52
important strides have been made in skin cancer prevention across several countries,
they have not been sufficient to curb the rising rates of skin cancer incidence.
The increase in harmful UV rays as a consequence of ozone hole expansion is
another key factor responsible for the rise of skin cancer incidence. Numerous
actions have therefore been taken in order to diminish this ozone depletion in the
stratosphere. While the application of the Montreal Protocol has allowed the ozone
hole to reduce and remain stable, no clear data is available regarding a reduction on
the levels of UV rays reaching the Earth’s surface. Moreover, the total reduction of
the ozone hole is expected to happen slowly due to the long half-life of ozone
depleting molecules. The WHO estimates that a 10% decrease in ozone levels will
result in additional 300,000 non-melanoma and 4500 melanoma skin cancer cases.
Beyond the serious consequences for life, skin cancer also represents a huge
problem for public health. It is clear that management of skin cancer exerts a sizable
burden on health systems. Economists in Europe believe that the current growth in
healthcare spending is not sustainable (Gordon and Rowell 2015). Skin cancer prevention programs require exorbitant amounts of money, while diagnostics and treatments are also expensive. In most studies, doctor visits, biopsies, surgical excisions,
therapies, and hospital stays are the major direct treatment costs related to skin
cancers. Although the costs of squamous or basal cell carcinomas per lesion are not
high, the high numbers of cancers being treated produce high aggregate costs
(Gordon and Rowell 2015).
In order to reduce the number of patients reaching advance stages of cancer, and
therefore, reduce the number of fatalities, better diagnosis and prognosis tests are
required. Early detection and treatments can be improved by a better understanding
of the events activated after UV radiation reaches human cells. Particularly relevant
is the field of the DDR after UV radiation as it helps to gain better understanding
regarding the genetic regulation and/or dysregulation which leads to skin cancer.
Research on this field has helped in the development of new biomarkers which can
be identified by modern molecular genetic methods. Until recently these biomarkers
have not been thought to be involved in progression and metastasis of skin tumors
or to be used as prognostic markers (Greinert 2009). Although these new biomarkers predict future and successful tests, some points need to be evaluated in greater
detail. Future research should determine (1) all the lesions generated by UV on the
DNA molecule (e.g., pyrimidine dimers, DSBs, oxidative lesion) and characterize
their role as carcinogenic agents; (2) the different effects of UV-A, UV-B, and UV-C
on the DNA molecule, malignant transformation, and skin tumor development; and
(3) biomarkers of UV exposure on early effects of the skin cancer. Also, it is important to keep in mind that successful implementation of these diagnostic/treatment
tools will depend not only on the basic research but also on the precision value of
the test, the cost, and speed of the assay.
Acknowledgments I would like to thank Dr. Vanesa Gottifredi, Head of the Cell Cycle and
Genomic Stability Laboratory at Leloir Institute, for being an excellent mentor and transmitting
me her knowledge about DNA damage response and UV radiation.
M. B. Federico
important strides have been made in skin cancer prevention across several countries,
they have not been sufficient to curb the rising rates of skin cancer incidence.
The increase in harmful UV rays as a consequence of ozone hole expansion is
another key factor responsible for the rise of skin cancer incidence. Numerous
actions have therefore been taken in order to diminish this ozone depletion in the
stratosphere. While the application of the Montreal Protocol has allowed the ozone
hole to reduce and remain stable, no clear data is available regarding a reduction on
the levels of UV rays reaching the Earth’s surface. Moreover, the total reduction of
the ozone hole is expected to happen slowly due to the long half-life of ozone
depleting molecules. The WHO estimates that a 10% decrease in ozone levels will
result in additional 300,000 non-melanoma and 4500 melanoma skin cancer cases.
Beyond the serious consequences for life, skin cancer also represents a huge
problem for public health. It is clear that management of skin cancer exerts a sizable
burden on health systems. Economists in Europe believe that the current growth in
healthcare spending is not sustainable (Gordon and Rowell 2015). Skin cancer prevention programs require exorbitant amounts of money, while diagnostics and treatments are also expensive. In most studies, doctor visits, biopsies, surgical excisions,
therapies, and hospital stays are the major direct treatment costs related to skin
cancers. Although the costs of squamous or basal cell carcinomas per lesion are not
high, the high numbers of cancers being treated produce high aggregate costs
(Gordon and Rowell 2015).
In order to reduce the number of patients reaching advance stages of cancer, and
therefore, reduce the number of fatalities, better diagnosis and prognosis tests are
required. Early detection and treatments can be improved by a better understanding
of the events activated after UV radiation reaches human cells. Particularly relevant
is the field of the DDR after UV radiation as it helps to gain better understanding
regarding the genetic regulation and/or dysregulation which leads to skin cancer.
Research on this field has helped in the development of new biomarkers which can
be identified by modern molecular genetic methods. Until recently these biomarkers
have not been thought to be involved in progression and metastasis of skin tumors
or to be used as prognostic markers (Greinert 2009). Although these new biomarkers predict future and successful tests, some points need to be evaluated in greater
detail. Future research should determine (1) all the lesions generated by UV on the
DNA molecule (e.g., pyrimidine dimers, DSBs, oxidative lesion) and characterize
their role as carcinogenic agents; (2) the different effects of UV-A, UV-B, and UV-C
on the DNA molecule, malignant transformation, and skin tumor development; and
(3) biomarkers of UV exposure on early effects of the skin cancer. Also, it is important to keep in mind that successful implementation of these diagnostic/treatment
tools will depend not only on the basic research but also on the precision value of
the test, the cost, and speed of the assay.
Acknowledgments I would like to thank Dr. Vanesa Gottifredi, Head of the Cell Cycle and
Genomic Stability Laboratory at Leloir Institute, for being an excellent mentor and transmitting
me her knowledge about DNA damage response and UV radiation.
M. B. Federico