A Novel Role For CBF? As A Regulator Of Breast Cancer
Funder
National Health and Medical Research Council
Funding Amount
$682,415.00
Summary
Whole genome sequencing studies of human breast tumours identified a handful of common significantly mutated genes, all previously linked to breast cancer, except one, CBF?. Preliminary data from our lab now show that CBF? may be a new regulator of human breast cancer and metastasis. Using mice with altered CBF? levels, breast cancer models and human patient cohorts, this study aims to identify a novel role for CBF? as a new regulator of human breast cancer and potential therapeutic target.
Determination Of The Cellular Origins Of Breast Cancer
Funder
National Health and Medical Research Council
Funding Amount
$705,563.00
Summary
Breast cancer is a highly heterogeneous disease with multiple molecular and histological subtypes. We propose to use novel genetically engineered mice to understand breast inter-tumoral heterogeneity by dissecting the cells of origin of breast cancer in vivo. Initially, we will examine whether long-lived stem or progenitor cells are the targets of breast carcinogenesis induced by a progesterone derivative using our state-of-the-art multi-coloured reporter models to track the cells in vivo.
Determing Whether Breast Stem Cells Mediate The Risk Of Developing Breast Cancer
Funder
National Health and Medical Research Council
Funding Amount
$433,894.00
Summary
Whilst the outcomes for women with breast cancer have improved significantly, the incidence of breast cancer continues to increase. Research needs to focus on prevention now to try to stop the increase. Apart from age, our reproductive behaviour is the largest risk factor for breast cancer. If a woman does not bear children, or has them after 35 years of age, she is at 25-50% increased risk of breast cancer. We would like to determine whether the breast stem cells play a role in this and why.
The Role Of The Asymmetric Cell Division Regulator GPSM2 In Mammary Gland Development And Breast Cancer
Funder
National Health and Medical Research Council
Funding Amount
$647,539.00
Summary
Tissues are built by small populations of progenitor cells which divide unequally to generate different cell types. Recent studies suggest defective progenitor cells are founders of some breast cancers and that progenitor-like cancer cells resist therapy to regenerate tumours. We have shown a progenitor division regulator called GPSM2 controls these cells and inhibits breast cancer. Examination of this new anti-tumour pathway promises to identify therapeutic targets for breast cancer recurrence.
Early Antecedents Of Food Allergy: Defining The Pathways Underlying Very Early Sensitisation To Foods.
Funder
National Health and Medical Research Council
Funding Amount
$607,193.00
Summary
With such a dramatic rise in food allergy, and many infants now showing established food-sensitization before starting complimentary foods at 4-6 months, there is a pressing need to define events around much earlier allergen encounter. This project addresses critical questions that form an essential platform for earlier strategies to prevent the rising burden of food allergy and other allergic diseases.
Improving Cancer Management By Direct Detection With Diffusion-weighted Magnetic Resonance Imaging.
Funder
National Health and Medical Research Council
Funding Amount
$421,549.00
Summary
Despite reliable methods of prostate and breast cancer diagnosis there remains considerable uncertainty as to whether the detected disease will have a significant impact on a patient’s quality of life. This uncertainty is largely due to the inability of current detection methods to show the extent of disease. This project will address this problem by developing new MRI methods that directly measure the microscopic tissue properties that define cancer.
Psychosocial Predictors Of Developing Breast Cancer In Women From High Risk Breast Cancer Families
Funder
National Health and Medical Research Council
Funding Amount
$1,109,214.00
Summary
Over the past 20 years, studies have highlighted the possible roles of stressful life events and distress, possibly mediated by social support and personality, in causing or speeding up the development of breast cancer. This possibility is of strong concern to consumers. To date, there have been few well designed, prospective studies of this issue. Furthermore, no previous studies have specifically targeted women at increased risk because of their family history. In recent years, it has become p ....Over the past 20 years, studies have highlighted the possible roles of stressful life events and distress, possibly mediated by social support and personality, in causing or speeding up the development of breast cancer. This possibility is of strong concern to consumers. To date, there have been few well designed, prospective studies of this issue. Furthermore, no previous studies have specifically targeted women at increased risk because of their family history. In recent years, it has become possible to identify 2 breast cancer genes (BRCA1 and BRCA2). Female carriers of mutations in these genes with a strong family history have an estimated lifetime risk of between 35% and 85%. The Kathleen Cuningham Consortium for Research into Familial Breast Cancer (kConFab) was established 11 years ago to coordinate the collection of genetic, epidemiological and clinical data in Australian and New Zealand families with a dominantly inherited predisposition to breast cancer. Due to the high rate of breast cancer diagnoses in this group, and the systematic recruitment of large numbers of high risk women by kConFab, there is a unique and temporary opportunity to conduct a rigorous study to resolve this question, with sufficient numbers involved. The study is a world first, and will provide the best data to date in this area. If the study demonstrates a relationship between psychosocial factors and the development of breast cancer in women from high risk breast cancer families, subsequent identification of vulnerable individuals and the implementation of appropriate interventions may have a real impact on reducing morbidity and mortality in this population. Furthermore, the results may have implications for all women in reducing breast cancer incidence.Read moreRead less
Endocrine Therapy Tolerance As A Cancer Cell Survival Mechanism For Late Recurring Breast Cancer
Funder
National Health and Medical Research Council
Funding Amount
$450,083.00
Summary
~25% of breast cancer deaths are attributable to cancers that have failed endocrine therapy and recur >5 years after primary diagnosis. These cancers are not well understood because their long latency makes them difficult to study. We have new models of this disease that identify a “therapy tolerant” population, and this is likely to re-emerge to cause late recurrence. Our work could potentially identify new biological tests and therapeutic strategies to treat late recurring breast cancer.
Reduction Of Breast Lymphoedema Symptoms Secondary To Breast Cancer: A Randomised Controlled Trial
Funder
National Health and Medical Research Council
Funding Amount
$600,395.00
Summary
Breast lymphoedema is a consequence of treatment for breast cancer that is not typically discussed, despite more than 1/3 of women with lymphoedema reporting symptoms in the breast. To date, no study has investigated the impact of exercise on breast lymphoedema symptoms. The aim of this study is to determine if a general exercise program is safe, acceptable and effective in reducing symptoms for women with breast lymphoedema.
Identification Of Target Genes At Breast Cancer-risk Loci With Potential For Drug Repositioning
Funder
National Health and Medical Research Council
Funding Amount
$757,478.00
Summary
Genome wide association studies have been extremely successful at identifying regions of the genome associated with breast cancer risk. However, to fully translate this information to prevention and treatment of breast cancer, we need to understand the molecular mechanisms responsible for increasing breast cancer susceptibility, and the genes that are involved.