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Content archived on 2023-03-09

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EU-funded scientists uncover gene that causes spread of skin cancer

A new EU-funded study has pinpointed the specific gene that must be present before malignant melanoma, the most dangerous form of skin cancer, can spread. The gene P-Rex1 causes cancer cells to break away from the original tumour and spread or metastasise to other organs like ...

A new EU-funded study has pinpointed the specific gene that must be present before malignant melanoma, the most dangerous form of skin cancer, can spread. The gene P-Rex1 causes cancer cells to break away from the original tumour and spread or metastasise to other organs like the brain, something which can cause them to fail. Cancer's ability to metastasise is what makes it so dangerous, so understanding what triggers metastatic behaviour is vital for furthering our knowledge of the disease and reducing high death rates. Although survival rates have been on the up over the past 25 years and are now amongst the highest for any cancer, malignant melanoma still causes around 46 000 deaths worldwide each year, and it is particularly prevalent in young people: in the United Kingdom, for instance, at least two young adults are diagnosed with the disease every day. EU funding for the study came in the form of a Marie Curie Industry-Academia Partnership and Pathway grant, as part of the 'People' Theme of the Seventh Framework Programme (FP7). The aim of the Marie Curie Industry-Academia Partnerships and Pathways programme is to boost skills exchange between the commercial and non-commercial sectors working on joint research projects. With contributions from researchers hailing from a variety of different institutions in Canada, France, Ireland, Switzerland, the United Kingdom and the United States, the findings from this new study, published in the journal Nature Communications, could play an important part in this fight against malignant melanoma. The team found that the gene P-Rex1 plays a key role in the spread of malignant melanoma in mice samples. The researchers observed that if P-Rex1 was absent from cells, the melanoma tumours were unable to spread. After further investigation, they worked out the exact mechanism that P-Rex1 uses to drive metastasis. Their results were confirmed when they found that in human melanoma samples taken from patients' tumours, raised levels of P-Rex1 were present. Lead study author Professor Owen Sansom from the Beatson Institute for Cancer Research in Glasgow, United Kingdom comments: '... P-Rex1 is not present in most other normal human cell types, pointing up its suitability as a gene to be 'switched off' with chemotherapeutic drugs, as there are unlikely to be any unwanted side effects on nearby healthy cells. As malignant melanoma is resistant to many forms of chemotherapy, these findings are encouraging. Earlier studies using cancer cell lines implicated P-Rex1 in prostate, breast and ovarian cancer, but this is the first time it has been shown to be involved in the metastasis of melanoma in mice models as well as being present at high levels in human tumours and cell lines where it drives invasion into surrounding tissue.' Dr Lara Bennett, scientific communications manager for the cancer charity Association for International Cancer Research (AICR), which also provided funding for the study, expressed her delight at the discovery: the results will act as a building block towards future treatments. She remarked: 'Although it is early days and more research is needed, if drugs could be designed to block the effects of P-Rex1, melanoma could be prevented from metastasising. This would ensure it remained on the surface of the skin where it could easily be removed through surgery, leading to higher survival rates. If malignant melanoma is caught sufficiently early - while still only a very thin tumour in the top layers of the skin - survival rates are much higher.'For more information, please visit:Beatson Institute for Cancer Research:http://www.beatson.gla.ac.uk/

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Canada, Switzerland, France, Ireland, United Kingdom, United States

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