Leah Prentice

Leah raising money for cancer research atop Mt Kilimanjaro.

 lprentice@bccrc.ca

Department:	Molecular Oncology and Breast Cancer Program (@ the BCCRC since 2005)
Research Role:	Graduate Student
Degree Sought:	PhD,  Pathology & Laboratory Medicine,  UBC
Thesis Topic:	Expression of KiSS1 and GPR54 in breast cancer and other hormonally responsive tumours.
Advisor:	Sam Aparicio
Education:	BSc (Pathology), University of British Columbia, Canada, 2004
Phone:	604-675-8000 ext.7558
Fax:	675 8218

Research Interests:

Kisspeptin, GPR54, breast cancer, metastasis, prostate cancer, ovarian cancer, hormonally responsive cancer

Hormone-responsive tumours represent a serious health burden in Canada and around the world. For instance, breast and prostate cancers are the most frequently diagnosed malignancies in Canadian women and men, respectively, while ovarian cancer has the highest mortality rates of all gynecological cancers. Cancer mortality is associated with the ability of the initial tumour to spread to other sites in the body. My research focuses on the role of two genes called KiSS1 and GPR54 in this process.

The KiSS1 gene produces several small protein molecules that bind to the GPR54 protein. This interaction has been shown to prevent cancer cells from moving around the body, and also affects hormone release. The role of these genes in hormonally responsive tumours is therefore especially significant. My research studies how KiSS1 / GPR54 interaction affects the progression of breast, prostate and ovarian cancer.

The first part of my research will involve studying different breast cancer cells that have different characteristics. The less invasive MCF-7 cells contain exceptionally high levels of GPR54, whereas the highly invasive MDA-MB-231 cells have very low levels of GPR54. The proposed research will determine whether the relatively benign phenotype of the MCF-7 cells will become more invasive when GPR54 expression is inhibited. Conversely, other studies will determine if malignant MDA-MB-231 cells become less invasive when forced to express high levels of GPR54. Similar studies will be conducted in hormonally responsive prostate and ovary cancer cell lines.

I am also working on developing a mouse model in which the GPR54 gene can be deleted at will. The mice I plan to use have been demonstrated to develop primary mammary and prostate tumours that eventually progress to metastatic disease. By comparing tumour response in the presence and absence of GPR54 expression, GPR54's role in tumour invasion can be determined. Specifically, the incidence and extent of tumour metastasis will be compared between the two models.

I am jointly supervised by Drs. Sam Aparicio and David Huntsman.

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