Current projects approved for access to the 100,000 Genomes Project data set.
Only specific staff within the groups or organisations listed below will have access.
Cancer is a genetic disease. It is caused by changes to DNA that control the way our cells function, especially how they grow and divide. The exact changes affect various characteristics of a tumour. As a cancer grows, new changes occur and a tumour becomes a mix of different cells – or a “population” – all with different characteristics. Find out more about the genetics of cancer.
That’s why we’re looking at cancer in the 100,000 Genomes Project; to understand cancer genomes better and try to improve diagnosis, prognosis and treatment for cancer patients. Read more.
More about cancer
Cancer starts in our cells. Cells are tiny building blocks that make up the organs and tissues of our body. We have about 10 trillion cells in our bodies.
Normally, cells grow and divide to form new cells as the body needs them. When cells grow old or become damaged, they die and new cells take their place. But when cancer develops, this orderly process breaks down. Old or damaged cells survive when they should die, and new cells form when they are not needed. These extra cells can divide without stopping, and may form tumours.
Cancerous tumours are malignant. This means they can spread into, or “invade”, nearby tissues. As tumours grow, some cancer cells can break off and travel to distant places in the body. They can form new tumours far from the original tumour, called metastases.
Research questions in cancer GeCIP domains
The different cancer GeCIP domains will focus on the same questions, tailored to cancer in their particular area.
Subtype identification – can we use the DNA sequence from the tumour, and changes to that DNA, to better classify the tumour type? Can we use this to better identify a tumour, beyond where it is and what the cells look like through a microscope?
Tumour evolution – by looking at changes that have happened in the tumour’s DNA, can we more accurately spot tumours likely to spread and create metastases elsewhere in the body?
Response to treatment – can we identify changes in DNA that are important in determining whether or not the tumour will respond to the standard courses of treatment?
Alternative, ‘off label’ treatment – are there changes to DNA in tumours that mean medicines usually used for a one tumour type, could also be effective in another?
Inherited drivers – are there changes in ‘normal’ DNA that put that person more at risk of cancer in the future?
DNA and Environment interactions – do environmental or lifestyle factors interact with changes in the DNA? Are there changes in the DNA that will only cause cancer if that person is also a heavy smoker, or is exposed to a lot of UV light?