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Advances in dermatology and venereology Acta Dermato-Venereologica
CLINICAL REPORT
1/6
Acta Derm Venereol 2020; 100: adv00128
This is an open access article under the CC BY-NC license. www.medicaljournals.se/acta
Journal Compilation © 2020 Acta Dermato-Venereologica.
doi: 10.2340/00015555-3486
SIGNIFICANCE
Actinic keratosis is a common skin lesion associated with
chronic exposure to sun. In most cases actinic keratosis is
harmless, but it occasionally transforms into squamous cell
carcinoma. This study included 2,893 patients with actinic
keratosis, and investigated their 10-year risk of developing
skin cancer, compared with a control group of 14,668 pa-
tients without actinic keratosis. Patients with actinic kera-
tosis were found to have a more than 5 times increased risk
of getting skin cancer. With regard to specic types of skin
cancer, this increased risk in patients with actinic keratosis
was highest (greater than 7 times higher) for squamous
cell carcinoma, greater than 4 times higher for basal cell
carcinoma, and almost 3 times higher for malignant mela-
noma. In conclusion, actinic keratosis is an important indi-
cator of increased risk of skin cancer.
Actinic keratosis is the most common actinic lesion in
fair-skinned populations. It is accepted as an indicator
of actinic skin damage and as an occasional precursor
of squamous cell carcinoma. The aim of this study was
to investigate, in a cohort of patients with a diagnosis
of actinic keratosis, the relative risk of developing skin
cancer during a follow-up period of 10 years. This re-
gistry-based cohort study compared a cohort of 2,893
individuals in south-eastern Sweden, who were diag-
nosed with actinic keratosis during the period 2000 to
2004, with a matched-control cohort of 14,668 indivi-
duals without actinic keratosis during the same inclu-
sion period. The subjects were followed for 10 years
to identify skin cancer development in both cohorts.
Hazard ratios with 95% condence intervals (95% CI)
were used as risk measures. Individuals in the actinic
keratosis cohort had a markedly higher risk for all skin
cancer forms compared with the control cohort (hazard
ratio (HR) 5.1, 95% CI 4.7–5.6). The relative risk was
highest for developing squamous cell carcinoma (SCC)
(HR 7.7, 95% CI 6.7–8.8) and somewhat lower for ba-
sal cell carcinoma (BCC) (HR 4.4, 95% CI 4.1–5.0) and
malignant melanoma (MM) (HR 2.7 (2.1–3.6). Patients
with a diagnosis of actinic keratosis were found to be
at increased risk of developing SCC, BCC and MM in
the 10 years following diagnosis of actinic keratosis.
In conclusion, a diagnosis of actinic keratosis, even
in the absence of documentation of other features of
chronic sun exposure, is a marker of increased risk of
skin cancer, which should be addressed with individu-
ally directed preventive advice.
Key words: skin cancer; actinic keratosis; cohort study; mela-
noma; squamous cell carcinoma; basal cell carcinoma.
Accepted Apr 21, 2020; Epub ahead of print Apr 21, 2020
Acta Derm Venereol 2020; 100: adv00128.
Corr: Magnus Falk, Department of Health, Medicine and Caring Sciences,
Linköping University, SE-581 83, Linköping, Sweden. E-mail: magnus.
falk@liu.se
Actinic keratosis (AK) is a common skin condi-
tion caused by long-term exposure to the sun in
susceptible individuals. AK typically develops on sun-
exposed areas, such as the face, neck, balding scalp,
chest, shoulders, and the back of arms and hands of
mainly Caucasian adults (1–5), presenting as a rough,
dry, scaly or crusted lesion which can be skin-coloured
or tanned, sometimes with an erythematous base. Clini-
cally, AK is sometimes difcult to differentiate from
other benign skin conditions, such as lichenoid keratosis
and other benign keratotic lesions (6, 7). AKs are often
asymptomatic, but can sometimes be sore or itchy (1, 8).
The diagnosis of AK is, in practice, often set clinically,
based on its typical appearances, without histopatholo-
gical conrmation, and the condition is therefore not
regularly recorded in pathology databases (4, 8). Data
about the prevalence of AK are thus relatively sparse,
and originate mostly from Australia and the USA, with
only a few studies available from Europe and Asia and
no information from Africa and South America (9, 10).
On the one hand, as is the case for the majority of
lesions, a single AK lesion may be completely harmless,
with only cosmetic consequences for patients. On the
other hand, however, the potential for malignant transfor-
mation is well documented; AKs are the most common
precursor of invasive SCC (11). Any single AK lesion
may have 1 of 3 possible outcomes: it can enter spon-
taneous remission; remain stable without further pro-
gression; or transform over time into in situ or invasive
squamous cell carcinoma (SCC) (1, 2, 12). The reported
risk of malignant progression of AK is widely variable. A
systematic review found that the estimated risk of a single
AK lesion becoming malignant ranged between 0.075%
and 0.096% per year, or approximately1% over 10 years,
with some estimates as high as 10% over 10 years (2). In
another review the risk of progression of AK to invasive
SCC varied between 0.025% and 16% per year (12). AK,
Actinic Keratosis Diagnosis and Increased Risk of Developing Skin
Cancer: A 10-year Cohort Study of 17,651 Patients in Sweden
Ghassan GUORGIS
1
, Chris D. ANDERSON
2
, Johan LYTH
1,3
and Magnus FALK
1
1
Department of Health, Medicine and Caring Sciences,
2
Department of Biomedical and Clinical Sciences, Division of Dermatology, Linköping
University, and
3
Research and Development Unit in Region Östergötland, Linköping, Sweden
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and non-melanoma skin cancer (NMSC), are both also
risk factors for the development of malignant melanoma
(MM); a study in Italy (13) has shown that more than
40% of patients with a previous diagnosis of multiple
AKs developed a NMSC or a MM during a follow-up
period of 5–11 years. Solid-organ transplanted patients,
such as those with heart, lung and kidney transplants,
are at specically increased risk of developing malig-
nancies, including skin cancer and, especially, SCC,
due to immunosuppression (14–19). The risk of SCC
has been found to increase for those with more than 5
AKs, and the majority of SCCs arise from AKs (2). AKs
on sun-exposed body surfaces indicate previous chronic
exposure to ultraviolet (UV) radiation, and may, together
with other factors, such as age, duration, and skin type,
be sufcient to facilitate malignant change. Just as for
basal cell carcinomas (BCC) and SCC, the prevalence
of AK is typically higher in sun-intense geographical
regions, but the specic pathogenic factors associated
with progression of AK to SCC are not clear (20).
Although the most common reason for treatment of AK
is prevention of malignancy, lesions are also treated for
cosmetic purposes and to provide relief from symptoms,
such as tenderness or itch (4), and can either be lesion
directed, such as curettage and cryotherapy, or eld di-
rected, by means of a variety of topical, pharmacological
treatments and photodynamic therapy (PDT) (1, 8, 21).
Some national guidelines or consensus reports recom-
mend treatment of AK, and subsequent clinical follow-up
of treated patients, due to its malignant potential (22, 23),
whereas other are less dogmatic (24). Routine obligatory
treatment of AK would entail a substantial burden on
general practitioners and on dermatological specialist
care, which, in many cases, is already strained by the
diagnostic process and care of increasing number of
cutaneous malignancies (4).
With increasing incidence of skin cancer, research into
prevention and early detection measures to counteract
its development is important, not least from a primary
healthcare perspective. This includes the identication
of individuals who are at particular risk of developing
skin cancer, among whom patients with AK emerge as
an identiable and potentially important category. The
aim of the present study was to investigate, in a cohort
of patients with a documented diagnosis of AK, the re-
lative risk of developing skin cancer during a follow-up
period of 10 years.
MATERIALS AND METHODS
The study was approved by the Regional Ethics Review Board in
Linköping, Sweden (number 2015/182-31).
The study was a registry-based cohort study on patients resident
in the County of Östergötland, south-eastern Sweden, which has
a total population of approximately 453,600 inhabitants (2017).
As population-based data source, an administrative healthcare
registry, The Care Data Warehouse in Östergötland, (CDWÖ)
was used. The registry consists of administrative records of all
publicly produced healthcare utilization in the county, including
inpatient and outpatient care for all medical specialties, covering
more than 95% of the total healthcare utilization in the county,
from 1998 onwards (25). All patients aged 18 years or over who
were clinically or histopathologically diagnosed with AK (ICD-10
code L57.0), during a 5-year time-period from January 2000 to
December 2004, were identied from the registry as the AK cohort.
The date of diagnosis of AK was set as the patient’s index date.
Patients were included independently of the number of lesions or
form of treatment, and were only included once, even if they were
treated on more than one occasion. Patients were excluded if they
had a previous history of skin cancer (in the form of MM (ICD-
10 code C43.0–C43.9), SCC (ICD-10 code: C44.0S–C44.9S) or
BCC (ICD-10 code: C44.0D–C44.9D)) prior to the study baseline,
according to data from the national Swedish Cancer Register. The
Swedish Cancer Register contains data on MM and SCC from
January 1958 and on BCC from January 2004.
As a control cohort, up to 5 matched individuals without a
diagnosis of AK during the inclusion period 2000 to 2004 were
identied in the CDWÖ. As in the study cohort, individuals with
a previous history of skin cancer were excluded based on data
from the national Swedish Cancer Register. Remaining cases were
included in the control cohort, frequency-matched by age, sex and
index year. The corresponding index date was used to set the start
date for the matched controls.
During a follow-up period from baseline to 2014, data from the
national Swedish Cancer Register was used to identify whether
the participants had been diagnosed with MM, SCC or BCC. Each
individual was monitored from the index date until diagnosis with
skin cancer, or until they were omitted due to loss to follow-up,
death, or until the end of the study in 2014. Events of MM, SCC
and BCC were identied for each cohort.
Statistical analysis
A χ2 test was used to analyse categorical data, and an independent
t-test to analyse continuous data. The Kaplan–Meier method was
used to estimate the cumulative incidence for patients and controls
for different endpoints (1: all skin cancers; 2: SCC; 3: BCC; 4:
MM), and multivariable Cox regression, with the same endpoints
as listed above, to determine the hazard ratios (HR) and 95%
condence intervals (95% CI) between patients and controls. To
investigate whether the HRs between patients and controls varied
according to sex and age, the sex- and age-specic HRs were
calculated for each endpoint and the p-values for the interaction
with group were presented. All Cox models were adjusted for
age and sex.
RESULTS
The median follow-up time was 10.6 years (range
0.1–14.99 years). Follow-up was stopped if the person
had an event. Consequently, if there were fewer events
in a group, then the follow-up time would be longer in
that group. Patients in the AK cohort were thus followed
for a shorter time compared with the control cohort 9.6
(0.1–14.99) and 10.7 (0.1–14.99) years, respectively.
Eligible study individuals consisted of 3,422 indivi-
duals in the AK cohort and 17,110 individuals in the
non-AK control cohort. A history of prior skin cancer
was an exclusion criterion. In the AK cohort 439 indi-
viduals (12.8%) were excluded, whereas only 332 (1%)
individuals were excluded from the control cohort. After
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exclusion of individuals with a previous history of skin
cancer the AK cohort comprised 2,983 patients and the
control cohort comprised 16,778 individuals. If an AK
patient was excluded due to previous skin cancer, its
identied matched controls were also excluded, unless
they matched another AK patient with fewer than 5
identied controls (85 of 2,110 excluded controls were
re-matched to the AK cohort). In the analysable material,
2,983 individuals remained in the AK group and 14,668
in the control group (Fig. 1).
The characteristics of the study cohort of patients with
AK and the matched controls are shown in Table I. There
was a somewhat greater proportion of women (56.3%),
and a higher representation of individuals within the age
interval 70–79 years, representing 55.9% of our popu-
lation. The lack of statistically signicant differences
between the 2 groups regarding sex, age and year of
inclusion conrmed that the controls were successfully
matched to the patients.
Table II shows the cumulative incidences of SCC,
BCC and CMM in the 2 cohorts, and also the HR for each
diagnosis. As seen, the AK cohort had a higher risk for
all 3 cancer forms than did the control cohort. Patients
with AK had 5.1 (95% CI: 4.7–5.6) times higher risk of
developing some form of skin cancer within 10 years
compared with the control group, i.e. individuals without
AK. The difference was signicant for all types of skin
cancer, but most pronounced for SCC.
Table III shows the HRs for each of the different skin
cancer types, as well as for all skin cancers. The HR of
developing BCC was signicantly lower for women than
for men (p
interaction
< 0.001). The age group ≤ 59 years had
the highest HR of developing SCC (p
interaction
< 0.01) and
BCC (p
interaction
< 0.01) compared with the other age groups.
DISCUSSION
The most important result of this study is the nding
of a strong relationship between a diagnosis of AK and
Identified patients with a diagnosis
of actinic keratosis (n=3,422)
Five matched (age, sex and year of
diagnosis) controls per patient added
(controls: n=17,110)
Exclusions:
Skin cancer before date of inclusion
(patients: n=439 and controls n=332)
Controls related to patients with
previous skin cancer n=2,110
Final number of patients and
controls to be analysed (patients:
n=2,983, controls: n=14,668)
Fig. 1. Flow chart of the distribution of study participants, by means
of patients with actinic keratosis and matched controls.
Table I. Characteristics of the patients in the actinic keratosis
cohort and the control cohort
Patients Controls p-value
All patients, n (%) 2,983 (100) 14,668 (100)
Sex, n (%) 0.97
Men 1,304 (43.7) 6,417 (43.7)
Women 1,679 (56.3) 8,251 (56.3)
Age, n (%) 0.95
< 60 years 618 (20.7) 3,071 (20.9)
60–69 years 697 (23.4) 3,449 (23.5)
70–79 years 926 (31.0) 4,576 (31.2)
≥ 80 years 742 (24.9) 3,572 (24.4)
Age, mean (SD) 70.0 (12.5) 69.8 (12.4) 0.55
Year of inclusion, n (%) 1.00
2000 731 (24.5) 3,607 (24.6)
2001 715 (24.0) 3,527 (24.0)
2002 529 (17.7) 2,592 (17.7)
2003 516 (17.3) 2,517 (17.2)
2004 492 (16.5) 2,425 (16.5)
Controls per patient, n (%) –
≤ 3 101 (1.3) –
4 160 (5.4) –
5 2785 (93.4) –
Number of controls, mean (SD) 4.92 (0.34) – –
SD: standard deviation.
Table II. Hazard ratio and 5- and 10-year cumulative incidence of skin cancera in 2,983 patients with actinic keratoses (AK) compared
with 14,668 matched (age, sex and year of diagnosis) controls
Patients/controls
n
Events
n (%) Hazard ratio (95% CI) p-value
Cumulative incidence (95% CI)
5-year 10-year
Skin cancera*
Patients 2,983 1,007 (33.8) 5.1 (4.7–5.6) < 0.0001 19 (18–21) 33 (31–35)
Controls 14,668 1,062 (7.2) 1.0 (ref) 3.1 (2.8–3.4) 7.6 (7.1–8.0)
Squamous cell carcinoma
Patients 2,983 561 (18.8) 7.7 (6.7–8.8) < 0.0001 9.5 (8.5–11) 17 (16–19)
Controls 14,668 355 (2.4) 1.0 (ref) 0.9 (0.8–1.1) 2.4 (2.1–2.7)
Basal cell carcinoma
Patients 2,983 626 (21.0) 4.4 (4.1–5.0) < 0.0001 11 (10–12) 21 (20–23)
Controls 14,668 692 (4.7) 1.0 (ref) 2.0 (1.8–2.2) 5.1 (4.7–5.5)
Cutaneous malignant melanoma
Patients 2,983 86 (2.9) 2.7 (2.1–3.6) < 0.0001 1.2 (0.8–1.6) 2.6 (1.9–3.2)
Controls 14,668 142 (1.0) 1.0 (ref) 0.3 (0.2–0.4) 0.9 (0.7–1.1)
aSquamous cell carcinoma (SCC), basal cell carcinoma (BCC) and cutaneous malignant melanoma (CMM). *Multiple skin cancer types where present in 247 patients and
124 controls with the following distribution: BCC+SCC=200 (patients), 91 (controls), BCC+CMM=16 (patients), 21 (controls), SCC+CMM=12 (patients), 9 (controls),
BCC+SCC+CMM=19 (patients), 3 (controls).
CI: condence interval.
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development of skin cancer. Patients with AK were found
to have a 5 times higher risk of developing some form of
skin cancer during 10 years’ follow-up compared with pa-
tients in the control cohort. This was more prominent for
patients with AK aged ≤ 59 years at inclusion, for which
the HRs for developing BCC and SCC were particularly
high (6.9 and 16, respectively). Another notable nding
was that the exclusion criteria “previous skin cancer” was
applied for 12.8% of the AK group, but for only 1% of
the control group, indicating the general association of
AK with both keratinocyte and melanocyte malignancy.
Study limitations and strengths
This study has some limitations. Firstly, the diagnoses
are based on registration in the local registry (CDWÖ),
which, although it covers 95% of all cases reported in
patients’ medical records (25), does not provide data
on probable under-reporting of AK. Under-reporting is
likely, not only because an unknown number of patients
probably never seek medical help for their AK, but also
because the diagnosis is, in most cases, set clinically,
and not by histopathology, hence it is not certain that the
diagnosis is always correct. In addition, an AK may be
discovered as a secondary diagnosis, in which case the
likelihood of its registration as a diagnosis can be ex-
pected to be lower than for a primary diagnosis. Finally,
it is important to consider that the results of this study
do not refer to patients with AK in general, but only to
those who choose to seek healthcare.
Another limitation is that registration of BCC was
not initiated before January 2004, i.e. after the start of
our inclusion period; hence, cases of BCC may also
have been under-reported in both cohorts. An additional
limitation is that the ICD coding mixes all subtypes of
SCC and MM. In cases of uncertainty during the diag-
nostic process, the physician registers the non-specic
diagnosis code “other and non-specied skin changes”
before having the histopathological answer. The actual
frequency with which the histopathology report resulted
in a revision of the initial diagnosis set at the time of
clinical examination is unknown. Neither does the data
collection allow for determination of whether there were
multiple (or single) AKs or whether solar lentigines or
actinic elastosis (common other features of “actinically
damaged skin”) were present. Nor is it possible to draw
any conclusions about possible connections between sites
of AK, possible treatment modality and subsequent skin
cancer development, which prohibits any interpretation
of the possible malignication of an individual AK.
An important strength of the study is that it includes
healthy individuals in the control group, i.e. not only
those who had had contact with healthcare. This is an
advantage, since these are, as a group, closer in character
to a general population. Another strength is that this is
a full population-based study, based on a whole county,
thus eliminating selection biases. The 10-year follow-up
interval may be discussed and may have been extended,
but we think that it is a reasonably long time period for
this age group and sample size of individuals to present
with a sufcient incidence of skin malignancies, and to
detect and compare differences with the control cohort.
Overall, and despite the limitations mentioned above, we
believe that this relatively large cohort study provides
novel and important information concerning the risk of
skin cancer development in patients with AK.
The HR for patients with AK to develop SCC was
much higher (approximately double) than the correspon-
ding HRs for MM and BCC, possibly because there is a
stronger relationship between AK and SCC in addition
to the general effect of chronic sun exposure. Regarding
the proportion of patients with AK developing any form
of skin cancer (SCC; BCC; MM), the current study sho-
wed this to be somewhat lower (33.8%) than in an Italian
study by Dika et al. (13) (41.5%), even though we had
a longer follow-up period. This may be due to possible
discrepancies in documentation of skin cancer diagnosis
in the different registries used for the studies, or other
selection biases, but it cannot be excluded that the Italian
population, for some reason, may have a higher risk of
developing skin cancer. It is likely that the difference
Table III. Hazard ratios, stratied by sex and age, for the incidence of skin cancera in 2,983 patients with actinic keratoses (AK) compared
with 14,668 matched (age, sex and year of diagnosis) controls
Skin cancera* SCC BCC CMM
HR (95% CI) pInteraction HR (95% CI) pInteraction HR (95% CI) pInteraction HR (95% CI) pInteraction
Overall 5.1 (4.7–5.6) 7.7 (6.7–8.8) 4.4 (4.1–5.0) 2.7 (2.1–3.6)
Sex <0.01 0.56 <0.001 55
Men 5.8 (5.1–6.6) 8.0 (6.6–9.7) 5.4 (4.7–6.4) 3.0 (2.0–4.3)
Women 4.6 (4.1–5.2) 7.4 (6.1–8.9) 3.8 (3.3–4.4) 2.5 (1.7–3.7)
Age 0.03 <0.01 0.01 0.78
≤ 59 years 6.9 (5.5–8.6) 16 (10–26) 6.9 (5.3–9.1) 2.3 (1.3–4.1)
60–69 years 4.5 (3.8–5.4) 6.0 (4.6–8.0) 4.3 (3.5–5.4) 3.2 (2.0–5.2)
70–79 years 4.9 (4.2–5.6) 7.3 (5.9–9.1) 4.1 (3.5–4.9) 2.5 (1.5–4.0)
≥ 80 years 5.4 (4.5–6.5) 7.9 (6.1–10) 4.1 (3.2–5.2) 3.2 (1.6–6.3)
aSquamous cell carcinoma (SCC), basal cell carcinoma (BCC) and cutaneous malignant melanoma (CMM). *Multiple skin cancer types where present in 247 patients and
124 controls with the following distribution: BCC+SCC=200 (patients), 91 (controls), BCC+CMM=16 (patients), 21 (controls), SCC+CMM=12 (patients), 9 (controls),
BCC+SCC+CMM=19 (patients), 3 (controls).
HR: hazard ratio; CI: condence interval.
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in insolation between the study populations lies behind
this difference in outcome, although this requires further
research. There was a female dominance in our AK co-
hort (56%, see Table I), a nding that is in contrast with
that of previous studies (1–3). On the other hand, men
had a higher risk of developing skin cancer compared
with women (Table III). This is in concordance with
other studies (1–3, 26). We also noticed that women had
signicantly lower HRs for developing BCC compared
with men (3.8 vs. 5.4).
The localization of AK lesions and developed skin
cancers were not specied in our study, since we wan-
ted to assess the relative risk of developing skin cancer
in general, unrelated to the body location of a specic
lesion. Neither did we have access to information about
the treatments received by the patients with AK and its
possible effect on individual risk of developing skin can-
cer from the specic (or other co-existing) lesion treated.
The considerable differences in risk levels for cancer
development from a single AK (from 0.025% to 16% per
year), shown in previous studies (12), is probably related
to the fact that the studies were conducted in different
modalities. Also, in our study the median follow-up time
of patients with AK was shorter than that of controls, due
to a larger number of events.
This study has some bearing on the logic of mana-
gement issues in patients with AK. Whilst the current
study has little to add to the question of the fate of an
individual with AK, the results support the consensus of
opinion that the likelihood of progression is extremely
small. On the other hand, the fact that a clinical diag-
nosis of AK has been made is clearly associated with
an increased risk for future (or present) skin cancer at
an undetermined site in the same patient. Although not
evaluated in our study, histopathological features of AK
can, as described previously (27), be correlated with the
risk of developing other cutaneous neoplasms. Thus,
we regard AK as a marker of chronic sun exposure over
the patient’s lifetime, increasing the risk of skin cancer,
rather than AKs per se being dangerous. In conclusion,
this calls for the provision of structured prevention in-
formation for patients even with their rst AK, and of
providing information on early detection. A consequence
of that is the necessity for the healthcare systems to meet
the patient’s need for repeated examination as required.
The question of whether a planned follow-up should be
provided requires further discussion, since healthcare
resources are not unlimited and efforts may be best put
into making the routines for “as required” examinations
more effective. There is currently no existing technology
or prognostic markers that allow clinicians to distinguish
between individual lesions of AK that will resolve,
remain stable, or progress to invasive disease, thus the
treatment (or not) of an AK lesion is left to an individual,
clinical management decision.
Conclusion
In conclusion, patients for whom a clinical diagnosis
of AK has been set have a considerably higher risk of
developing SCC, BCC or MM compared with sex- and
age-matched controls, within 10 years from diagnosis.
Although an individual AK is usually considered a harm-
less skin lesion, with a considerable rate of spontaneous
resolution and with progression to SCC as a relatively
rare event, the results of this study illustrate an opportu-
nity to use the identication and documentation of AKs,
even without documentation of other manifestations of
solar damage, as motivation for the targeted provision
of appropriate skin cancer prevention information. This
may be an important and achievable part of our efforts
to reduce the incidence and burden of skin cancer.
The authors have no conicts of interest to declare.
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