Chemotherapy for brain tumours

5 min read

How does chemotherapy work for brain tumours?

Chemotherapy drugs attack cancer cells that are actively dividing, usually by damaging the RNA or DNA that contains the instructions that enable cells to copy themselves and multiply. This causes the cells to stop growing and ultimately to die. A cell division process that has become faulty is what enables tumours to grow in an uncontrolled way and forms the definition of cancer, which is why chemotherapy drugs are designed to attack this process.

Why does chemotherapy give you side effects?

Chemotherapy drugs cannot identify the difference between a cancer cell and a healthy cell, but healthy cells can repair the damage caused by the drug and recover, whilst the tumour cells are unable to do this. This is why you can experience side effects when taking the chemotherapy drug, but given time to recover, those side effects tend to improve.

A lot of research including the pioneering work funded by us at our UK Centres of Excellence is focused on developing a new generation of drugs, designed to attack only the cancer cells. The aim is to reduce and potentially avoid the current side effects of chemotherapy drug based cancer treatment.

When is chemotherapy used for brain tumours?

Sometimes chemotherapy is used alone to treat some forms of brain tumour, but it is more commonly used after surgery and/or radiotherapy has reduced the size of the tumour. Not all brain tumours will respond positively to chemotherapy, which is why it is only offered when there has been evidence in a clinical trial to prove that it is worthwhile undergoing the treatment.

What is PCV triple therapy?

'PCV triple therapy’ is a combination of procarbazine, CCNU (lomustine) and vincristine. Procarbazine and lomustine are given in capsule form, whilst vincristine is given via a drip into a vein in your arm during a hospital appointment.

How is PCV therapy administered for brain tumour patients?

PCV is given as up to 6 cycles of treatment, with each cycle lasting about 6 weeks.

On the first day of each cycle the patient attends hospital in order to have vincristine administered via a drip into a vein in their arm. The actual infusion only takes a few minutes. Lomustine and vincristine are given as capsules once on the first day. Procarbazine capsules are then taken once a day for a total of 10 days, then nothing is taken for the rest of the six weeks, until the process is repeated.

The number of cycles administered depends on how the patient responds to the treatment, which is closely monitored via blood tests and scans.

How does Temozolomide work in brain tumours?

Temozolomide is usually taken in capsule form at home, although it can also be infused intravenously. Intravenous means that it is given directly into a vein, so that it can be carried in the bloodstream to the site of the cancer. An infusion means that the drug is given slowly over time: for example, 90 minutes.

Temozolomide is converted into its anti-cancer form by your body’s metabolism. Temozolomide is an “alkylating agent”, meaning that it affects the ability of a cell to replicate itself by affecting its DNA, and it acts when the cell is during a resting phase rather than when it is actively dividing. This is why it is given in multiple cycles, to ensure that it affects all of the cells in your tumour as they go through their natural cyles of resting and activity.

What are Gliadel Wafers (Carmustine)?

Gliadel Wafers contain the chemotherapy drug Carmustine. They are approved for use in the UK for patients with newly diagnosed high-grade malignant glioma, and for those with glioblastoma multiforme (GBM) that has recurred after treatment.

How does Avastin work in brain tumours?

Avastin is the trade name of the drug Bevacizumab. It works by binding to a protein called vascular endothelial growth factor (VEGF) that stimulates tumour blood vessel growth.

This process of growing new blood vessels around a cancer is known as angiogenesis  and a brain tumour is dependent upon angiogenesis in order to draw more nutrients into itself via the increased blood supply, giving it the energy it needs in order to grow.

Drugs such as Avastin that block angiogenic signals can potentially help to halt tumour growth. However, side effects are often an issue because such drugs can also affect the growth of new blood vessels required by healthy cells in the body.

Avastin is a type of monoclonal antibody drug currently used in the UK for glioblastoma multiforme (GBM) brain tumours.

Monoclonal antibodies (MABs) for brain tumours

Monoclonal antibodies (MABs) are drugs that can specifically target tumour cells, and allow recognition and destruction of that cell by the immune system. However because they don’t directly stimulate an increased immune response, they are not usually classed as a form of immunotherapy.

These drugs consist of copies of a particular antibody that is designed to target a specific protein found on cancer cells.

Monoclonal antibodies are used to treat many diseases, including some types of cancer. To make a monoclonal antibody, researchers first have to identify the right antigen to attack.

Much of the research in brain tumours is focused on antigens that mark cells involved in particular signalling pathways: named because these are pathways of molecules that work together to give certain signals to cancer cells that enable them to grow. These pathways are promoting cancer rather than healthy cell function because an aspect of their molecular structure is changed (mutated) at some point in their development, so if a monoclonal antibody can block a mutated molecule’s function, it can stop it from continuing along its destructive path.

How do monoclonal antibodies (MABs) work in brain tumours?

After being made in a laboratory, monoclonal antibodies (MABs) are injected into the patient so that the antibodies can circulate in the bloodstream until they find and then stick to the specific target on the cancer cells. Once attached to the antigen they can alert the immune system to the fact that the cells are a danger, and recruit other cells of the immune system to destroy the cells that they have “highlighted”.

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