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Recent trends in cutaneous melanoma
incidence among whites in the United States.
BACKGROUND: It is not yet clear whether increasing melanoma
incidence is real or whether recent incidence trends mainly reflect improved
diagnosis. To address this question, we examined the most recent melanoma
incidence patterns among the white population stratified by sex, age,
tumor stage, and tumor thickness by use of data from the Surveillance,
Epidemiology, and End Results Program. METHODS: We examined log-transformed
age-specific rates for melanoma by 5-year age groups and time periods
by year of diagnosis and birth cohort. Melanoma trends were further examined
among broader age groups (<40 years, 40-59 years, and > or =60 years)
by tumor stage and tumor thickness. Rates were age-adjusted to the 1970
U.S. standard population, and trends were tested by use of a two-sided
Student's t test. RESULTS: Melanoma incidence increased in females born
since the 1960s. From 1974-1975 through 1988-1989, upward trends for the
incidence of localized tumors and downward trends for the incidence of
distant-stage tumors occurred in the age group under 40 years. In the
more recent time period, 1990-1991 through 1996-1997, age specific rates
among females compared with males generally remained stable or declined
more for distant-stage tumors and increased less for local-stage tumors.
Thin tumors (<1 mm) increased statistically significantly in all age
groups (P<.05 for all), except in men under age 40 years. In contrast,
rates for thick tumors (> or =4 mm) increased statistically significantly
(P =.0003) only in males aged 60 years and older. CONCLUSION: Melanoma
incidence may well continue to rise in the United States , at least until
the majority of the current population in the middle-age groups becomes
the oldest population. The recent trends may reflect increased sunlight
exposure.
J Natl Cancer Inst. 2001 May 2;93(9):678-83
Ultraviolet radiation: sun exposure, tanning beds, and vitamin
D levels. What you need to know and how to decrease the risk of skin
cancer.
This year, more than one million new cases of skin cancer will be diagnosed
in the United States and an estimated 9800 individuals will die of the disease.
Despite recent public education efforts and increased public awareness about
the importance of the use of sunscreen and avoidance of ultraviolet radiation,
the incidence of melanoma has more than tripled among white Americans from
1980 to 2001. This increase in cancer rates means that one person dies of melanoma
in this country every hour of every day. The answer to this increasing problem
is not a simple one, but public education seems to be a common starting point.
The American Cancer Society and the American Academy of Dermatology have published
recommendations with regard to sun exposure and sunscreen use. However, patients
often ask questions that are not as easily answered. Questions such as, Which
sunscreens are the safest? Are tanning beds safe? If I limit my sun exposure,
do I need to take vitamin D supplements? If I tanned as a teenager, is the
damage already done? How do I treat sunburn? This article provides a review
of the current literature regarding these issues and provides the facts family
physicians need to answer common patient questions. The author discusses the
mechanisms of sun damage, the facts on tanning beds, and the importance of
supplementing vitamin D.
Am Osteopath Assoc . 2003 Aug;103(8):371-5
Common skin disorders in the elderly.
Skin diseases commonly seen in the elderly are more often than not the effects
of sun damage or vascular disease. The effects of a lifetime of even casual
sun exposure can be dramatic. Chronically sun-exposed skin becomes thin,
loses collagen, and has disrupted elastin and decreased glycosaminoglycans.
The result is skin that breaks easily, bruises, sags, irritates easily, and
itches. The spots and bumps that patients associate with age are all sun-induced.
Consider how lesionless a 60-year-old's buttock is compared to the extensor
forearm. The reason that bruising attributed to anticoagulation seems to
occur exclusively on the extensor forearm and not the volar aspect of the
arm is that sun-induced elastin degradation is greatest on the extensor forearm.
Even trivial trauma will cause unsupported capillaries to shear and bleed
whether the patient is anticoagulated or not. This article reviews the primary
skin disorders associated with the elderly and some of the management approaches
that the primary care physician can use.
Clin Cornerstone . 2001;4(1):39-44
Elderly and sun-affected skin. Distinguishing between changes
caused by aging and changes caused by habitual exposure to sun.
OBJECTIVE: To review and distinguish between skin changes produced by aging
and changes produced by habitual exposure to sun. QUALITY OF EVIDENCE: The
literature was searched from 1969 to 1999 for articles on dermatoheliosis and
sun-damaged skin. Surprisingly few were found comparing the difference between
elderly skin and sun-damaged skin. A few articles focused on certain small
aspects of sun-damaged skin. Many excellent articles described particular changes
(e.g., actinic keratosis), but few covered all the changes due to aging and
to sun. MAIN MESSAGE: Skin changes due to aging can be distinguished from those
due to sun damage. All changes due to sun exposure can be grouped under the
term dermatoheliosis; five parts of the skin are involved: epidermis (actinic
keratosis), dermis (solar elastosis), blood vessels (telangiectasia), sebaceous
glands (solar comedones), and melanocytes (diffuse or mottled brown patches).
Habitual exposure to sun and a white skin are prerequisites for developing
these changes. Knowing the difference between changes caused by sun and by
aging can help physicians predict which patients are most likely to get skin
cancers. CONCLUSION: Knowledge of these common skin changes will help physicians
diagnose and manage the skin abnormalities of elderly people and of people
with dermatoheliosis.
Can Fam Physician. 2001 Jun;47:1236-43
Cutaneous photobiology. The melanocyte vs. the sun:
who will win the final round?
Solar ultraviolet radiation (UV) is a major environmental factor that dramatically
alters the homeostasis of the skin as an organ by affecting the survival, proliferation
and differentiation of various cutaneous cell types. The effects of UV on the
skin include direct damage to DNA, apoptosis, growth arrest, and stimulation
of melanogenesis. Long-term effects of UV include photoaging and photocarcinogenesis.
Epidermal melanocytes synthesize two main types of melanin: eumelanin and pheomelanin.
Melanin, particularly eumelanin, represents the major photoprotective mechanism
in the skin. Melanin limits the extent of UV penetration through the epidermal
layers, and scavenges reactive oxygen radicals that may lead to oxidative DNA
damage. The extent of UV-induced DNA damage and the incidence of skin cancer
are inversely correlated with total melanin content of the skin. Given the
importance of the melanocyte in guarding against the adverse effects of UV
and the fact that the melanocyte has a low self-renewal capacity, it is critical
to maintain its survival and genomic integrity in order to prevent malignant
transformation to melanoma, the most fatal form of skin cancer. Melanocyte
transformation to melanoma involves the activation of certain oncogenes and
the inactivation of specific tumor suppressor genes. This review summarizes
the current state of knowledge about the role of melanin and the melanocyte
in photoprotection, the responses of melanocytes to UV, the signaling pathways
that mediate the biological effects of UV on melanocytes, and the most common
genetic alterations that lead to melanoma.
Pigment Cell Res. 2003 Oct;16(5):434-47
Determinants of melanocyte density in adult human skin.
The distribution of melanocytes in human skin has been observed to vary within
and among individuals, yet little is known of the factors that determine
the density of these pigment cells. These factors were explored in a molecular
epidemiological study conducted among a population-based sample of 97 male
subjects aged over 50 years in Queensland , Australia . Information relating
to environmental and phenotypic factors was collected through face-to-face
interviews and physical examination of all participants. In addition, 2-mm
biopsies of representative skin were taken from the dorsum of the hand and
another anatomical site. Melanocytes were identified by cytoplasmic staining
with the B8G3 (anti-TRP1) monoclonal antibody using standard immunohistochemical
techniques. Melanocyte counts were performed blind by two observers. On crude
analysis, melanocyte density decreased with advancing age (P = 0.0002), and
increased with increasing number of naevi (P = 0.01). Other pigmentary characteristics
(such as hair and eye colour and depth of tan) were not associated with epidermal
melanocyte density. Melanocyte density varied significantly by anatomical
site (P = 0.02), with highest densities observed on the back/shoulders (n
= 50, 17.1 +/- 8.8 cells/mm, mean +/- SD) followed by the upper limbs (n
= 11, 12.6 +/- 8.8 cells/mm) and lower limbs (n = 14, 14.4 +/- 5.9 cells/mm).
Lowest melanocyte densities were recorded on the anterior trunk (n = 3, 3.2
+/- 2.4 cells/mm). These findings confirm the results of earlier studies
in which site-specific differences in melanocyte density have been found.
We speculate that the unequal distribution of melanocytes may partially explain
the site-specific incidence of melanoma, offering fresh perspectives on the
aetiology of this cancer.
Arch Dermatol Res. 1999 Sep;291(9):511-6
Epidemiology of ultraviolet-DNA repair capacity and human
cancer.
The following conclusions are derived from an epidemiological study. Reduced
repair of ultraviolet (UV)-induced DNA damage contributes directly to basal
cell carcinoma (BCC) in individuals with prior sunlight overexposure. A family
history of BCC is a predictor of low DNA repair. Repair of UV-damaged DNA declines
at a fixed rate of approximately 1% per annum in noncancerous controls. The
DNA repair differences between young BCC cases and their controls disappear
as they age. Hence, BCC, in terms of DNA repair, is a premature aging disease.
The persistence of photochemical damage because of reduced repair results in
point mutations in the p53 gene and allelic loss of the nevoid BCC gene (Gorlin's
syndrome) located on chromosome 9q. The fact that environmental vulnerability
is gender oriented implicates hormones in regulating DNA repair. Xeroderma
pigmentosum appears to be a valid paradigm for the role of DNA repair in BCC
in the general population.
Environ Health Perspect . 1997 Jun;105 Suppl 4:927-30
Repair of UV light-induced DNA damage
and risk of cutaneous malignant melanoma.
BACKGROUND: The mechanism underlying the role of UV light exposure from sunlight
in the etiology of cutaneous malignant melanoma (CMM) is unclear. Patients
with xeroderma pigmentosum, a disease characterized by severe sensitivity to
UV radiation and a defect in nucleotide excision repair, have a high incidence
of CMM, which suggests that DNA repair capacity (DRC) plays a role in sunlight-induced
CMM in the general population as well. METHODS: We conducted a hospital-based
case-control study of DRC and CMM among 312 non-Hispanic white CMM patients
who had no prior chemotherapy or radiation therapy, and 324 cancer-free control
subjects who were frequency-matched to case patients on age, sex, and ethnicity.
Information on demographic variables, risk factors, and tumor characteristics
was obtained from questionnaires and medical records. We used the host-cell
reactivation assay to measure the DRC in study subjects' lymphocytes. All statistical
tests were two sided. RESULTS: Case patients had a 19% lower mean (+/- standard
deviation [SD]) DRC (8.5 +/- 3.4%) than control subjects (10.5 +/- 5.1%), a
statistically significant difference (P<.001). DRC that was at or below
the median value (i.e., 9.4%) in control subjects was associated with increased
risk for CMM after adjustment for age, sex, and other covariates (odds ratio
[OR] = 2.02, 95% confidence interval [CI] = 1.45 to 2.82). We observed a dose-response
relationship between decreased DRC and increased risk of CMM (P(trend)<.001).
Patients with tumors on sun-exposed skin had statistically significantly lower
DRC than patients with tumors on unexposed skin (8.2 +/- 3.3% versus 9.5 +/-
3.5%; P =.004). CONCLUSIONS: Reduced DRC is an independent risk factor for
CMM and may contribute to susceptibility to sunlight-induced CMM among the
general population.
J Natl Cancer Inst.
2003 Feb 19;95(4):308-15 |