New insight into the origins of lung cancer


Monday, 02 February, 2015

Researchers at Sydney’s Centenary Institute are working to find new insights into the origins of lung cancer, in the hope of creating avenues for personalising patient therapy.

Genes provide the instructions for each cell in each organ or tissue in the human body to function. Genetic abnormalities that cause lung and other types of cancer are mistakes in our genes that alter the normal genetic ‘program’ for cell function and behaviour. To date, research has centred on identifying abnormalities directly in genes that provide the instructions for how cells grow and behave - processes which are defective in cancer.

However, the Centenary Institute has found that the molecular machinery within cells that ‘reads’ the instructions encoded in genes is just as important as the message itself in determining whether cellular programs go awry and cause cancer. The institute now aims to determine how the malfunction of protein molecules that influence how the human genome is ‘read’ - not just abnormalities in genes that directly provide instructions for cell growth and survival - contributes to cancer.

Dr Adam Cook is leading the Centenary research.

Centenary scientists have recently showed that tNASP, a ‘chaperone’ protein that controls the packaging and therefore function of our genes, is inappropriately switched on in cancer cells grown in the lab. Along with previous work, this finding hints that the protein tNASP plays a role in cancer patients, promoting the growth or survival of cancer cells or directly causing cancer to form.

What remains unknown, however, is whether NASP levels are altered in tumours within patients or whether NASP could be a valuable clinical marker for customising patient treatment. The Centenary Institute is currently seeking to fund a project that would explore this question.

The project aims to establish reagents to measure tNASP and its molecular partners in patient tumour samples. It would later evaluate tNASP levels in patient lung tumour and leukemia samples, calculating whether it is a predictor of patient diagnosis or prognosis. The purpose of the research is also to determine whether tNASP contributes to cancer formation, which would be tested with mouse models.

It is anticipated that the project will lead to tNASP being used in the clinic as a new marker for determining cancer type, severity and patient prognosis. This will help personalise patient chemotherapy, thereby improving patient survival and reducing side effects.

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