Sub-type Specific Genomic Mutations in Serous Borderline Ovarian Tumors
Trial Snapshot
- Phase
- Not Applicable
- Status
- Active, not recruiting
- Enrollment
- 20
- Locations
- 1
- Primary Endpoint
- genetic mutations
Study Overview
Brief 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.
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.
Study Design
- Study Type
- Observational
- Observational Model
- Case Only
- Time Perspective
- Retrospective
Eligibility Criteria
- Ages
- 18 Years to — (Adult, Older Adult)
- Sex
- Female
- Accepts Healthy Volunteers
- No
Inclusion Criteria
- •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.
Exclusion Criteria
- •Presence of invasive ovarian carcinoma.
Arms & Interventions
sBOT with micropapillary grow pattern
BOT ovarian tissue presenting with micropapillary grow pattern
Intervention: genomic mutations study (Genetic)
serous BOT
simple serous BOT ovarian tissue
Intervention: genomic mutations study (Genetic)
serous BOT with non-invasive implants
BOT ovarian tissue presenting with non-invasive implants
Intervention: genomic mutations study (Genetic)
serous BOT with invasive implants
sBOT ovarian tissue presenting with invasive implants at the time of diagnosis
Intervention: genomic mutations study (Genetic)
Outcomes
Primary Outcomes
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?
Secondary Outcomes
No secondary outcomes reported
Investigators
Stefan Cosyns
Principal Investigator
Universitair Ziekenhuis Brussel