A study reveals that a number of different pathways lead to ovarian cancer, depending on the genes involved.
Mutated versions of the tumour suppressor genes BRCA1 and BRCA2 account for five to ten per cent of all cases of ovarian cancer. But how do these genetic forms of the disease compare to the more common ‘sporadic’ cases (arising for no obvious reason)? Thanks to advances in gene technology, scientists can now analyse differences in gene activity in different kinds of diseased tissue quite readily.
Researchers at the National Cancer Institute have analysed the activity of 6,500 different genes in three groups of women. One group had BRCA1 mutations, another BRCA2 mutations, and the third comprised women with sporadic ovarian cancer. They found 110 gene activities to differ between BRCA1 and BRCA2, suggesting these are two different sub-types of the disease. But these differences were also found within the various sporadic tumours. So there are similarities between genetic and sporadic forms of the disease - some sporadic cases resemble the BRCA1 cases, others the BRCA2 cases.
This takes us a step further towards understanding ovarian cancer at a molecular level. The findings could open up exciting new possibilities for diagnosis and treatment of this disease.
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