Ovarian Neoplasm EpithelialNCT03883542
Sub-type Specific Genomic Mutations in sBOTs
An observational study of Ovarian Neoplasm Epithelial, run by Universitair Ziekenhuis Brussel at 1 site in Belgium.
Trial summary
The aim of this study is to identify different origin in carcinogenesis between serous borderline ovarian tumors presenting a. without implants, b. with non-invasive implants, c. with invasive implants and d. with micropapillary pattern. Read more about this study
- Who is it for?
- Ages 18 years and older, women only
- Conditions the study is for
- Ovarian Neoplasm Epithelial
- What is being tested?
- genomic mutations study
- How many people
- 20 participants
- Where
- 1 siteBelgium
- Study dates
- Jan 2017to 30 Jul 2027
- Phase
- Observational
- Are there results?
- Not yet: the study is under way
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 18 years and older
- Women only
- No healthy volunteers
- Adult, Older adult
Study population: Patients with proven serous bordeline ovarian tumors.
Who may be able to join
- Paraffin embedded material from the original borderline ovarian tumor must be present and of good quality for DNA extraction.
- Original slides are available for central pathological review.
Who cannot join
- Presence of invasive ovarian carcinoma.
Trial locations and contacts
1 site in 1 country.
About this study
Official title: Sub-type Specific Genomic Mutations in Serous Borderline Ovarian Tumors
The aim of this study is to identify different origin in carcinogenesis between serous borderline ovarian tumors presenting a. without implants, b. with non-invasive implants, c. with invasive implants and d. with micropapillary pattern.
The presence of specific mutations could suggest for a more aggressive primary treatment if a higher risk of recurrence can be expected.
Read the detailed description
Introduction Borderline Ovarian Tumors (BOTs) behave indolently in the vast majority of cases and the prognosis is usually favorable. There is more evidence that two subtypes of BOTs represent a higher risk of recurrence or even progression to an invasive ovarian cancer. In case of a presentation with a micro-papillary grow pattern or when invasive implants are diagnosed the prognosis tend to be less favorable.
Genome sequencing in ovarian cancer helped to differentiate two different pathways in the carcinogenesis.
Low grade serous carcinomas evolving from adenofibromas or borderline tumors over non-invasive micropapillary serous borderline tumors to invasive micropapillary serous carcinoma, show frequent mutations in the Kirsten Rat Sarcoma gene (KRAS), B-Raf Kinase gene(BRAF), Erb-B2 Receptor Tyrosine Kinase 2 gene (ERBB2), Phosphatase and Tensin homolog gene (PTEN), Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha gene (PIK3CA) and Catenin Beta 1 gene (CTNNB1). This pathway is called Type I and is characterized by a slow step-wise process. These low-grade invasive tumors are indolent and are known with a better outcome than high-grade invasive tumors.
In contrast the Type II pathway development of invasive tumors is rapid and vast majority of tumors show a Tumor Protein p53 (TP53) mutation and loss of Breast Cancer type 1 susceptibility protein (BRCA1).
The aim of this study is to identify different origin in carcinogenesis between serous borderline ovarian tumors presenting a. without implants, b. with non-invasive implants, c. with invasive implants and d. with micropapillary pattern.
The presence of specific mutations could suggest for a more aggressive primary treatment if a higher risk of recurrence can be expected.
- Conditions
- Ovarian Neoplasm Epithelial
- Being tested
- genomic mutations study
- Keywords
- low malignant potential, serous
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
genomic mutations studyGenetic
Sequencing of the DNA samples extracted from the subgroups
- serous BOT tissue,
- serous BOT tissue with non-invasive implants and
- serous BOT tissue with micropapillary grow pattern will undergo a panel testing for Type 1 genes (small panel 15-40 mutations) AND p53 AND BRCA testing
Sequencing of the DNA samples extracted from the serous BOT tissue with invasive implants will undergo a more comprehensive examination (large panel +- 1000 genes checked)
| Study group | Role | What they receive |
|---|---|---|
| serous BOT | simple serous BOT ovarian tissue Receives: Genetic: genomic mutations study | |
| serous BOT with non-invasive implants | BOT ovarian tissue presenting with non-invasive implants Receives: Genetic: genomic mutations study | |
| sBOT with micropapillary grow pattern | BOT ovarian tissue presenting with micropapillary grow pattern Receives: Genetic: genomic mutations study | |
| serous BOT with invasive implants | sBOT ovarian tissue presenting with invasive implants at the time of diagnosis Receives: Genetic: genomic mutations study |
What is being measured
The primary outcome is the main question the study is designed to answer.
genetic mutations
amount and type of genetic mutations in different subgroups will be analyzed and compared between the different subgroups. Are the mutations suggestive for a type I or type II pathway differentiation?
Measured: 2020
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted21 Mar 2019
- Study startJan 2017
- Primary completion31 Dec 2026 (estimated)
- Study completion30 Jul 2027 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (4)Papers the sponsor has linked to this study.
- Other trials for Ovarian Neoplasm EpithelialStudies of the same condition, open and under way.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Observational
- Observational model
- Case only
- Time perspective
- Retrospective
- Enrolment
- 20 participants (actual)
Sponsor and investigators
- Lead sponsor
- Universitair Ziekenhuis Brussel
- Sponsor type
- University, hospital or other
- Responsible party
- Principal investigator, Stefan Cosyns, Universitair Ziekenhuis Brussel
- Investigators
- stef cosyns, dr, Principal investigator, UZBrussel
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT03883542
- Sponsor's protocol ID
- sBOT
- Status last verified
- Apr 2026
- First submitted
- 26 Feb 2019
- Last updated
- 4 May 2026
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- No
Publications
Morice P, Uzan C, Fauvet R, Gouy S, Duvillard P, Darai E. Borderline ovarian tumour: pathological diagnostic dilemma and risk factors for invasive or lethal recurrence. Lancet Oncol. 2012 Mar;13(3):e103-15. doi: 10.1016/S1470-2045(11)70288-1.
PubMed 22381933Vang R, Shih IeM, Kurman RJ. Ovarian low-grade and high-grade serous carcinoma: pathogenesis, clinicopathologic and molecular biologic features, and diagnostic problems. Adv Anat Pathol. 2009 Sep;16(5):267-82. doi: 10.1097/PAP.0b013e3181b4fffa.
PubMed 19700937Despierre E, Lambrechts D, Neven P, Amant F, Lambrechts S, Vergote I. The molecular genetic basis of ovarian cancer and its roadmap towards a better treatment. Gynecol Oncol. 2010 May;117(2):358-65. doi: 10.1016/j.ygyno.2010.02.012. Epub 2010 Mar 7.
PubMed 20207398Kurman RJ, Shih IeM. The origin and pathogenesis of epithelial ovarian cancer: a proposed unifying theory. Am J Surg Pathol. 2010 Mar;34(3):433-43. doi: 10.1097/PAS.0b013e3181cf3d79.
PubMed 20154587
Study at a glance
From the registry record, last updated by the sponsor on 4 May 2026. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Sub-type Specific Genomic Mutations in Serous Borderline Ovarian Tumors
- ClinicalTrials.gov ID
- NCT03883542
- Acronym / sponsor ID
- sBOT
- Conditions
- Ovarian Neoplasm Epithelial
- Keywords
- low malignant potential, serous
- Study type
- Observational
- Recruitment status
- Active, not recruiting
- Enrolment
- 20 participants (actual)
- Lead sponsor
- Universitair Ziekenhuis BrusselUniversity, hospital or other
- Study start
- Jan 2017 (actual)
- Primary completion
- 31 Dec 2026 (estimated)
- Study completion
- 30 Jul 2027 (estimated)
- First posted
- 21 Mar 2019 (actual)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
The aim of this study is to identify different origin in carcinogenesis between serous borderline ovarian tumors presenting a. without implants, b. with non-invasive implants, c. with invasive implants and d. with micropapillary pattern.
The presence of specific mutations could suggest for a more aggressive primary treatment if a higher risk of recurrence can be expected.
Detailed description
Introduction Borderline Ovarian Tumors (BOTs) behave indolently in the vast majority of cases and the prognosis is usually favorable. There is more evidence that two subtypes of BOTs represent a higher risk of recurrence or even progression to an invasive ovarian cancer. In case of a presentation with a micro-papillary grow pattern or when invasive implants are diagnosed the prognosis tend to be less favorable.
Genome sequencing in ovarian cancer helped to differentiate two different pathways in the carcinogenesis.
Low grade serous carcinomas evolving from adenofibromas or borderline tumors over non-invasive micropapillary serous borderline tumors to invasive micropapillary serous carcinoma, show frequent mutations in the Kirsten Rat Sarcoma gene (KRAS), B-Raf Kinase gene(BRAF), Erb-B2 Receptor Tyrosine Kinase 2 gene (ERBB2), Phosphatase and Tensin homolog gene (PTEN), Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha gene (PIK3CA) and Catenin Beta 1 gene (CTNNB1). This pathway is called Type I and is characterized by a slow step-wise process. These low-grade invasive tumors are indolent and are known with a better outcome than high-grade invasive tumors.
In contrast the Type II pathway development of invasive tumors is rapid and vast majority of tumors show a Tumor Protein p53 (TP53) mutation and loss of Breast Cancer type 1 susceptibility protein (BRCA1).
The aim of this study is to identify different origin in carcinogenesis between serous borderline ovarian tumors presenting a. without implants, b. with non-invasive implants, c. with invasive implants and d. with micropapillary pattern.
The presence of specific mutations could suggest for a more aggressive primary treatment if a higher risk of recurrence can be expected.
Study design
- Observational model
- Case only
- Time perspective
- Retrospective
- Number of arms
- 4
| Arm | Type | Receives |
|---|---|---|
| serous BOT | – | Genetic: genomic mutations studysimple serous BOT ovarian tissue |
| serous BOT with non-invasive implants | – | Genetic: genomic mutations studyBOT ovarian tissue presenting with non-invasive implants |
| sBOT with micropapillary grow pattern | – | Genetic: genomic mutations studyBOT ovarian tissue presenting with micropapillary grow pattern |
| serous BOT with invasive implants | – | Genetic: genomic mutations studysBOT ovarian tissue presenting with invasive implants at the time of diagnosis |
Who may qualify
- Ages
- 18 years and older
- Sex
- Female only
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
- Study population
- Patients with proven serous bordeline ovarian tumors.
Key inclusion criteria (2 listed)
- Paraffin embedded material from the original borderline ovarian tumor must be present and of good quality for DNA extraction.
- Original slides are available for central pathological review.
Key exclusion criteria (1 listed)
- Presence of invasive ovarian carcinoma.
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| genomic mutations studySequencing of the DNA samples extracted from the subgroups 1. serous BOT tissue, 2. serous BOT tissue with non-invasive implants and 3. serous BOT tissue with micropapillary grow pattern will undergo a panel testing for Type 1 genes (small panel 15-40 mutations) AND p53 AND BRCA testing Sequencing of the DNA samples extracted from the serous BOT tissue with invasive implants will undergo a more comprehensive examination (large panel +- 1000 genes checked) | Genetic | sBOT with micropapillary grow pattern, serous BOT, serous BOT with invasive implants, serous BOT with non-invasive implants |
Primary outcome
genetic mutations
Time frame: 2020
amount and type of genetic mutations in different subgroups will be analyzed and compared between the different subgroups. Are the mutations suggestive for a type I or type II pathway differentiation?
Results and safety
This study is still under way. Results are not available in the source record yet.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 4 May 2026.
- Background: PubMed 22381933Morice P, Uzan C, Fauvet R, Gouy S, Duvillard P, Darai E. Borderline ovarian tumour: pathological diagnostic dilemma and risk factors for invasive or lethal recurrence. Lancet Oncol. 2012 Mar;13(3):e103-15. doi: 10.1016/S1470-2045(11)70288-1.
- Background: PubMed 19700937Vang R, Shih IeM, Kurman RJ. Ovarian low-grade and high-grade serous carcinoma: pathogenesis, clinicopathologic and molecular biologic features, and diagnostic problems. Adv Anat Pathol. 2009 Sep;16(5):267-82. doi: 10.1097/PAP.0b013e3181b4fffa.
- Background: PubMed 20207398Despierre E, Lambrechts D, Neven P, Amant F, Lambrechts S, Vergote I. The molecular genetic basis of ovarian cancer and its roadmap towards a better treatment. Gynecol Oncol. 2010 May;117(2):358-65. doi: 10.1016/j.ygyno.2010.02.012. Epub 2010 Mar 7.
- Background: PubMed 20154587Kurman RJ, Shih IeM. The origin and pathogenesis of epithelial ovarian cancer: a proposed unifying theory. Am J Surg Pathol. 2010 Mar;34(3):433-43. doi: 10.1097/PAS.0b013e3181cf3d79.
- Individual participant dataSharing planned: No
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
stef cosyns, dr principal investigator
UZBrussel
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
An observational study of Ovarian Neoplasm Epithelial, run by Universitair Ziekenhuis Brussel at 1 site in Belgium.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 2 inclusion and 1 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: under way, not looking for participants, as of the sponsor's last update on 4 May 2026. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in Belgium. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
This study is still under way. Results are not available in the source record yet.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
genetic mutations (time frame: 2020). It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT03883542, which also lists 4 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 4 May 2026.