Funded projects

Genesis Oncology Trust palliative care breakfast lecture series

Now in its 8th year, the Genesis Oncology Trust Lecture Series continues to provide a low cost and easily accessible palliative care education opportunity. Delivered via teleconference, the eleven lecture series is attended by on average over 250 people each month, more than 50 sites throughout the country are registered to hold the series. Thanks to the generosity of the Genesis Oncology Trust the lectures continue to be available without charge to registered participants. The goal for 2011 is to increase participation in the series, reaching into the aged care sector and developing rural area sites.

Melanoma Summit 2010: Genesis Oncology Trust Sponsorship

New Zealand health professionals will gather at Te Papa in Wellington on 11 March 2011 for the second national Melanoma Summit. The Summit will provide a unique and important opportunity for professionals working in all areas of melanoma control to be informed of recent developments and to identify priorities for action. The programme will include four international experts, speakers on NZ innovations and workshops on prevention, diagnosis, research and consumer action. New Zealand has one of the highest melanoma incidence rates in the world. The Summit will provide an important opportunity for professionals to work more closely to reduce its incidence and impact.

Partial funding (0.3FTE) of a Gynaecology Cancer Research Nurse. Christchurch Women's Hospital

The gynaecological cancer unit at Christchurch Women's Hospital provides services for women throughout the South Island of New Zealand. Participating in international clinical research enables us to maintain treatments at the best international standards. Our research also answers questions relevant to New Zealand women. We also support collaborating researchers who are assessing new tests used in screening and prevention of cervical cancer, understanding cancer growth and developing a new tests for gynaecological cancers. Clinical research can only be performed in the presence of a suitable infrastructure. The research nurse/study coordinator position performs an essential role in managing and coordinating research activities and obtaining participant informed consent.

Modulatory effects of phytochemicals and pharmaceutical drugs on ABC transporters and their potential in reversing multidrug resistance in pancreatic and colorectal cancer.

Resistance to chemotherapy has been one of the greatest hurdles towards effective treatment of cancer, and is the main reason for the poor prognosis of diagnosed patients despite the plethora of anticancer compounds currently available. A major mechanism of tumour resistance is the active extrusion of cancer drugs out of tumour cells by proteins called ABC transporters. The aim of this project is to identify natural plant compounds and existing drugs which can stop the action of these transporters and hopefully reverse tumour resistance and improve treatment outcome.

MicroRNA expression as a biomarker for pancreatic neuroendocrine tumours and adenocarcinomas.

A gene is a set of instructions that tells the cells in our body how to behave. Some genes have instructions that tell cells how to grow, and a mistake (or mutation) might cause abnormal growth, which might result in a cancer. Other factors also control whether a mistake in a gene will cause problems. For example, sometimes a gene with a mistake does not cause any problem because it is "switched off" so that it can't be read. One way that genes can be switched "off" or "on" is by tiny molecules called microRNA's.

This research will look for microRNA's that turn off and on cancers that grow in the pancreas. The two types of cancer in the pancreas are called neuroendocrine tumours and adenocarcinomas. The research aims to understand why these tumours are so hard to treat, when to give treatment, and how we can detect cancer earlier.

The role of germline DNA copy number variation in familial breast cancer risk.

A significant proportion of breast cancers arise in a subset of women who inherit genetic changes that increase risk of developing the disease. However, for most women the changes underlying their disease remain undetermined. Genomic DNA copy number variations (CNVs) are a major source of inherited human genetic variation and to date there have no in depth studies exploring such DNA variations in relation to breast cancer risk. This research aims to explore whether inherited CNVs contribute to increased risk in breast cancer affected families, and thus may ultimately impact on future diagnostic protocols to facilitate improved care in families.

To attend the Joint Scientific Meeting of the International Epidemiological Association Western Pacific Region (IEA-WPR) and the Japan Epidemiological Association (JEA) in Japan in January 2010.

To attend the International Society of Nurses in Cancer Care (ISNCC) in Atlanta Georgia. March 2010.

To attend the Trans-Tasman Radiation Oncology Group (TROG) Study Coordinator Workshop and Annual Scientific Meeting 2010, to be held in Queenstown from the 24th March -27th March.

Development of prodrug-activating enzymes for anti-cancer gene therapy.

This project aims to identify and improve enzymes from bacteria that are able to activate non-toxic "prodrugs" into highly toxic anticancer drugs. These enzymes can then be delivered to cancer cells by tumour-specific viruses, making them sensitive to the prodrugs. Normal human cells lack these enzymes, which minimises side-effects in healthy tissue. As well as having the potential to target both dormant and rapidly dividing tumour cells, these particular enzymes will allow us to follow the progression of virus in the body - a vital safety control which has been lacking in previous cancer gene therapy work.

Metabolic Constraints on Tumour Metastasis.

Tumour metastasis is the main cause of mortality in cancer. Our novel finding that metastatic melanoma cells that have no mitochondrial genome, and whose energy metabolism is therefore purely glycolytic, fail to form tumours in the lung, raises the question of whether metabolic flexibility is essential for metastasis. We will investigate this phenomenon in metastatic melanoma and breast carcinoma cells. Manipulating mitochondrial metabolism is a potential therapeutic approach to metastatic cancer.

Chemotherapy response in an obese mouse model with colorectal cancer

Colorectal cancer kills over 1200 New Zealanders every year, and obesity is a major risk factor. Obese cancer patients often have a poorer survival than normal weight patients, but it is not known why. This study will test the theory that obesity may lead to less successful chemotherapy treatment. Tumour shrinkage after treatment will be compared between obese and normal weight mice with colorectal cancer. Factors in the blood, liver and tumours of obese mice will be studied to determine if they could interfere with successful chemotherapy treatment.

Understanding the activity of IAP antagonists

Programmed cell death (apoptosis) is required for normal development and disruption of this process is a major factor that leads to tumour development and chemoresistance. ‘Inhibitor of apoptosis' (IAP) proteins regulate cell death and compounds that bind to IAPs are in clinical trials. Instead of blocking the association of two molecules as predicted, these compounds trigger degradation of one protein. Using purified proteins we will determine how drug binding alters protein function. This project will indicate how this promising class of therapeutic molecules functions, and pave the way for development of improved compounds.

Investigating the cell of origin of epithelial ovarian cancer through BRCA1 knockdown.

Mutations in the tumour-suppressor gene BRCA1 specifically increase the risk of both breast and epithelial ovarian cancers. Loss of BRCA1 expression in breast cancer cells increases oestrogen synthesis and reduces response to oestrogen, suggesting a possible causal link for the tissue specificity of cancers in women with BRCA1 mutations. However little is known about these relationships in ovarian cells. This proposal aims to determine if tissue-specific roles exist for BRCA1 in steroidogenesis and oestrogen responsiveness. This will increase our understanding of BRCA1-induced carcinogenesis in breast and ovary and may lead to more specific biomarkers of carcinogenesis in these tissues.

Cancer-causing papillomaviruses: reprogramming of the immune response.

The second biggest cancer killer in women is cancer of the cervix. Cervical cancer is caused by persistent infection of high-risk human papillomavirus (HPV). It is likely that the ability of HPV to cause persistent infection is attributable to immune evasion mechanisms harboured by the virus. The focus of this research is to investigate how HPV reprogrammes the host immune response. Through understanding this, interventions to disrupt these processes can be developed, leading to better treatments for women with pre-cancerous changes resulting from HPV.