Islamabad-A new research from the University of Southampton in the United Kingdom investigates the way in which cancer takes over certain cell types and uses them as a life support. Finding a way to target these turncoat cells could help to reduce a tumour’s success.

They have also shown that CAFs protect cancer cells from chemotherapy and suppress the immune system’s anti-cancer response.

The relationship between CAF levels and survival could make them a potential target for pharmacological intervention. To date, however, attempts to interact with them have been unsuccessful.

“I think what surprised us was the fact that there is a common mechanism that regulates the formation of CAFs in multiple cancer types. [...] This common mechanism suggests that we can adopt a similar strategy for targeting the cells in different types of cancer.”

Prof Thomas and his team embarked on a new project looking at the potential of a specific enzyme, called NOX4, to interrupt CAFs. This enzyme is essential for the conversion of fibroblasts into CAFs.

The team demonstrated that by blocking NOX4, the size of tumours in mice was reduced by up to 50 per cent.

The drug that blocks NOX4 is currently being developed to treat organ fibrosis, which is a condition characterized by the formation of excessive fibrous connective tissue. If follow-up studies go well, it might be a useful medication to be taken alongside existing cancer treatments.

“By looking at many types of cancer, we have identified a common mechanism responsible for CAF formation in tumours. These cells make cancers aggressive and difficult to treat, and we can see exciting possibilities for targeting CAFs in many patients who don’t respond well to existing therapies.”Prof Thomas informed us that, to date, little is known about CAFs. Although it has been shown that the “myofibroblastic CAF subtype is associated with aggressive cancers,” there are presumably a number of CAF subtypes, all of which could have different functions that need to be unpicked.

Prof Thomas is currently involved in a study involving the collection of cells directly from patients with head and neck cancers; the plan is “to identify different CAF subtypes and examine their similarity between different cancer types.”

Additionally, Prof Thomas talked to MNT about new questions that have opened up about the importance of the immune system in this process. The team found that when tumours have high levels of CAF, there is a significant reduction in immune response.

“This suggests that CAF may be a mechanism by which cancers evade the immune response, an important consideration given the current interest in immunotherapy. Our experiments in murine models have confirmed this, and we have recently shown (unpublished) that targeting CAF through NOX4 inhibition can improve the immune response to anti-cancer vaccination.”

The team is casting its net wide: they are also investigating another enzyme pathway involved in the generation of CAFs alongside NOX4.

Although there is much to learn about CAFs and their role in cancer, the hunt is on and Prof. Thomas and his team are leading from the front. Meanwhile, the results of a Parkinson’s disease clinical trial suggest that the type 2 diabetes drug exenatide may work as a treatment that can slow or even stop the disease. Patients who injected the drug every week for 48 weeks performed better in movement tests than those who injected a placebo.

The difference between the two groups was still detectable 12 weeks after they stopped the injections, according to a report on the trial.

The investigators, led by University College London (UCL) in the United Kingdom, say that the drug was well tolerated and that the encouraging results pave the way for a larger trial to formally test whether or not the drug actually stops nerve cells from dying.

He explains that current treatments for Parkinson’s disease can relieve many of the symptoms, sometimes for years, but they do not stop the disease from getting worse.

Parkinson’s disease is a brain-wasting disorder that primarily attacks a part of the brain known as the substantia nigra. As it progresses, it destroys the neurons, or nerve cells, that make dopamine, which is a chemical messenger important for controlling movement.

The drug exenatide is already licensed for the treatment of type 2 diabetes. It is a synthetic version of a substance that was originally discovered in the saliva of the Gila monster lizard.

In the treatment of diabetes, exenatide stimulates GLP-1 hormone receptors in cells of the pancreas, causing them to produce insulin.

Previous studies have discovered GLP-1 receptors in the brain, and laboratory tests have also shown that activating them produces a number of changes that might be useful for treating Parkinson’s disease. These effects include an increase in dopamine connections, improvement in energy production, reduced inflammation, and switching on of survival signals in nerve cells.

Prof Foltynie and colleagues also refer to studies of animal models of Parkinson’s disease that have shown that exenatide can cross the blood-brain barrier.