Scientists from the Wellcome Trust Sanger Institute, UK, where one-third of the human genome was sequenced, have studied more than 500 genes in over 200 cancers. The results of the Cancer Genome Project reveal mutations in 120 genes that could cause cancer, most of which not been encountered previously.

Analysing the human genome to determine the specific genes that contribute towards the development of cancer is a crucial step towards developing new, targeted therapies to combat the disease.

The need for more cancer treatments was highlighted when, last month, the World Health Organization's Cancer Research Agency revealed that cases of cancer are on the rise. Last year in Europe alone, there were 3.2m new cases of the disease - up 10 per cent from 2005 - resulting in 1.7m deaths.

"The human genome is a vast place and this, our first deep systematic exploration in cancer, has thrown up many surprises," said Professor Mike Stratton, co-leader of the Cancer Genome Project.

"We have found a much larger number of mutated driver genes produced by a wider range of forces than we expected."

The mutations found in cancers can be divided into two types. 'Driver' mutations are the ones that actually cause cancer whereas 'passenger' mutations don't affect the development of the disease.

"It turns out that most mutations in cancers are passengers," explained Dr Andy Futreal, co-leader of the Cancer Genome Project.

"However, buried amongst them are much larger numbers of driver mutations than was previously anticipated. This suggests that many more genes contribute to cancer development than was thought."

The team studied kinase genes - many of which are already popular targets for anticancer drug development. For example, the pilot of this project found that the BRAF gene is mutated in around 70 per cent of malignant melanomas and 10 per cent of colon cancers. Most of the mutations involved the same letter of DNA code and several pharma companies have since developed drugs to exploit the observation. The new research sheds further light on this group of genes.

"We found that a group of kinases involved in the Fibroblast Growth Factor Receptor signalling pathway was hit much more than we expected, particularly in colorectal cancers," said Dr Futreal.

The type of mutation varies between different cancers, depending on what caused the defect. Deciphering the patterns of mutations

The trick will be to decipher which mutations are drivers and which are just along for the ride. To do this, scientists may have to analyse many more genes for each cancer type. New DNA sequencing technology could play an important role in this.

"The time is right to apply the powerful tools of genomics to obtain a comprehensive view of what goes wrong at the DNA level in cancer," said Dr Francis Collins, director of the National Human Genome Research Institute at the US National Institutes of Health.

"The important and interesting data on protein kinases...further encourages the conclusion that a full assault on the cancer genome will yield many opportunities to revolutionise diagnosis and treatment."