A drug that will supress tumour growth in the most common type of lung cancer may open up life-saving treatment options for the 1.8 million people worldwide diagnosed with the cancer each year.
Lung adenocarcinoma is the most common form of lung cancer and the leading cause of cancer death worldwide. It is associated with a high risk of tumour re-occurrence following surgery and treatments, such as chemotherapy, and has poor overall survival rates. Many patients are given five years to live, or less, when diagnosed.
PhD student Mohamed Saad and Research Group Head Professor Brendan Jenkins have made an important discovery, identifying a drug that slows down tumour growth by targeting an enzyme that makes cancer cells proliferate more rapidly.
Opening up new treatment options
Prof Jenkins said, “We have found a drug that rapidly slows tumour growth, which brings a lot more treatment options to the table. If we can slow down growth, we then open up the possibility that the size of tumours can reduce to a point where surgery could be more effective.
“In lung adenocarcinoma, the diagnosis is often late, progression is rapid, and life-expectancy outlook is very dire. Being able to drastically supress tumour growth gives a lot of hope,” he said.
“While chemotherapy, as well as radiation therapy, reduces the size of tumours in a number of different cancers, when people are diagnosed with lung adenocarcinoma, tumour growth is too advanced for these treatments to be much help.
“And while surgery may be an option for many cancers, it’s often not possible for lung adenocarcinoma as the size of the tumour is too large and has spread to other parts of the body. The implications for this drug, used in combination with other therapies, is very promising.”
A Hudson Institute-led team is exploring the development of the drug in collaboration with colleagues at the Weizmann Institute of Science in Israel and support from Kiel University in Germany. Together they are looking
to improve the drug that they have previously trialled to maximise its activity and stability, and find an easy way to administer it to patients.
Once the drug is ready for market, Prof Jenkins hopes the next stage could be a phase I trial, where the drug is trialled with chemotherapy to assess the extent of impact it could have for patients.
Collaborators: Garvan Institute, Kiel University (Germany), Monash University, Nagoya University (Japan), RMIT University, Weizmann Institute of Science (Israel).
LUNG ADENOCARCINOMA FACTS
Each year, 1.8 million people worldwide are diagnosed with lung cancer. About 85 per cent of the people diagnosed have non-small lung cancer and about 40 per cent of these will have lung adenocarcinoma.
HOW DOES THE DRUG WORK?
The KRAS gene is a common cause of lung adenocarcinoma. When the gene mutates unexpectedly it can lead to the development and spread of cancer cells. For many years, researchers have unsuccessfully tried to find a way to inhibit the KRAS gene to stop it creating cancer cells.
Mohamed Saad and Prof Jenkins took a different approach, and decided not to target KRAS directly. Instead they looked for different interactions with the gene they could control. Mohamed Saad said, “From our research we have found that a particular enzyme, ADAM17, when activated, amplifies the effect of the KRAS gene, causing it to also have greater activity and make more cancer cells. “Based on this finding, we found a drug that reduced the activity of the enzyme ADAM17. This meant the enzyme was no longer putting KRAS in overdrive and telling cancer cells to grow faster than normal. By slowing down KRAS we were able to rapidly reduce tumour growth.” “The drug needs some development before it is ready for patients, and we are working on this now with colleagues in Israel and Germany,” Mr Saad said.