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New research helps detect ovarian cancer earlier; offers personalised treatment

Ovarian cancer is widely known as the ‘silent cancer’ as in most cases, there are no symptoms until the condition has progressed to an advanced stage.

Over 7,000 women are diagnosed with cancer each year in the UK, so new research which has revealed new methods and clues to early detection of the disease, as well as personalised treatments, can offer hope to millions of women who are susceptible to ovarian cancer or those who are already suffering from it.

The A*STAR Institute of Medical Biology (IMB) and the Bioinformatics Institute have identified a naturally-occurring molecule known as Lgr5 within ovarian stem cells. With this presence of the molecule, experts are optimistic that ovarian cancers could be detected early.

The molecule Lgr5 is usually present on the ovarian surface and is part of an important subset of tissue which control the development of the ovary – something which would contribute to the development of cancerous cells within the organ. The presence of Lgr5 within a patient is a significant sign of ovarian cancer.

Using previously sourced information on cancer genomes, scientists identified a specific set of genes and their mutational status which can be used for prognosis and the development of personalised treatment for high-grade serous ovarian carcinoma.

One gene, Checkpoint Kinase 2 (CHEK2) has been identified as an effective prognostic marker of patient survival. The main role of this gene if to act as a tumour suppressor and keep the uncontrolled growth of cancer cells in check, so if it is present within an ovarian cancer patient, the patient is more likely to have an increased chance of survival. However, in some people, the CHEK2 gene is slightly mutated, meaning that should they develop ovarian cancer, their chances of survival are not as increased as those with the ‘normal’ CHEK 2 genome.

Patients with Lgr5 may be susceptible or already suffering from the effects of ovarian cancer, but if they have the fully-functioning CHEK2 gene, they have a better chance of survival.

Due to the effectiveness of the CHEK2 gene in suppressing ovarian tumours, it’s likely that it will become the object of many studies in the future. If scientists can develop a treatment which can help the mutated forms of the CHEK 2 gene produce the effects of a ‘normal’ CHEK 2 gene, then ovarian cancer survival rates could be set to dramatically increase.

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