High-factor sunscreen doesn’t cut melanoma risk “High-factor sun cream cannot…protect against the deadliest form of skin cancer,” The Guardian reports. Research involving mice with a predisposition to develop melanoma found that sunscreen only delayed, rather than prevented, the onset of melanoma.
Malignant melanoma occurs when cells that produce melanin – pigment that darkens the skin – rapidly divide and grow uncontrollably.
A mutation in a gene crucial for cell growth, BRAF, has been found in several cancers, including around half of melanoma cases. Mice in this study were given this mutation, and all of them developed melanoma when exposed to UV light.
Sunscreen factor 50 delayed the onset and reduced the number of tumours, but did not prevent melanoma.
The study also found that in the mice with the BRAF mutation, UV light damaged another part of the DNA that stops cells dividing too rapidly – tumour suppressor genes called TP53. Sunscreen did not prevent this damage, which means that the cells could grow unchecked.
Mutations in the BRAF gene found in melanomas are not the inherited type, and in humans may be caused by UV exposure and other environmental factors.
It should not be interpreted from this study that sunscreen is useless, but you cannot rely on it solely, especially if you have risk factors for melanoma, such as pale skin and having lots of moles.
Sunscreen should be used in combination with other preventative methods, such as wearing appropriate clothing when the sun is at its hottest.
Where did the story come from?
The study was carried out by researchers from the University of Manchester, the Institute of Cancer Research and the Royal Surrey County Hospital. It was funded by Cancer Research UK, the Wenner-Gren Foundations and a FEBS Long-Term Fellowship.
The study was published in the peer-reviewed medical journal Nature.
It was accurately covered in the UK media, with many news sources including useful quotes from independent experts about the research's implications.
What kind of research was this?
This was a laboratory study that used mice to look at how effective sunscreen is at reducing the risk of developing melanoma, following exposure to UV light.
Melanoma is the most malignant form of skin cancer. It is the fifth most common cancer in the UK, with 13,348 new cases occurring each year, according to figures from 2011.
Melanoma occurs when melanocytes grow uncontrollably. These are the cells that produce the protective pigment melanin, which gives skin its colour. People with darker skin have more active melanocytes, which transfer more melanin to other cells to protect them from UV light.
A mutation in the BRAF gene that regulates growth and division of cells has been found in melanoma. It is known as an “oncogene”, as it can cause normal cells to become cancerous if it has a mutation. Several different BRAF gene mutations have been found in melanoma and some cancers of the colon, rectal, ovary and thyroid.
It is not known how UV light causes melanoma, but an abnormal BRAF gene has commonly been found at an early stage in the development of melanoma. The researchers wanted to study the process, so used mice that had this particular BRAF gene mutation (called BRAF [V600E]).
Another gene, tumour protein 53 (TP53), makes a protein called tumour suppressor 53 (Trp53) that stops cells dividing too rapidly or uncontrollably. If there is a mutation in this gene, there is no safety check and the cells can grow and multiply unchecked, causing a tumour. Trp53 has been implicated in non-melanoma skin cancer, but was not thought to be involved in melanoma.
What did the research involve?
Mice with the BRAF gene mutation in their melanocytes were used in a variety of experiments and compared to mice without the BRAF mutation.
The backs of the mice were shaved and one half was protected with a cloth.
Newborn mice were given a single exposure to UV light at a dose that would mimic mild sunburn in humans. Those also given the BRAF mutation were compared to those without.
Adolescent mice were given the BRAF mutation and then either:
not exposed to UV light
given weekly exposure to UV light for up to six months
repeated exposure to UV light 30 minutes after sunscreen factor 50 had been applied
What were the basic results?
The newborn mice given the BRAF mutation developed melanoma. This was found to be due to the inflammatory response of the skin.
In the adolescent mice given the BRAF mutation:
melanoma occurred in 70% of the mice with no UV exposure after about 12.6 months. They had, on average, 0.9 tumours (this somewhat unusual average is due to the fact that some mice had no tumours – much like the famous example of 2.4 children)
all mice developed melanoma after repeated UV exposure within 7 months. They had, on average, 3.5 tumours each; 98% of them were on the skin exposed to the UV light
all mice given sunscreen developed melanoma within 15 months. They had, on average, 1.5 tumours each, and were more common on the sunscreen-protected skin than the cloth-protected skin
Mice without the BRAF gene mutation did not develop melanoma after exposure to UV rays.
UV light caused damage to the DNA. This was evidenced by finding mutations in the Trp53 tumour suppressor protein in 40% of cases. These mutant Trp53 proteins increased the BRAF-driven growth of the melanoma.
How did the researchers interpret the results?
The researchers conclude that this study reveals “two UVR melanoma pathways: one driven by inflammation in neonates and one driven by UVR-induced mutations in adults”. They also found that “sunscreen (UVA superior, UVB sun protective factor [SPF] 50) delayed the onset of UVR-driven melanoma, but only provided partial protection”. They “advocate combining it with other sun avoidance strategies, particularly in at-risk individuals with BRAF-mutant naevi [moles]”.
Conclusion
This study found that in mice given the BRAF mutation, sunscreen did not prevent them from developing melanoma, although it did delay it and reduce the number of tumours. The mechanism for this appears to include damage to a tumour suppressor gene, TP53, which has previously been implicated in other skin cancers. Sunscreen did not prevent mutations occurring in this gene, but did reduce the number of mutations.
The study's authors accepte that sunscreen protects against squamous cell carcinoma – a type of skin cancer – but that there was uncertainty around its ability to protect against malignant melanoma – a second type of skin cancer. This study indicated that sunscreen did reduce the risk of developing melanoma in the mice, but that protection was not 100%. These preliminary findings in mice will need to be confirmed in humans for the results to be more credible and reliable.
These results were applicable only to those with an existing mutation in the BRAF gene. Mutations in the BRAF gene can be inherited, but these are not thought to be linked to skin cancers. Acquired mutations in the BRAF gene do increase the risk of melanoma, and can be present in moles. These people have a heightened risk of skin cancer. The complication that arises from this is that UV light might cause this mutation, setting off a cycle of cell and DNA damage, leading to cancer. This means that overexposure to the sun still increases your risk of skin cancer risk factors, whether you have the mutation or not.
People with known risk factors for melanoma should use high-factor sunscreen in combination with other preventative methods, such as wearing appropriate clothing and staying in the shade when the sun is at its hottest (between 11am and 3pm). If you are desperate for a tan, fake is the best way to go.
Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter. Join theHealthy Evidence forum.
Links To The Headlines
High-factor sunscreen cannot give complete protection against skin cancer. The Guardian, June 12 2014
Skin cancer: Sunscreen 'not complete protection'. BBC News, June 11 2014
Wearing sunscreen may NOT prevent skin cancer, study claims. Mail Online, June 12 2014
Sunscreen does not protect against deadliest skin cancer. The Daily Telegraph, June 12 2014
Links To Science
Viros A, Sanchez-Laorden B, Pedersen M, et al. Ultraviolet radiation accelerates BRAF-driven melanomagenesis by targeting TP53. Nature. Published online June 11 2014
Malignant melanoma occurs when cells that produce melanin – pigment that darkens the skin – rapidly divide and grow uncontrollably.
A mutation in a gene crucial for cell growth, BRAF, has been found in several cancers, including around half of melanoma cases. Mice in this study were given this mutation, and all of them developed melanoma when exposed to UV light.
Sunscreen factor 50 delayed the onset and reduced the number of tumours, but did not prevent melanoma.
The study also found that in the mice with the BRAF mutation, UV light damaged another part of the DNA that stops cells dividing too rapidly – tumour suppressor genes called TP53. Sunscreen did not prevent this damage, which means that the cells could grow unchecked.
Mutations in the BRAF gene found in melanomas are not the inherited type, and in humans may be caused by UV exposure and other environmental factors.
It should not be interpreted from this study that sunscreen is useless, but you cannot rely on it solely, especially if you have risk factors for melanoma, such as pale skin and having lots of moles.
Sunscreen should be used in combination with other preventative methods, such as wearing appropriate clothing when the sun is at its hottest.
Where did the story come from?
The study was carried out by researchers from the University of Manchester, the Institute of Cancer Research and the Royal Surrey County Hospital. It was funded by Cancer Research UK, the Wenner-Gren Foundations and a FEBS Long-Term Fellowship.
The study was published in the peer-reviewed medical journal Nature.
It was accurately covered in the UK media, with many news sources including useful quotes from independent experts about the research's implications.
What kind of research was this?
This was a laboratory study that used mice to look at how effective sunscreen is at reducing the risk of developing melanoma, following exposure to UV light.
Melanoma is the most malignant form of skin cancer. It is the fifth most common cancer in the UK, with 13,348 new cases occurring each year, according to figures from 2011.
Melanoma occurs when melanocytes grow uncontrollably. These are the cells that produce the protective pigment melanin, which gives skin its colour. People with darker skin have more active melanocytes, which transfer more melanin to other cells to protect them from UV light.
A mutation in the BRAF gene that regulates growth and division of cells has been found in melanoma. It is known as an “oncogene”, as it can cause normal cells to become cancerous if it has a mutation. Several different BRAF gene mutations have been found in melanoma and some cancers of the colon, rectal, ovary and thyroid.
It is not known how UV light causes melanoma, but an abnormal BRAF gene has commonly been found at an early stage in the development of melanoma. The researchers wanted to study the process, so used mice that had this particular BRAF gene mutation (called BRAF [V600E]).
Another gene, tumour protein 53 (TP53), makes a protein called tumour suppressor 53 (Trp53) that stops cells dividing too rapidly or uncontrollably. If there is a mutation in this gene, there is no safety check and the cells can grow and multiply unchecked, causing a tumour. Trp53 has been implicated in non-melanoma skin cancer, but was not thought to be involved in melanoma.
What did the research involve?
Mice with the BRAF gene mutation in their melanocytes were used in a variety of experiments and compared to mice without the BRAF mutation.
The backs of the mice were shaved and one half was protected with a cloth.
Newborn mice were given a single exposure to UV light at a dose that would mimic mild sunburn in humans. Those also given the BRAF mutation were compared to those without.
Adolescent mice were given the BRAF mutation and then either:
not exposed to UV light
given weekly exposure to UV light for up to six months
repeated exposure to UV light 30 minutes after sunscreen factor 50 had been applied
What were the basic results?
The newborn mice given the BRAF mutation developed melanoma. This was found to be due to the inflammatory response of the skin.
In the adolescent mice given the BRAF mutation:
melanoma occurred in 70% of the mice with no UV exposure after about 12.6 months. They had, on average, 0.9 tumours (this somewhat unusual average is due to the fact that some mice had no tumours – much like the famous example of 2.4 children)
all mice developed melanoma after repeated UV exposure within 7 months. They had, on average, 3.5 tumours each; 98% of them were on the skin exposed to the UV light
all mice given sunscreen developed melanoma within 15 months. They had, on average, 1.5 tumours each, and were more common on the sunscreen-protected skin than the cloth-protected skin
Mice without the BRAF gene mutation did not develop melanoma after exposure to UV rays.
UV light caused damage to the DNA. This was evidenced by finding mutations in the Trp53 tumour suppressor protein in 40% of cases. These mutant Trp53 proteins increased the BRAF-driven growth of the melanoma.
How did the researchers interpret the results?
The researchers conclude that this study reveals “two UVR melanoma pathways: one driven by inflammation in neonates and one driven by UVR-induced mutations in adults”. They also found that “sunscreen (UVA superior, UVB sun protective factor [SPF] 50) delayed the onset of UVR-driven melanoma, but only provided partial protection”. They “advocate combining it with other sun avoidance strategies, particularly in at-risk individuals with BRAF-mutant naevi [moles]”.
Conclusion
This study found that in mice given the BRAF mutation, sunscreen did not prevent them from developing melanoma, although it did delay it and reduce the number of tumours. The mechanism for this appears to include damage to a tumour suppressor gene, TP53, which has previously been implicated in other skin cancers. Sunscreen did not prevent mutations occurring in this gene, but did reduce the number of mutations.
The study's authors accepte that sunscreen protects against squamous cell carcinoma – a type of skin cancer – but that there was uncertainty around its ability to protect against malignant melanoma – a second type of skin cancer. This study indicated that sunscreen did reduce the risk of developing melanoma in the mice, but that protection was not 100%. These preliminary findings in mice will need to be confirmed in humans for the results to be more credible and reliable.
These results were applicable only to those with an existing mutation in the BRAF gene. Mutations in the BRAF gene can be inherited, but these are not thought to be linked to skin cancers. Acquired mutations in the BRAF gene do increase the risk of melanoma, and can be present in moles. These people have a heightened risk of skin cancer. The complication that arises from this is that UV light might cause this mutation, setting off a cycle of cell and DNA damage, leading to cancer. This means that overexposure to the sun still increases your risk of skin cancer risk factors, whether you have the mutation or not.
People with known risk factors for melanoma should use high-factor sunscreen in combination with other preventative methods, such as wearing appropriate clothing and staying in the shade when the sun is at its hottest (between 11am and 3pm). If you are desperate for a tan, fake is the best way to go.
Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter. Join theHealthy Evidence forum.
Links To The Headlines
High-factor sunscreen cannot give complete protection against skin cancer. The Guardian, June 12 2014
Skin cancer: Sunscreen 'not complete protection'. BBC News, June 11 2014
Wearing sunscreen may NOT prevent skin cancer, study claims. Mail Online, June 12 2014
Sunscreen does not protect against deadliest skin cancer. The Daily Telegraph, June 12 2014
Links To Science
Viros A, Sanchez-Laorden B, Pedersen M, et al. Ultraviolet radiation accelerates BRAF-driven melanomagenesis by targeting TP53. Nature. Published online June 11 2014
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