16 out of 51 (31.4%) borderline tumors and 6 out of 40 (15.0%) invasive cancers had no solid components and a color score 1 or 2 and were considered benign by the sonologist.
  • Conversely, 96 out of 287 (33.4%) benign mucinous cystadenomas exhibited solid components and/or a color score of 3 or 4.
  • Overall, substantial overlap in sonographic features limits accurate preoperative discrimination between benign, borderline, and malignant mucinous ovarian tumors.
Limitations: Retrospective observational design.; Study excluded women with ultrasound evidence of intra-abdominal disease spread, which may bias the sample toward less advanced cases.; Abstract reports substantial overlap in imaging features, limiting diagnostic discrimination.; No diagnostic accuracy metrics (sensitivity, specificity, predictive values) are reported in the abstract..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

Animal studyMechanismReported positivePreclinical onlyTier 2 · animal

Mutant p53 Promotes Epithelial Ovarian Cancer by Regulating Tumor Differentiation, Metastasis, and Responsiveness to Steroid Hormones

Cancer research · Apr 2016

epithelial ovarian cancerserous epithelial ovarian cancermucinous ovarian tumorsovarian neoplasms

The authors introduced the Trp53(R172H) mutant allele into a Pten/Kras(G12D) mouse model of epithelial ovarian cancer and examined tumor behavior. They found that heterozygous WT/Trp53(R172H) promoted stromal invasion, faster intraperitoneal metastasis, reduced TP53 transactivation but retained responsiveness to nutlin-3a, and showed estradiol-driven growth linked to high estrogen receptor α. Homozygous Trp53(R172H) tumors were undifferentiated, highly metastatic, and had minimal TP53 transactivation. Heterozygous mice also developed mucinous cystadenocarcinomas, modeling human mucinous ovarian tumors.

Key findings
  • Introduction of Trp53(R172H) into a Pten/Kras(G12D) mouse strain affected epithelial ovarian cancer features and progression depending on presence of WT TP53.
  • Heterozygous WT/Trp53(R172H) alleles facilitated invasion into the ovarian stroma and accelerated intraperitoneal metastasis.
  • Heterozygous tumors showed reduced TP53 transactivation activity but retained responsiveness to nutlin-3a, an activator of WT TP53.
  • High levels of estrogen receptor α in heterozygous tumors enhanced growth of primary and metastatic tumors in response to estradiol.
  • Homozygous Trp53(R172H) tumors were undifferentiated, highly metastatic, and exhibited minimal TP53 transactivation activity.
  • Heterozygous WT/Trp53(R172H) mice developed mucinous cystadenocarcinomas at 12 weeks, recapitulating features of human mucinous ovarian tumors.
Limitations: Findings are from a mouse model and may not fully translate to humans.; Abstract provides no sample size or detailed methods in this summary, limiting assessment of robustness.; Functional mechanisms beyond gene expression (causal pathways) are not fully established in the abstract.; Therapeutic implications were not tested in human patients..

AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Human · observationalMechanismReported positiveLimited evidenceTier 3 · early humann = 82

Mutational landscape of mucinous ovarian carcinoma and its neoplastic precursors

Genome medicine · Aug 2015 · Exome sequencing of a discovery cohort of 24 mucinous ovarian tumors (benign, borderline, carcinoma) with a validation cohort of 58 tumors assessed for specific gene regions including exons 4-9 of TP53.

mucinous ovarian carcinomamucinous ovarian tumors

The authors performed exome sequencing on 24 mucinous ovarian tumors (5 benign, 8 borderline, 11 carcinomas) and examined a validation cohort of 58 tumors for selected TP53 exons. They observed a predominant C>T mutational signature in an NpCpG context and identified mutations in known drivers (KRAS, BRAF, CDKN2A). A high percentage of carcinomas had TP53 mutations (52%), and recurrent mutations were reported in RNF43, ELF3, GNAS, ERBB3 and KLF5. The authors conclude that these tumors are genetically heterogeneous and generally distinct from other ovarian subtypes.

Reported effects: discovery_cohort_size 24 · benign_tumors_in_discovery_cohort 5 · +4 more

Key findings
  • Exome sequencing performed on 24 mucinous ovarian tumors (discovery cohort) with a validation cohort of 58 tumors for selected TP53 regions.
  • Predominant mutational signature was C>T transitions in an NpCpG context, consistent with deamination of methyl-cytosines.
  • Mutations were found in known driver genes KRAS, BRAF and CDKN2A.
  • A high percentage of carcinomas had TP53 mutations (52%).
  • Recurrent mutations identified in RNF43, ELF3, GNAS, ERBB3 and KLF5.
  • Overall mutational diversity suggests multiple routes to tumorigenesis and distinction from other ovarian subtypes.
Limitations: Relatively small discovery cohort (24 tumors) and modest validation cohort (58 tumors).; Validation was targeted to specific gene regions (including TP53 exons 4-9) rather than whole-exome in the larger cohort.; No functional validation or assessment of clinical outcomes reported in the abstract.; Findings are descriptive/genomic and do not establish causality or therapeutic efficacy..

AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Human · observationalMechanismReported positiveLimited evidenceTier 3 · early human

The role of the REG4 gene and its encoding product in ovarian epithelial carcinoma

BMC cancer · Jun 2015 · cell line experiments plus human tissue expression and survival analysis

ovarian epithelial carcinomaovarian cancermucinous ovarian tumorsserous carcinomas

This study looked at REG4 in ovarian epithelial carcinoma using SKOV3 cells and ovarian tissue samples. In cells, adding REG4 or making cells overexpress REG4 reduced apoptosis and increased proliferation, migration, invasion, and G2/S cell-cycle progression. In patient tissues, REG4 was more highly expressed in tumor samples than in normal ovarian tissue, and higher REG4 expression was linked with worse survival outcomes.

Key findings
  • REG4 overexpression and recombinant REG4 inhibited apoptosis in SKOV3 cells.
  • REG4 increased proliferation, migration, invasion, and G2/S progression in SKOV3 cells.
  • Wnt5a, p70s6k, survivin, and VEGF increased, while Bax decreased with REG4 overexpression.
  • REG4 mRNA and protein were higher in ovarian tumor tissues than in normal ovarian tissue.
  • Higher REG4 expression was associated with poorer cumulative and relapse-free survival.
Limitations: Primarily cell-line and tissue-expression study; no therapeutic intervention in patients.; Observational survival association cannot establish causality.; Abstract does not report sample sizes, effect sizes, or detailed statistical estimates.; Findings are based on one ovarian cancer cell line (SKOV3) and may not generalize to all ovarian cancers..

REG4 was studied as a biomarker and functional regulator in ovarian cancer, not as a repurposed drug or natural compound.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Browse all studies mentioning Mucinous Ovarian Tumors →

Study mix

10 published studies by what they were done in. Lab and animal findings often do not carry over to people.

7 Human1 Animal2 Review/other
Reported directionReported positive5Mixed results3Inconclusive2

What the research shows for Mucinous Ovarian Tumors

A plain-language summary of the reviewed studies OncoForge tracks for Mucinous Ovarian Tumors. It reports what those studies described, not a claim that any compound or therapy helps or harms Mucinous Ovarian Tumors. Most of this evidence is early, and findings often conflict.

  • Studies report that in SKOV3 ovarian epithelial carcinoma cells, adding recombinant REG4 or forcing REG4 overexpression reduced apoptosis.
  • Studies report that in the same SKOV3 cell experiments, REG4 manipulation increased cell proliferation, migration, invasion, and progression through the G2/S cell-cycle phase.
  • Studies report that the investigation also included analysis of REG4 in ovarian tissue samples (including mucinous ovarian tumors), although the provided summary does not specify the detailed tissue-level findings.
  • Studies report that the evidence is limited and primarily preclinical/observational (one cell line model plus patient tissue analyses); consistency across models and clinical relevance remain unclear.

Supportive & alternative options discussed

  • Exercise / prehabilitation: Also discussed as a supportive option for people with ovarian cancer to help maintain physical function and quality of life; the studies above did not evaluate exercise or its effects on mucinous ovarian tumors.
  • Acupuncture: Also discussed as a supportive option for symptom management (for example, pain or nausea) in ovarian cancer care; the studies above did not assess acupuncture in mucinous ovarian tumors.
  • Mind–body (MBSR / CBT): Also discussed as a supportive approach (stress reduction, coping, and quality-of-life support) for people with ovarian cancer; the studies above did not investigate mind–body interventions for mucinous ovarian tumors.
  • Ketogenic / metabolic therapy: Also discussed by some as a complementary dietary approach in cancer care, but the studies above did not examine ketogenic diets or metabolic therapies in mucinous ovarian tumors.
  • Hyperthermia (heat): Also discussed as an adjunctive modality in some ovarian cancer treatment contexts; the studies above did not evaluate hyperthermia for mucinous ovarian tumors.
These findings are preliminary and based mainly on controlled cell-line experiments with limited patient tissue observations; they do not establish clinical relevance for people with mucinous ovarian tumors.

Clinical trials in Mucinous Ovarian Tumors

20 ongoing · 58 completed · tracked from ClinicalTrials.gov. Recruiting is not the same as proven, and completed is not the same as positive — read the results. Not a recommendation.

Completed
19 stopped (terminated / withdrawn / suspended)

Search all trials on ClinicalTrials.gov →

Getting care & support

Nonprofit / Gov

Practical, vetted help for Mucinous Ovarian Tumors — advocacy, paying for treatment, second opinions, and caregivers.

If you’re struggling emotionally, you don’t have to wait.

Advocacy & community

No dedicated organization for this specific cancer is curated yet — these general organizations can help in the meantime.

Financial help

  • PAN Foundation ↗ — Copay assistance funds by diagnosis (funds open and close as money allows). · status changes often — check the fund’s site
  • HealthWell Foundation ↗ — Copay and premium assistance funds by disease. · status changes often — check the fund’s site
  • CancerCare — financial assistance ↗ — Limited grants plus free financial counseling. · status changes often — check the fund’s site
  • Family Reach ↗ — Help with everyday living costs (rent, transport, food) during treatment. · status changes often — check the fund’s site
  • NeedyMeds ↗ — Searchable directory of drug patient-assistance and discount programs. · status changes often — check the fund’s site
What you’ll typically need to apply
  • Your diagnosis and, if you have it, the specific drug/treatment name (from your care team).
  • Insurance details — your member ID card, or a note that you're uninsured (some funds require active insurance, some don't).
  • Proof of income and household size (recent pay stubs, a tax return, or a benefits letter) — most funds are income-based.
  • Your prescriber's contact information; some programs need the clinic to submit part of the application.
  • Apply early and re-check: funds open and close as money is available, so a closed fund may reopen.

General guidance — each program sets its own eligibility. Confirm requirements on the program’s site.

Second opinions

Caregiver support

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