Advances in basic research
Basic research is the study of how cells work. Scientists who carry out basic research don’t focus on finding a new treatment for disease or developing a new drug. Instead, they want to understand what makes cancer cells different from normal cells. Find out more about 'basic research'.
The cell cycle
Their discoveries have greatly enhanced our understanding of how cells grow and divide, and how this is regulated. This knowledge may lead to new ways of preventing the growth and proliferation of cancer cells and should open up new possibilities for cancer therapy.
The p53 gene
In 1979, Professor Sir David Lane, who has been funded by the charities for over 25 years, co-discovered a gene called p53. This is one of the most important genes involved in the development of cancer; it is damaged or inactive in the vast majority of cancers.
His work is now moving from the laboratory into the clinic as his team develops ways to repair or reactivate the faulty copy of the p53 gene in the tumours of patients.
The APC gene
In the mid-1980s, scientists Sir Walter Bodmer and Professor Ellen Solomon located an extremely important gene called APC. Faults in this gene are known to cause an inherited syndrome that dramatically increases a person’s risk of bowel cancer. The gene is also known to be involved in the development of bowel cancer in the general population.
This work has huge implications for the prevention and early detection of bowel cancer.
The RET gene
In 1993, Professor Bruce Ponder and Dr Lois Mulligan in Cambridge were the first to identify a gene, called RET, responsible for an inherited form of thyroid cancer known as ‘multiple endocrine neoplasia 2A’. This was the first discovery of a dominant mutation that causes cancer in individuals who carry it.
The BRCA breast cancer susceptibility genes
In 1993, Professor Doug Easton in Cambridge headed an international team of researchers who showed that the inherited breast cancer susceptibility gene, BRCA1, was responsible for the vast majority of families with multiple cases of breast and ovarian cancer, and a large proportion of those families with breast cancer only.
In 1995, a team led by Professor Mike Stratton at the Institute of Cancer Research identified and isolated a second breast cancer susceptibility gene, BRCA2. The gene is associated with a substantially increased risk of female breast cancer as well as an increased risk of ovarian, prostate and male breast cancer.
This research paved the way for the development of tests that detect faults in the BRCA1 and BRCA2 genes. This allows doctors to identify high-risk individuals and help them, by referring them for counselling and regular screening, and by providing advice about prevention.
Telomerase
In 1997, Cancer Research UK scientist Dr Nicol Keith and colleagues were the first to locate a gene called hTERC, which makes up part of a protein called telomerase. This protein helps regulate cell ageing and appears to be involved in cancer cell immortality. Telomerase is active in over 80% of cancers but is switched off in normal tissues. This important discovery could lead to new treatments for a wide variety of cancers, including lung, bowel and breast cancer.
The CHEK2 gene
In April 2003, Professor Stratton and Professor Easton, in collaboration with researchers in Rotterdam, showed that inheriting a damaged version of a gene called CHEK2 nearly doubles a woman’s risk of developing breast cancer. The faulty gene also substantially increases men’s risk of the disease. Screening high-risk individuals could help save lives, while understanding the genetic causes of the disease is vital for developing new treatments.
The EMSY gene
In late 2003, Dr Luke Hughes-Davies and colleagues in Cambridge discovered a new gene linked to breast and ovarian cancer. This discovery provided a ‘missing link’ in an enduring medical mystery. The gene, which they named EMSY, finally joins the dots between the inherited susceptibility to breast cancer and the sporadic cases, where there is no family history of the disease.
While inheriting faulty BRCA genes can trigger breast and ovarian cancers, no one could find a role for these genes within sporadic tumours. But the team discovered that EMSY shuts down the action of functional BRCA2, thus fuelling a cancer’s development. It is not only a key advance in understanding how and why cancers develop, but may pave the way for new tests to predict how the disease may progress.
The E2F3 gene
In June 2004, Cancer Research UK scientists in London, led by Professor Colin Cooper, identified a gene which could help doctors identify how aggressive a man's prostate cancer is. One of the key issues in prostate cancer care is how to treat men once they have been diagnosed with the disease.
Many men‘s prostate cancers grow so slowly that they will probably die of other causes, but other prostate cancers can grow very quickly. Until now, doctors had no way to distinguish between these two types, and this often led to men receiving treatment they did not need. Professor Cooper's team discovered that the E2F3 gene is more active in aggressive prostate cancers. This paves the way for a test that may allow doctors to diagnose and treat men more accurately in the future.
