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2012/2013 Fellowship Grant Abstracts

Dr-Christine-Bruce.jpgCancerCare Manitoba – Dr. Christine Bruce 

Investigating recruitment of S6K1 and mTOR to estrogen response elements in ER+ breast cancer cells

The majority of breast cancers express higher than normal levels of the receptor for the hormone estrogen, called ER. In healthy cells, the role of ER is to promote cell proliferation and growth but deregulation of this pathway leads to uncontrolled growth and tumorigenesis, as is the case for ER-positive breast cancers. Therapies targeting ER are successful in treating and preventing breast cancer, however, the usefulness of these relatively non-toxic treatments are limited by the development of resistance. Understanding the cellular mechanisms leading to drug resistance is the most promising avenue for improving therapy and circumventing this problem.

Modification of the ER protein by enzymes within the cell affects protein function and has been linked to the development of resistance and a poor therapeutic response. In this proposal, I hypothesize a novel role for two enzymes which have been shown to modify ER. I will investigate further their role in ER modification and development of resistance using well-established laboratory techniques. This information will aid in the development of more precise biomarkers of therapy response, allowing the most effective therapies to be administered quickly and with minimal side-effects. Furthermore, this research may offer specific targets and alternative approaches for development of new endocrine therapies or for combination therapies, capable of overcoming resistance.

DrJie-Chen.jpgUniversity of Calgary – Dr. Jie Chen 

MicroRNA components of the p33ING1b in breast cancer

Using results proven through earlier studies, Dr. Chen and the team from the University of Calgary know that ING1b and some miRNAs regulated by ING1b are growth inhibitory. With this knowledge, they hypothesize miRNAs that are regulated by ING1b might play critical roles in the regulation of cell growth, apoptosis and senescence, all of which are relevant to the genesis and development of breast cancer. This team aims to use the growth inhibitory miRNAs to develop a strategy to kill breast cancer cells.

Within this project, the team will identify miRNAs regulated by ING1b, identify and confirm the target genes of selected miRNAs, determine whether the identified miRNAs are directly regulated by ING1b, evaluate the effects of the identified miRNAs in the breast cancer cell line and complete an evaluation of miRNAs regulating cell growth or suicide for the ability to affect tumour growth and survival in animal tumour models.

This team predicts a subset of the miRNAs that are induced by ING1b will regulate cell growth, suicide and aging since ING1b has been shown to impinge upon all of these processes. The results will provide further understanding of the pathways used by the ING1b tumor suppressor to regulate cell growth and death, and shed new light on the functions of miRNAs in cell cycle regulation. Since it may be more effective to use miRNAs, rather than chemotherapeutic agent or virus, due to low toxicity and high efficiency of delivery, it is believed that identification of a series of growth inhibitory and/or cell death inducing miRNAs may provide some clinical effective tools for breast cancer treatment as suggested by the recent initiation of miRNA clinical trial. Specifically, this knowledge should allow us to discover potential new therapeutic targets for the future treatment of breast cancer and builds upon our expertise with the ING family of tumor suppressor.

University of Alberta – Dr. Xiaoyun Tang

Roles of lipid mediators in chemo-resistance and metastasis in breast cancer

Treatment of breast cancer by a combination of surgery and drugs often fails and patients die. This is explained in two ways: 1.some tumor cells survive the surgery or they may have already spread to other areas of the body; 2. these cells fail to be killed since the drugs often become ineffective because of the development of resistance to these agents. The survival and spread of breast tumors to other organs is promoted by growth factors. My project concentrates on a newly discovered growth factor called lysophosphatidate (LPA), which has now been shown to play an important role in promoting the progression of breast cancer. Our group showed that LPA causes breast cancer cells to migrate to other organs and to resist being killed by drugs. So far, relatively little is know about how to diminish the effects of LPA in promoting the progression of breast cancer. This work will investigate how to modify the responses of breast cancer cells to stimulation by LPA and other growth factors. This knowledge will be used to devise treatments that inhibit tumor growth and migration to other argans. It should lead to the introduction of companion therapies that can be used to increase the effectiveness of existing treatments and to overcome the development of resistance to chemotherapy and radiotherapy. Overall, my work is directed to enhancing our ability to increase the quality of life for breast cancer patients and maximize the chance of a successful treatment and survival from this disease.

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