Glioblastoma is the most common high grade (cancerous) primary brain tumour in adults. Glioblastoma belongs to a group of brain tumours known as gliomas as it grows from a type of brain cell called a glial cell.

Glioblastomas are grade 4, as they are fast growing and likely to spread.

There are different types of glioblastoma:

  • Primary - this means the tumour originated in the brain instead of spreading from elsewhere (its first appearance was as a grade 4 glioblastoma (GBM))
  • Secondary - this means the tumour developed from a lower grade astrocytoma

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What causes glioblastoma?

There is nothing you could have done, or avoided doing, that would have prevented you from developing a brain tumour.

As with most brain tumours, the cause of glioblastoma is not known. The Brain Tumour Charity is funding research into possible causes, focussed around our genes.

How brain tumours are formed

Our genes control the way our cells grow and divide. Mutations (changes) in our genes can cause this process to go wrong, resulting in the cells growing uncontrollably and forming a tumour. These changes are often the result of a mistake being made when the cell copies its DNA before dividing.

These changes are known as 'biomarkers'. Research, including that funded by The Brain Tumour Charity, is gradually discovering which genes are involved in which tumours.

These biomarkers are starting to be used (and may be able to be used more accurately in the future) to predict how people may respond to certain treatments and also the length of their overall survival (prognosis).

Learn more about how and why brain tumours form.

How are glioblastomas treated?

The best treatment currently is surgery to remove as much of the tumour as possible, followed by chemoradiation. This is a combination of chemotherapy and radiotherapy.

Glioblastoma, however, are 'diffuse', meaning they have threadlike tendrils that extend into other parts of the brain making it difficult to remove it all. The chemoradiation is needed to target those cells which cannot be removed by surgery.

Generally it involves radiotherapy given over a period of weeks alongside rounds of the chemotherapy drug temozolomide (TMZ). TMZ is also usually taken for a further 6 months after the radiotherapy has finished.

Read more about treatments for brain tumours.

Effectiveness of treatment

Unfortunately glioblastomas are aggressive tumours and often appear resistant to treatment. This is probably due to the fact that the cells within the tumour are not all of the same type. This is known as 'heterogeneity'. This means that certain treatments will kill off certain types of glioblastoma cell but leave the others.

However, some of the research into the genes, which play a role in glioblastoma (GBM) development, are starting to give us information about who may respond better to certain treatments. For example biomarker tests, such as:

  • MGMT gene methylation test

This shows how likely you are to respond to temozolomide.

  • Mutations in the IDH-1 and TERT gene

These mutations are associated with effects on overall survival.

Many centres routinely test for these gene mutations, but if your hospital does not and you would like to have a test, ask your neuro-oncologist for information and advice about whether you are suitable.

Research is ongoing to find the keys to tumour progression in glioblastomas.

What is the prognosis?

Information about prognosis can be difficult to receive - some people do not want to know, whilst others do. There is no wrong or right answer as to whether or when to receive such information. If you would like information about prognosis, please see our brain tumour prognosis page.

Support and information

We've here to help you cope with a brain tumour diagnosis.

Visit our Living with a brain tumour pages for information on side-effects, managing finances and caring for someone with a brain tumour.

For details of our telephone support line and peer-to-peer support groups, please see our brain tumour support hub.

Page last reviewed: 01/2015
Next review due: 01/2018

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