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Garvan Institute

Sections
 

Mammary Development

 

Group Leader
Associate Professor Chris Ormandy

 

Development of the mammary gland occurs in defined stages that are governed by the hormones that regulate reproductive events. Our hypothesis is that the genes that control normal mammary development can become mutated or dysregulated in breast cancer, altering or subverting their normal function and so contributing to the disease process. We must understand how genes program normal development if we are to understand how the program goes awry in cancer. Key genes in these processes may provide targets for future therapies. Our current focus is on discovering the genes that respond to prolactin - a hormone that plays an important role in normal mammary cell proliferation, differentiation and lactation, but when in excess can increase the risk of developing breast cancer.

 

Staff

Sam OakesSenior Research Officer
Dr Samantha Oakes
d_gallego-ortega90.jpgSenior Research Officer
Dr David Gallego-Ortega
Daniel RodenResearch Bioinformatician
Dr Daniel Roden
Anita LedgerResearch Assistant
Anita Ledger
Maria Comas SoberatsResearch Officer
Dr Maria Comas Soberats
Christina ChoResearch Assistant
Christina Cho
Stephanie AllerdicePhD Student
Stephanie Allerdice
Catherine PigginPhD Student
Dr Catherine Piggin
Matthew NaylorVisiting Scientist
Dr Matt Naylor
Adelaide YoungPhD Student
Adelaide Young
Anne-Marie MooneyPhD Student
Anne-Marie Mooney
Alison FergusonPhD Student
Alison Ferguson

 

 

News

 

The factor that could determine future breast cancer treatment

MEDIA RELEASE: 28 Dec 2012
Garvan scientists have shown how a ‘transcription factor’ causes breast cancer to develop an aggressive subtype that lacks sensitivity to oestrogen and does not respond to anti-oestrogen therapies such as Tamoxifen and aromatase inhibitors. Transcription factors are molecules that switch genes on or off. In this case, the transcription factor known as ‘ELF5’ inhibits sensitivity to oestrogen very early in the life of a breast cancer cell.
 
 

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