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Cystadenoma

Cancer and Oncology · NLM MeSH · updated 2026-10-29 · version 1

Citations verified against PubMedNot yet clinician-reviewed10 referencesApproximately 5 min read

A benign neoplasm derived from glandular epithelium, in which cystic accumulations of retained secretions are formed.

Table of Contents

1. Definition2. Research landscape3. Reading the evidence4. Open-access studies5. Key reviews6. References7. About this article

Definition and research guide

This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.

Content available: 4 complete abstracts (999 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.

Definition

A benign neoplasm derived from glandular epithelium, in which cystic accumulations of retained secretions are formed. In some instances, considerable portions of the neoplasm, or even the entire mass, may be cystic. (Stedman, 25th ed)

Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.

Also known as: Cystadenomas.

Where it fits in the MeSH classification

Broader topics
Adenoma; Neoplasms, Cystic, Mucinous, and Serous
Narrower topics
Cystadenoma, Mucinous; Cystadenoma, Papillary; Cystadenoma, Serous

Research landscape

PubMed indexes 6,544 records tagged with the MeSH heading “Cystadenoma” (counts retrieved 2026-10-29). 368 of them (5.6%) were published from 2020 onward, and the busiest period so far is through 1999 with 3,600 records.

Reviews account for 677 records (10.3%) and meta-analyses for 4. Randomized controlled trials number 6 (0.1%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.

PubMed records by publication periodthrough 1999: 3,600 records; 2000-2009: 1,427 records; 2010-2019: 1,149 records; 2020 onward: 368 records3,600through 19991,4272000-20091,1492010-20193682020 onward
Records in PubMed indexed with this heading, by publication period. Real counts from NCBI E-utilities; the final period covers only part of the current year. Volume reflects how much has been published, not how strong the evidence is.
Show the data
PeriodRecords
through 19993,600
2000-20091,427
2010-20191,149
2020 onward368
Share of records by publication typeReviews: 10.3 percent; Meta-analyses: 0.1 percent; Randomized controlled trials: 0.1 percentReviews10.3% (677)Meta-analyses0.1% (4)Randomized controlled trials0.1% (6)
Share of all PubMed records on this heading that carry each publication type. Types overlap with other records, so the shares do not sum to 100%.
Publication-type chart data
Publication types among 6,544 PubMed records
TypeRecordsShare
Reviews67710.3%
Meta-analyses40.1%
Randomized controlled trials60.1%

Method: PubMed query "Cystadenoma"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.

Reading the evidence in cancer and oncology

Cancer research spans very different kinds of evidence. Laboratory studies in cell lines and animal models reveal mechanisms but often do not translate to patients. Early-phase trials mainly test safety and dosing, while phase 3 randomized trials and their meta-analyses are the usual basis for treatment conclusions. Outcomes also differ in meaning: tumour shrinkage, progression-free survival and overall survival are not interchangeable, and screening studies can be distorted by lead-time and overdiagnosis. When reading a result, check the cancer type and stage studied, the comparison treatment, and which outcome was measured.

Evidence from open-access studies

These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.

Study comparison — selected abstracts, not a systematic review
Study / authorsYearSource label / designEurope PMC citationsLicence / source
Exosomal microRNAs as tumor markers in epithelial ovarian cancer
Pan C, Stevic I, Müller V, Ni Q, Oliveira-Ferrer L, Pantel K, et al.
2018Clinical trial
Design not recorded in structured metadata
150cc by
PMID 30107086 · DOI · PMC6210043
Polyploid giant cancer cells with budding and the expression of cyclin E, S-phase kinase-associated protein 2, stathmin associated with the grading and metastasis in serous ovarian tumor
Lv H, Shi Y, Zhang L, Zhang D, Liu G, Yang Z, et al.
2014Research article
Design not recorded in structured metadata
83cc by
PMID 25106448 · DOI · PMC4137091
Identification of receptor tyrosine kinase, discoidin domain receptor 1 (DDR1), as a potential biomarker for serous ovarian cancer
Quan J, Yahata T, Adachi S, Yoshihara K, Tanaka K
2011Research article
Design not recorded in structured metadata
63cc by
PMID 21541037 · DOI · PMC3083684
Hypervascular solid-appearing serous cystadenoma as a mimic of nonfunctioning pancreatic neuroendocrine tumour: a systematic review
Annecchiarico M, Loiaco G, Argenio G, Varricchio A, Rompianesi G, Cannella R
2026Systematic review
Design not recorded in structured metadata
0cc by
PMID 42033641 · DOI · PMC13672579

Exosomal microRNAs as tumor markers in epithelial ovarian cancer [1]

Clinical trial Pan C, Stevic I, Müller V, Ni Q, Oliveira-Ferrer L, Pantel K, et al. · · 2018 · cited 150 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
Specific microRNAs (miRNAs) are packaged in exosomes that regulate processes in tumor development and progression.
Closing excerpt
Our findings reveal specific exosomal miRNA patterns in EOC and ovarian cystadenoma patients, which are indicative of a role of these miRNAs in the pathogenesis of EOC.
Interpretation limits
Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (231 words)

Specific microRNAs (miRNAs) are packaged in exosomes that regulate processes in tumor development and progression. The current study focuses on the influence of exosomal miRNAs in the pathogenesis of epithelial ovarian cancer (EOC). MiRNA profiles were determined in exosomes from plasma of 106 EOC patients, eight ovarian cystadenoma patients, and 29 healthy women by TaqMan real-time PCR-based miRNA array cards containing 48 different miRNAs. In cell culture experiments, the impact of miR-200b and miR-320 was determined on proliferation and apoptosis of ovarian cancer cell lines. We report that miR-21 (P = 0.0001), miR-100 (P = 0.034), miR-200b (P = 0.008), and miR-320 (P = 0.034) are significantly enriched, whereas miR-16 (P = 0.009), miR-93 (P = 0.014), miR-126 (P = 0.012), and miR-223 (P = 0.029) are underrepresented in exosomes from plasma of EOC patients as compared to those of healthy women. The levels of exosomal miR-23a (P = 0.009, 0.008) and miR-92a (P = 009, 0.034) were lower in ovarian cystadenoma patients than in EOC patients and healthy women, respectively. The exosomal levels of miR-200b correlated with the tumor marker CA125 (P = 0.002) and patient overall survival (P = 0.019). MiR-200b influenced cell proliferation (P = 0.0001) and apoptosis (P < 0.008). Our findings reveal specific exosomal miRNA patterns in EOC and ovarian cystadenoma patients, which are indicative of a role of these miRNAs in the pathogenesis of EOC.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 30107086 · DOI · PMC6210043

Polyploid giant cancer cells with budding and the expression of cyclin E, S-phase kinase-associated protein 2, stathmin associated with the grading and metastasis in serous ovarian tumor [2]

Research article Lv H, Shi Y, Zhang L, Zhang D, Liu G, Yang Z, et al. · · 2014 · cited 83 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
BackgroundWe previously reported that polyploid giant cancer cells (PGCCs) exhibit cancer stem cell properties and express cell cycle-related proteins.
Closing excerpt
ConclusionsThese data suggest that the cell cycle-related proteins cyclin E, SKP2, and stathmin may be valuable biomarkers to evaluate the metastasis in patients with ovarian serous carcinoma.
Interpretation limits
Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (306 words)

BackgroundWe previously reported that polyploid giant cancer cells (PGCCs) exhibit cancer stem cell properties and express cell cycle-related proteins. HEY PGCCs induced by cobalt chloride generated daughter cells and the daughter cells had a strong migratory and invasive ability. This study is to compare the expression of cyclin E, S-phase kinase-associated protein 2 (SKP2), and stathmin between PGCCs with budding and control HEY cells, and determine the clinicopathological significance of cell cycle-related protein expression in ovarian tumors.MethodsWe used western blot and immunocytochemical staining to compare the expression levels of cyclin E, SKP2 and stathmin between PGCC with budding daughter cells and control HEY cells. In addition, immunohistochemical staining for cyclin E, SKP2 and stathmin was performed on a total of 80 paraffin-embedded serous ovarian tumor tissue samples. The samples included 21 cases of primary high-grade carcinoma (group I) and their metastatic tumors (group II), 26 cases of primary low-grade carcinoma without metastasis (group III), and 12 cases of serous borderline cystadenoma (group IV).ResultsSingle PGCC with budding in the stroma showed high correlation with the metastasis of ovarian carcinoma. Group I had a significantly higher number of single PGCCs with budding in the stroma than group III (85.71% [18/21] vs. 23.08% [6/26] cases; χ2 = 18.240, P = 0.000). The expression of cyclin E, SKP2, and stathmin was compared among the four groups. The expression levels of cyclin E, SKP2, and stathmin increased with the malignant grade of ovarian tumors and group II had the highest expression levels. The expression of cyclin E (χ2 = 17.985, P = 0.000), SKP2 (χ2 = 12.384, P = 0.000), and stathmin (χ2 = 20.226, P = 0.000) was significantly different among the 4 groups.ConclusionsThese data suggest that the cell cycle-related proteins cyclin E, SKP2, and stathmin may be valuable biomarkers to evaluate the metastasis in patients with ovarian serous carcinoma.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 25106448 · DOI · PMC4137091

Identification of receptor tyrosine kinase, discoidin domain receptor 1 (DDR1), as a potential biomarker for serous ovarian cancer [3]

Research article Quan J, Yahata T, Adachi S, Yoshihara K, Tanaka K · · 2011 · cited 63 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
Ovarian cancer, one of the most common gynecological malignancies, has an aggressive phenotype.
Closing excerpt
Although its functional role and clinical utility remain to be examined in future studies, our results suggest that the expression of DDR1 may serve as both a potential biomarker and a molecular target for advanced ovarian cancer.
Interpretation limits
Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (204 words)

Ovarian cancer, one of the most common gynecological malignancies, has an aggressive phenotype. It is necessary to develop novel and more effective treatment strategies against advanced disease. Protein tyrosine kinases (PTKs) play an important role in the signal transduction pathways involved in tumorigenesis, and represent potential targets for anticancer therapies. In this study, we performed cDNA subtraction following polymerase chain reaction (PCR) using degenerate oligonucleotide primers to identify specifically overexpressed PTKs in ovarian cancer. Three PTKs, janus kinase 1, insulin-like growth factor 1 receptor, and discoidin domain receptor 1 (DDR1), were identified and only DDR1 was overexpressed in all ovarian cancer tissues examined for the validation by quantitative real-time PCR. The DDR1 protein was expressed in 63% (42/67) of serous ovarian cancer tissue, whereas it was undetectable in normal ovarian surface epithelium. DDR1 was expressed significantly more frequently in high-grade (79%) and advanced stage (77%) tumors compared to low-grade (50%) and early stage (43%) tumors. The expression of the DDR1 protein significantly correlated with poor disease-free survival. Although its functional role and clinical utility remain to be examined in future studies, our results suggest that the expression of DDR1 may serve as both a potential biomarker and a molecular target for advanced ovarian cancer.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 21541037 · DOI · PMC3083684

Hypervascular solid-appearing serous cystadenoma as a mimic of nonfunctioning pancreatic neuroendocrine tumour: a systematic review [4]

Systematic review Annecchiarico M, Loiaco G, Argenio G, Varricchio A, Rompianesi G, Cannella R · · 2026

Abstract reading summary — source excerpts
Opening excerpt
BackgroundSolid pancreatic serous cystadenoma (SCA) may present as a hypervascular mass and mimic nonfunctioning pancreatic neuroendocrine tumour (NF-pNET), potentially leading to pancreatic resection for benign disease.
Closing excerpt
These findings may support cautious multiparametric assessment in selected hypervascular solid-appearing pancreatic lesions, but should not be applied as definitive diagnostic thresholds without external validation.
Interpretation limits
Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (258 words)

BackgroundSolid pancreatic serous cystadenoma (SCA) may present as a hypervascular mass and mimic nonfunctioning pancreatic neuroendocrine tumour (NF-pNET), potentially leading to pancreatic resection for benign disease. We synthesized the available evidence on this diagnostic pitfall.MethodsA PRISMA 2020-aligned systematic review searched MEDLINE, Embase, and Web of Science (1 January 2000-1 December 2025). We included comparative cohorts of pathology-proven SCA versus NF-pNET reporting CT/MRI discriminative features and case reports/series of pathology-proven SCA preoperatively interpreted as NF-pNET. Comparative cohorts and case reports/series were synthesized separately; no meta-analysis was performed.ResultsThirty-five publications were included: four retrospective single-center comparative cohorts (50 SCA and 89 NF-pNET patients) and 31 case reports/series (39 SCA patients). In comparative cohorts, unenhanced CT attenuation was consistently lower in SCA than in NF-pNET (18.5-29.6 vs. 38.8-48.4 HU), with study-specific ROC-derived cutoffs in the low 30-HU range; attenuation ratios performed similarly. Diffusion-weighted MRI showed higher ADC values in SCA, with reported study-specific cutoffs of > 1.36 × 10- 3 mm2/s and > 1.99 × 10- 3 mm2/s. In case reports/series, arterial hyperenhancement occurred in 32/33 (97.0%), 68Ga-DOTA-peptide uptake in 17/39 (43.6%), and EUS-guided sampling was diagnostic in 9/17 (52.9%).ConclusionsNF-pNET-mimicking SCA is an uncommon but clinically consequential benign mimic. In the available retrospective comparative cohorts of resected, pathology-proven lesions, lower unenhanced CT attenuation (and attenuation ratios) and higher DWI-ADC values consistently favored SCA over NF-pNET, whereas arterial hyperenhancement and positive somatostatin receptor imaging uptake were not specific. These findings may support cautious multiparametric assessment in selected hypervascular solid-appearing pancreatic lesions, but should not be applied as definitive diagnostic thresholds without external validation.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42033641 · DOI · PMC13672579

Key reviews and meta-analyses

The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.

  • Research article ACG Clinical Guideline: Diagnosis and Management of Pancreatic Cysts [5]
    Elta GH, Enestvedt BK, Sauer BG, Lennon AM · Am J Gastroenterol · 2018 · cited 522 times (Europe PMC)
  • Research article Cyst fluid analysis in the differential diagnosis of pancreatic cystic lesions: a pooled analysis [6]
    van der Waaij LA, van Dullemen HM, Porte RJ · Gastrointest Endosc · 2005 · cited 391 times (Europe PMC)
  • Research article New insights into the pathogenesis of serous ovarian cancer and its clinical impact [7]
    Levanon K, Crum C, Drapkin R · J Clin Oncol · 2008 · cited 286 times (Europe PMC)
  • Research article Ovarian serous borderline tumors: a critical review of the literature with emphasis on prognostic indicators [8]
    Seidman JD, Kurman RJ · Hum Pathol · 2000 · cited 249 times (Europe PMC)
  • Research article Fallopian tube precursors of ovarian low- and high-grade serous neoplasms [9]
    Vang R, Shih IeM, Kurman RJ · Histopathology · 2013 · cited 192 times (Europe PMC)
  • Research article Cystic tumors of the pancreas [10]
    Fernández-del Castillo C, Warshaw AL · Surg Clin North Am · 1995 · cited 139 times (Europe PMC)

References

  1. Pan C, Stevic I, Müller V, Ni Q, Oliveira-Ferrer L, Pantel K, et al.. Exosomal microRNAs as tumor markers in epithelial ovarian cancer. . 2018. PMID 30107086 · DOI · PMC6210043
  2. Lv H, Shi Y, Zhang L, Zhang D, Liu G, Yang Z, et al.. Polyploid giant cancer cells with budding and the expression of cyclin E, S-phase kinase-associated protein 2, stathmin associated with the grading and metastasis in serous ovarian tumor. . 2014. PMID 25106448 · DOI · PMC4137091
  3. Quan J, Yahata T, Adachi S, Yoshihara K, Tanaka K. Identification of receptor tyrosine kinase, discoidin domain receptor 1 (DDR1), as a potential biomarker for serous ovarian cancer. . 2011. PMID 21541037 · DOI · PMC3083684
  4. Annecchiarico M, Loiaco G, Argenio G, Varricchio A, Rompianesi G, Cannella R. Hypervascular solid-appearing serous cystadenoma as a mimic of nonfunctioning pancreatic neuroendocrine tumour: a systematic review. . 2026. PMID 42033641 · DOI · PMC13672579
  5. Elta GH, Enestvedt BK, Sauer BG, Lennon AM. ACG Clinical Guideline: Diagnosis and Management of Pancreatic Cysts. Am J Gastroenterol. 2018. PMID 29485131 · DOI
  6. van der Waaij LA, van Dullemen HM, Porte RJ. Cyst fluid analysis in the differential diagnosis of pancreatic cystic lesions: a pooled analysis. Gastrointest Endosc. 2005. PMID 16111956 · DOI
  7. Levanon K, Crum C, Drapkin R. New insights into the pathogenesis of serous ovarian cancer and its clinical impact. J Clin Oncol. 2008. PMID 18854563 · DOI · PMC2652087
  8. Seidman JD, Kurman RJ. Ovarian serous borderline tumors: a critical review of the literature with emphasis on prognostic indicators. Hum Pathol. 2000. PMID 10836293 · DOI
  9. Vang R, Shih IeM, Kurman RJ. Fallopian tube precursors of ovarian low- and high-grade serous neoplasms. Histopathology. 2013. PMID 23240669 · DOI
  10. Fernández-del Castillo C, Warshaw AL. Cystic tumors of the pancreas. Surg Clin North Am. 1995. PMID 7660245 · DOI

About this article

Sources
NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
Verification
Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
Review state
automated source verified; no human expert review has been recorded yet.
Version
1, last updated 2026-10-29.

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At a glance

6,544
PubMed records on this heading
6%
published since 2020
677
review articles
6
randomized trials
10
verified references below

Counts come from PubMed on 2026-10-29; they show how much has been written, not how strong the evidence is.

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