42
incidence rate of melanoma for women (Moan and Dahlback 1992). The difference
between the numbers for men and women is almost significant and may be related
to the different intermittent exposure pattern to sunlight between the two sexes.
Getting a sunburn just once every 2 years can triple the risk of melanoma (Dennis
et al. 2008). Moreover, sunburn during childhood or adolescence can increase the
risk of skin cancer later on in life (Dennis et al. 2008; Gandini et al. 2005).
Extensive research using animal models has revealed a more active role of UV-B
in the induction of skin cancer than UV-A (Roy 2017). Although solar UV exposure
is known to be associated with several health problems beyond tumor generation
(e.g., accelerated skin aging, eye diseases, and a defective immune response), this
chapter will focus on the relationship between UV rays and cancer.
4.2.1.3 Skin Cancer: UV Radiation as a Mutagenic and Carcinogenic
Agent
The deoxyribonucleic acid molecule, better known as DNA, is a critical target for
UV radiation damage. DNA is a central component of all living organisms as it is
the genetic material responsible for guiding cell functions. DNA duplication is necessary to transfer the genetic information from the mother cell to its progeny, which
means this molecule must remain unaltered to allow next cell generations to preserve the information as accurately as possible. Unfortunately, there are several
DNA damaging agents which cause DNA lesions; these DNA damaging agents
include UV radiation which can generate 100,000 DNA lesions per cell per day
when exposed to peak hour sunlight (Ciccia and Elledge 2010).
The outcomes of DNA lesions differ according to their type, relative position in
the DNA molecule, and their quantity, but most are eventually repaired by one of the
multiple DNA repair mechanisms. However, damaged DNA is not always repaired
as DNA repair mechanisms are often inefficient or saturated. If a lesion goes unrepaired, it could change the DNA’s sequence in a permanent way, which results in a
mutation. The sources responsible for the generation of mutations, such as UV radiation, are called mutagenic agents (Ikehata and Ono 2011). UV radiation as a mutagenic agent has been broadly investigated, and the lesions generated by UV radiation
on the DNA molecule will be explained in detail within Sect. 4.2.2.1. UV rays are
also classified as carcinogenic agent, i.e., they promote cancer due to the transformation of a normal cell to a cancerous cell. The International Agency for Research on
Cancer (IARC) has extensively analyzed the carcinogenicity of UV and concluded:
“There is sufficient evidence in humans for the carcinogenicity of solar radiation.
Solar radiation causes cutaneous melanoma and non-melanocytic skin cancer.” The
increased rates of skin cancer in patients with xeroderma pigmentosum, who have a
deficiency in their capacity to repair UV-induced DNA damage, suggests that direct
UV DNA damage may be one of the key steps in the causation of these cancers
(World Health Organization 1995). Cancer’s development is a complex multistage
M. B. Federico
incidence rate of melanoma for women (Moan and Dahlback 1992). The difference
between the numbers for men and women is almost significant and may be related
to the different intermittent exposure pattern to sunlight between the two sexes.
Getting a sunburn just once every 2 years can triple the risk of melanoma (Dennis
et al. 2008). Moreover, sunburn during childhood or adolescence can increase the
risk of skin cancer later on in life (Dennis et al. 2008; Gandini et al. 2005).
Extensive research using animal models has revealed a more active role of UV-B
in the induction of skin cancer than UV-A (Roy 2017). Although solar UV exposure
is known to be associated with several health problems beyond tumor generation
(e.g., accelerated skin aging, eye diseases, and a defective immune response), this
chapter will focus on the relationship between UV rays and cancer.
4.2.1.3 Skin Cancer: UV Radiation as a Mutagenic and Carcinogenic
Agent
The deoxyribonucleic acid molecule, better known as DNA, is a critical target for
UV radiation damage. DNA is a central component of all living organisms as it is
the genetic material responsible for guiding cell functions. DNA duplication is necessary to transfer the genetic information from the mother cell to its progeny, which
means this molecule must remain unaltered to allow next cell generations to preserve the information as accurately as possible. Unfortunately, there are several
DNA damaging agents which cause DNA lesions; these DNA damaging agents
include UV radiation which can generate 100,000 DNA lesions per cell per day
when exposed to peak hour sunlight (Ciccia and Elledge 2010).
The outcomes of DNA lesions differ according to their type, relative position in
the DNA molecule, and their quantity, but most are eventually repaired by one of the
multiple DNA repair mechanisms. However, damaged DNA is not always repaired
as DNA repair mechanisms are often inefficient or saturated. If a lesion goes unrepaired, it could change the DNA’s sequence in a permanent way, which results in a
mutation. The sources responsible for the generation of mutations, such as UV radiation, are called mutagenic agents (Ikehata and Ono 2011). UV radiation as a mutagenic agent has been broadly investigated, and the lesions generated by UV radiation
on the DNA molecule will be explained in detail within Sect. 4.2.2.1. UV rays are
also classified as carcinogenic agent, i.e., they promote cancer due to the transformation of a normal cell to a cancerous cell. The International Agency for Research on
Cancer (IARC) has extensively analyzed the carcinogenicity of UV and concluded:
“There is sufficient evidence in humans for the carcinogenicity of solar radiation.
Solar radiation causes cutaneous melanoma and non-melanocytic skin cancer.” The
increased rates of skin cancer in patients with xeroderma pigmentosum, who have a
deficiency in their capacity to repair UV-induced DNA damage, suggests that direct
UV DNA damage may be one of the key steps in the causation of these cancers
(World Health Organization 1995). Cancer’s development is a complex multistage
M. B. Federico