Lung cancer occurs when cells divide in the lungs uncontrollably, causing tumours to grow. This can affect a patient’s breathing and the cancer can spread to other parts of the body.
Lung cancer is the leading cause of cancer deaths in the world and Australia.
What causes lung cancer?
Anyone can get lung cancer, but cigarette smoking is the biggest risk factor. About 90 per cent of lung cancer in men and 65 per cent in women is the result of smoking. However, nearly 15 per cent of lung cancer occurs in people who have never smoked. In addition, breathing in other hazardous substances, especially over a long period of time, can also cause lung cancer.
A type of lung cancer called mesothelioma is almost always caused by exposure to asbestos, which is increasing in incidence in line with the home renovation boom. While the lungs can repair acute damage caused by smoke to lung tissue, ongoing exposure makes it difficult for the lungs to maintain continual repair. Damaged cells increase the likelihood of lung cancer developing.
What are the types of lung cancer?
There are two major types of lung cancer, based on the type of cells affected. These two types grow differently and are treated differently.
- Small cell lung cancer (SCLC).Small cell lung cancer occurs mostly in smokers, spreads quickly and makes up about 15 per cent of lung cancers.
- Non-small cell lung cancer. Non-small cell lung cancer is an umbrella term for several types of lung cancers, making up around 85 per cent of lung cancers. These include squamous cell carcinoma, adenocarcinoma and large cell carcinoma.
What are lung cancer treatments?
The two types of lung cancers grow differently, therefore they are treated differently. Treatment options include surgery, radiation, chemotherapy, targeted therapy, immunotherapy and a combination of these approaches.
Lung cancer statistics
Lung cancer is the leading cause of cancer deaths in the world and Australia. More than 13,000 cases of lung cancer are diagnosed in Australia each year, and 8,500 people die.
The current survival rate is only about 17 per cent and for most lung cancer patients, current treatments do not cure the cancer.
Our lung cancer research
Hudson Institute researchers are working to understand how to prevent, detect and treat lung cancer.
Our teams are making significant progress in identifying an early detection test and new treatment targets for lung cancer patients.
Overcoming platinum resistant small cell lung cancer (SCLC)
Improved treatment. The majority of small cell lung cancer patients are diagnosed with advanced disease, which limits their treatment options to platinum-based chemotherapy. These patients typically respond well, but for a limited time before a drug resistant disease recurs. There is no effective second line therapy, and as a result more than 95 per cent of patients succumb to their disease. Dr Gough’s research is defining the mechanisms that drive platinum resistance to enable more durable responses to this key front-line agent. In addition, his team is identifying new therapies that can treat platinum resistant disease, which will improve the treatment arsenal. Dr. Gough’s laboratory uses combinations of patient derived material, resistant cell lines, pre-clinical mouse models of treatment naïve and platinum resistant disease, functional genomics, proteomics and drug screening technologies.
Re-engaging the immune system to kill SCLC
Improved treatment. The lung is a critical immune tissue harbouring cells of both the adaptive and innate immune system that enable rapid and potent immune responses. Small cell lung cancer typically arises in patients after chronic cigarette exposure which makes it the tumour type with the second highest DNA-mutation rate. This mutation rate, coupled with the immune infiltrate in the lung led to the hypothesis that the use of revolutionary new cancer therapies that harness the immune system (checkpoint inhibitors) would be an effective. However, these drugs are only effective in a small number of SCLC patients suggesting that SCLC suppresses the immune system. Importantly, it is possible to reanimate the immune system to limit SCLC growth and metastasis and to improve the efficacy of checkpoint inhibitor therapy. Dr Gough’s team uses sophisticated genetically engineered pre-clinical models, functional genomics, drug screening and biochemistry to find ways to re-engage the host immune system and improve outcomes for SCLC.
Targeting epigenetic dysregulation in lung cancer
Epigenetic and molecular studies. Epigenetics is the study of how your behaviours and environment can cause changes that affect the way your genes work. Some epigenetic changes increase your cancer risk. The mutations in genes needed for epigenetic regulation are frequent in non-small cell lung cancer. Using cell and pre-clinical models of lung cancer, Dr Cain’s team is investigating potential treatments that exploit the dependency of epigenetic dysregulation in lung cancer. It is hoped this information will provide a greater understanding of disease biology and lead to improved treatments and patient outcomes.
Lung cancer drug and diagnostic under development
Early detection and treatment. Professor Jenkins discovered that a drug called sgp130Fc could halt the progression of lung cancer and emphysema, the latter a risk factor for lung cancer. The team have also identified a unique signature that could be used as a biomarker to detect these diseases much earlier through a simple blood test. Earlier diagnosis will offer patients more treatment options and improved prognosis. The team is validating the clinical potential of these findings in additional lung cancer patient cohorts.
Breakthrough lung cancer drug
Treatment. The KRAS gene belongs to a class of genes known as oncogenes. When mutated, oncogenes have the potential to cause normal cells to become cancerous. For many years, researchers have unsuccessfully tried to find a way to inhibit the KRAS gene to stop it creating cancer cells. Prof Jenkins and Research Fellow Dr Mohammed Saad have identified, and are now developing, a drug that slows down tumour growth by targeting an enzyme, ADAM17, which amplifies the effect of the KRAS gene when it is activated.
What drives the muscle-wasting caused by cancer?
Molecular studies. Cachexia, or weight and muscle wasting, affects up to 80 per cent of advanced cancer patients. Prof Jenkins and his team have discovered a cytokine called Interleukin 6 (IL-6) that is responsible for driving cachexia in lung cancer patients through an alternative, trans-signalling cell pathway. They have also identified an antibody that blocks the trans-signalling process that may have clinical potential in the treatment of lung cancer cachexia.
Illuminating the role of ADAM17 in lung cancer
New treatment. ADAM17 is an enzyme that regulates the biological activity of more than 70 proteins, many of which are implicated in cancer. However, the role of ADAM17 in lung cancer is not clear. This project aims, for the first time, to define ADAM17 as a therapeutic target for lung cancer.
Inflammation and cancer
Molecular studies. Prof Brendan Jenkins and his team are looking at inflammation-associated cancers (stomach, lung, pancreatic) and emphysema/chronic obstructive pulmonary disease (COPD) using a combination of molecular biological and genetic approaches, alongside human translational studies. Their aim is to identify the mechanisms by which uncontrolled signal transduction from the interleukin (IL)-6 cytokine family, pattern recognition receptors (such as toll-like receptors) and inflammasomes lead to inflammation-associated cancers.
Lung cancer collaborators
Support for people with lung cancer
Hudson Institute scientists cannot provide medical advice.
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