Treating Healthy Cells to Prevent Cancer

On 4-7 November, at the 8th annual National Cancer Research Institute conference in Liverpool, two new strategies were put forward to prevent cancer cells from recruiting healthy cells to help them both grow and spread. The first would prevent the proliferation of surviving tumour cells through the dampening of the immune system post-cancer treatment. The other would stop breast cancer from reaching organs such as the lungs blocking an "accomplice" vital to any such spread.

The former strategy would essentially be implemented on women who have undergone breast cancer treatment previously in order to prevent cancer relapses by reducing the levels of regulatory T-cells (lymphocytes) which suppress the immune system. These cells are known to be more common in women with particularly large and aggressive breast cancers. This additional course would take place after the original treatment and would ideally be fairly cheap, using the relatively non-toxic anti-cancer drug: cyclophosphamide. A study of 35 women indicated that the drug may potentially be effective in preventing the spread of such harmful cells.

Regulatory T-cells (1)

"If you use cyclophosphamide at low doses, you can reduce [numbers of these cells] substantially without affecting other cancer defences,"claims Oleg Eremin of the Queen's Medical Centre at the University of Nottingham. He originally got the idea to use cyclophosphamide by monitoring the levels of regulatory T-cells in women with breast cancer before, during and after treatment. Each of the women had large breast tumours and some had six times the normal level of T-cells. This suggested that the cancer cells somehow ramp up the number of their "accomplices".

Regulatory T-cells (2)

Having shrunk the tumours through chemotherapy, which consisted the implementation of cyclophosphamide and two other drugs, then surgically removing any remaining tumours, Eremin and his team discovered that although the level of regulatory T-cells fell significantly, it was still above normal. Furthermore, they observed that once the chemotherapy had finished, these figures began to creep up again. His hypothesis is that it is the more resistant cancer cells that linger in the body and stimulate the production of the T-cells. Over the next six months or so, it is Eremin's wish to monitor the progress of these same women to see if their regulatory T-cell counts continue to rise. If this proves to be true, it is probably then worth attempting to keep these cells in check and prevent relapses with a second course of cyclophosphamide.

Meanwhile, a team at the Institute of Cancer Research in London, led by Clare Isacke, have made headway in the battle to prevent breast cancer cells from spreading into the lungs, liver and other tissues. The process begins with these cells binding into the surface of blood vessels in the lungs. Isacke has discovered that they can only do this if they are attached to a protein "accomplice" in the blood. It is this binding that can potentially be blocked by drugs.

Isacke also discovered that cancer cells were least invasive if they lacked the surface sugars required for grasping the protein. Blocking the protein, which she will name when she publishes her results in full, might be enough to reduce cancer's spread, and Isacke is confident that drugs can be found that are able to do this. "We'd like to find ways to disrupt this collusion without harming normal interactions between healthy cells," she says.