- Title
- Ovarian hormones through Wnt signalling regulate the growth of human and mouse ovarian cancer initiating lesions
- Creator
- Nagendra, Prathima B.; Goad, Jyoti; Nielsen, Sarah; Rassam, Loui; Lombard, Janine M.; Nahar, Pravin; Tanwar, Pradeep S.
- Relation
- NHMRC.ARC
- Relation
- OncoTarget Vol. 7, Issue 40, p. 64836-64853
- Publisher Link
- http://dx.doi.org/10.18632/oncotarget.11711
- Publisher
- Impact Journals
- Resource Type
- journal article
- Date
- 2016
- Description
- Ovarian cancer (OC) is the most deadly gynaecological disease largely because the majority of patients are asymptomatic and diagnosed at later stages when cancer has spread to other vital organs. Therefore, the initial stages of this disease are poorly characterised. Women with BRCA1/2 mutations have a genetic predisposition for developing OC, but not all of these women develop the disease. Epidemiological findings show that lifestyle factors such as contraceptive use and pregnancy, a progesterone dominant state, decrease the risk of getting OC. How ovarian hormones modify the risk of OC is currently unclear. Our study identifies activated Wnt signalling to be a marker for precursor lesions of OC and successfully develops a mouse model that mimics the earliest events in pathogenesis of OC by constitutively activating ßcatenin. Using this model and human OC cells, we show that oestrogen promotes and progesterone suppresses the growth of OC cells.
- Subject
- ovarian cancer; hormones; womens health
- Identifier
- http://hdl.handle.net/1959.13/1345191
- Identifier
- uon:29580
- Identifier
- ISSN:1949-2553
- Rights
- This is an open access article distributed under the Creative Commons Attribution License (Creative Commons Attribution 3.0 License).
- Language
- eng
- Full Text
- Reviewed
- Hits: 4637
- Visitors: 2354
- Downloads: 226
Thumbnail | File | Description | Size | Format | |||
---|---|---|---|---|---|---|---|
View Details Download | ATTACHMENT02 | Publisher version (open access) | 11 MB | Adobe Acrobat PDF | View Details Download |