Epidemiology of Malignant Melanoma

177 Pages·1986·13.1 MB·English

by  A. J. Worth (auth.), Richard P. Gallagher M.A. (eds.)

Recent Results 102
in Cancer Research
Founding Editor
P. Rentchnick, Geneva
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Recent Results in Cancer Research
Volume 95: Spheroids in Cancer Research
Edited by H. Acker, J. Carlsson, R. Durand, R. M. Sutherland
1984. 83 figures, 12 tables. IX, 183. ISBN 3-540-13691-6
Volume 96: Adjuvant Chemotherapy of Breast Cancer
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1984.98 figures, 91 tables. X, 243. ISBN 3-540-13738-6
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1985.44 figures, 47 tables. VII, 166. ISBN 3-540-13798-X
Volume 98: Perioperative Chemotherapy
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1985.48 figures, 45 tables. XII, 157. ISBN 3-540-15124-9
Volume 99: Peptide Hormones in Lung Cancer
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1985. 100 figures, 63 tables. XII, 248. ISBN 3-54O-15504-X
Volume 100:
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1986.163 figures, 104 tables. ISBN 3-540-16011-6
Volume 101:
Locoregional High-Frequency Hyperthermia and Temperature
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1986.96 figures, 8 tables. IX, 143. ISBN 3-540-15501-5
Epidemiology of
Malignant Melanoma
Edited by R. P. Gallagher
With 15 Figures and 70 Tables
Springer-Verlag
Berlin Heidelberg New York Tokyo
Richard P. Gallagher, M. A.
Cancer Control Agency of British Columbia
600 West 10th Avenue
Vancouver, B. C. V5Z 4E6, Canada
lSBN-13:978-3-642-82643-6 e-1SBN-13:978-3-642-82641-2
001: 10.1007/978-3-642-82641-2
Library of Congress Cataloging-in-Publication Data. Main entry under title: Epidemiology
of malignant melanoma. (Recent results in cancer research; v. 102) Based on a conference
held in Vancouver in 1984, sponsored by the Cancer Control Agency of British Columbia.
Includes bibliographies and index. 1. Melanoma·Congresses. 2. Carcinogenesis
Congresses. 3. Epidemiology-Congresses. 4. Environmentally induced diseases-Congresses.
I. Gallagher, R. P. (Richard P.), 1944-. II. Cancer Control Agency of British Columbia.
III. Series. [DNLM: 1. Melanoma-etiology-congresses. 2. Melanoma-occurrence
congresses. Wl REl06P v.l02/QZ 202 E639 1984) RC261.R35 vol. 102 616.99'4
[616.99'4071) 85-27796[RC280.S5)
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Preface
Interest in the etiology of malignant melanoma has increased enor
mously in the last 10 years, after it was realized that the incidence of
the cutaneous form of the disease was rising.
Treatment of the disease has not improved dramatically, and our
best hope for curtailing the rise in mortality and morbidity from the
disease appears to be primarily through early detection and, per
haps in the future, through prevention. It is thus very important for
the medical community to be able to recognize individuals and
groups at high risk of the disease because of either familial and con
stitutional factors and lifestyle or exposure to environmental risk
factors.
This book, arising from a meeting held in Vancouver in 1984, pro
vides a summary of the latest findings amo ~ Caucasian popula
tions along with perspectives on the most im, Jrtant environmental
risk factors identified to date. Comparison of results from the four
major analytic studies presented here also demonstrates that a num
ber of factors implicated in other common cancers are probably not
related to the incidence of melanoma. These include smoking, alco
hol consumption, and for the most part, diet.
The Vancouver conference was sponsored by the Cancer Control
Agency of British Columbia, and was financially supported by
Health and Welfare Canada (6610-1429-50), the Northern Califor
nia Cancer Program (NCCP), Miles Laboratories (Canada), Bristol
Myers Laboratories (Canada), and Plough Canada Inc.
I owe a special debt of gratitude to Mrs. Shirley Morton and in
particular to Mrs. Jean van den Broek, who managed most of the
details of the meeting and typed the manuscripts.
Vancouver, December 1985 Richard P. Gallagher
Contents
Pathology of Melanoma 1
A.J. Worth
Growth Patterns in Melanoma and Its Precursor Lesions 1
Descriptive and Analytic Studies of Cutaneous Melanoma . 8
A. (l)sterlind and O. M@ller Jensen
Trends in Incidence of Malignant Melanoma of the Skin in
Denmark 1943-1982 . . . . . . . . . . . . . . . . . . . . . . 8
C. D. J. Holman, B. K.Armstrong, P. J. Heenan, J. B. Blackwell,
F. J. Cumming, D. R. English, S. Holland, G. R. H. Kelsall,
L.R.Matz, I. L. Rouse, A.Singh, R.E.J. Ten Seldam, J.D. Watt,
and Z.Xu
The Causes of Malignant Melanoma: Results from the West
Australian Lions Melanoma Research Project . . . . . . . . .. 18
R. P. Gallagher, J. M. Elwood, and G. B. Hill
Risk Factors for Cutaneous Malignant Melanoma:
The Western Canada Melanoma Study . . . . . . . . .. 38
N. Dubin, M. Moseson, and B. S. Pasternack
Epidemiology of Malignant Melanoma:
Pigmentary Traits, Ultraviolet Radiation, and the Identification
of High-Risk Populations .. . . . . . . . . . . . . . . . . . .. 56
A. Green, C. Bain, R. McLennan, and V. Siskind
Risk Factors for Cutaneous Melanoma in Queensland . . . . .. 76
Current Issues in Melanoma Research: Occupation . . . . . . .. 98
D. F.Austin and P. Reynolds
Occupation and Malignant Melanoma of the Skin . . . . . . .. 98
VIII Contents
Current Issues in Melanoma Research:
Exogenous Hormones, Pregnancy .............. 108
E.A.Holly
Cutaneous Melanoma and Oral Contraceptives:
A Review of Case-Control and Cohort Studies . 108
E.A.Holly
Melanoma and Pregnancy . . . . . . . . . . . . ....... 118
Current Issues in Melanoma Research: Fluorescent Light ..... 127
J.M.Elwood
Could Melanoma Be Caused by Fluorescent Light?
A Review of Relevant Epidemiology . . . . . . . . . . . . . . . 127
K. J. Maxwell and J. M. Elwood
Could Melanoma Be Caused by Fluorescent Light?
A Review of Relevant Physics . . . . . . . . . . . . . . . . . . . 137
Dysplastic Nevus Syndrome and Familial Melanoma .. . . . . . 144
M. H. Greene and S. J. Bale
Genetic Aspects of Cutaneous Malignant Melanoma 144
G. C. Roush, J. M. Kirkwood, M. Ernstoff, S. J. Somma,
P.H.Duray, S. N. Klaus, K.S.Stenn, L.J. Titus, andA.B.Lerner
Reproducibility and Validity in the Clinical Diagnosis of the
Nonfamilial Dysplastic Nevus: Work in Progress ......... 154
Ocular Melanoma ......................... 159
M.A. Tucker, P.Hartge, and J.A.Shields
Epidemiology of Intraocular Melanoma . . . . . . . . . . . . . 159
Subject Index ............................ 166
List of Contributors *
Armstrong, B. K 181 Lerner, A B. 154
Austin, D. F. 98 Matz, L. R. 18
Bain, C. 76 Maxwell, KJ. 137
Bale, S.J. 144 McLennan, R. 76
Blackwell, J.B. 18 M0ller Jensen, O. 8
Cumming, F.J. 18 Moseson, M. 56
Dubin, N. 56 0sterlind, A 8
Duray, P. H. 154 Pasternack, B. S. 56
Elwood, J. M. 38, 127, 137 Reynolds, P. 98
English, D.R. 18 Rouse, 1. L. 18
Ernstoff, M. 154 Roush, G. C. 154
Gallagher, R. P. 38 Shields, J.A 159
Green, A 76 Singh, A 18
Greene, M. H. 144 Siskind, V. 76
Hartge, P. 159 Somma, S.J. 154
Hill, G. B. 38 Stenn, K S. 154
Heenan, P.J. 18 Ten Seldam, R. E.J. 18
Holland, S. 18 Titus, L.J. 154
Holly, E.A 108,118 Tucker, M. A 159
Holman, C.D.J. 18 Watt, J.D. 18
Kelsall, G.R.H. 18 Worth, AJ. 1
Kirkwood, J. M. 154 Xu, Z. 18
Klaus, S. N. 154
* The address of the principal author is given on the first page of each con
tribution
1 Page on which contribution begins
Pathology of Melanoma
Growth Patterns in Melanoma and Its Precursor Lesions
A. J. Worth
Head of Clinical Laboratories, Cancer Control Agency of British Columbia, 600 West 10th Avenue,
Vancouver, B. C. V5Z 4E6, Canada
In this presentation on the pathology of malignant melanoma I would like to consider
briefly some of growth patterns which are seen in melanomata and in associated melano
cytic precursor lesions. I shall attempt to relate the growth patterns to the biology of the
disease and to the clinical presentation.
Malignant melanoma appears to be increasing in incidence, the rate of increase in Can
ada exceeding that for every other tumor except lung cancer, while in southern Arizona
the incidence increased by 340% between 1969 and 1978 (Fitzpatrick et al. 1985). Fortu
nately, many melanomata are detected at an earlier stage, but late, deeply invasive lesions
are still frequently seen. Although the clinical features of dysplastic nevi and other precur
sor lesions are becoming more sharply defined and the role of ultraviolet radiation is un
der intense study, we are still not capable of determining who is actually at risk for devel
oping a melanoma with sufficient accuracy to develop adequate screening programs. At
present the detection of dysplastic nevi and early malignant transformation depends upon
clinical recognition of the lesion.
The cell of concern is, of course, the melanocyte. It is thought that the melanocytic pre
cursor cells migrate from the neural crest to the skin and other parts of the body very early
in life, melanocytes being found in the epidermis by the third month offetal development.
In the adult skin the melanocyte is seen as a small dendritic cell with clear cytoplasm,
which is located singly in the basal portions of the epidermis adjacent to the epithelial
basement membrane. The melanocyte is characterized by the presence of tyrosinase and
melanosomes, which differentiate it from the dendritic Langerhans' cells and intermediate
cells which may also be found within the epidermis. The melanosome, which is the specif
ic granule of the melanocyte, is found singly within the functional melanocyte, but when
transferred through the dendritic cytoplasm of the melanocyte to the adjacent epithelial
cells, the granules are aggregated into membrane-bound organelles, which may be visible
in tissue sections as melanin granules. In melanomas and in other melanocytic dysplasias
the melanosomes may assume an abnormal structure, or they may be absent in amelanotic
clones.
In future, with the advent of monoclonal antibodies, we may no longer have to depend
upon morphological characteristics to identify melanocytes and to evaluate melanocytic
disorders. Antimelanoma antibodies are already on the market, and they offer exciting
prospects for the future. An antibody which has already proved to be most useful in dis
tinguishing melanocytes from other connective tissue cells and from epithelial cells is
Sl00 protein.
Recent Results in Cancer Research. Vol 102
© Springer-Verlag Berlin· Heidelberg 1986
2 A.J. Worth
A B c
Fig. 1 A -CO Patterns of melanocytic proliferation. A Normal melanocytes growing as dendritic cells,
distributed along the basement membrane and interdigitating between the basal epithelial cells. B A
numeric abnormality is seen, the melanocytes being increased in number. There also is a positional
abnormality, as the melanocytes are clustering and becoming confluent in one of the rete pegs.
C Numeric and positional abnormalities are present, with the melanocytes (in addition to showing
confluent growth along the basement membrane) demonstrating upward invasion through the epi
dermis to the keratin layer. Melanocytes have broken through the basement membrane and are accu
mulating at and pressing against the papillary reticular dermal border. This growth pattern repre
sents an invasive level III melanoma.
Levels: I. cells confined to the epithelium above the basement membrane; II. malignant cells invad
ing the papillary dermis; III. malignant cells reach and accumulate at the papillary-reticular dermal
border; IV. invasion of the reticular dermis; V. invasion of the subcutaneous tissues
When looking at a section of nonnal skin one may have considerable difficulty in iden
tifying nonnal meianocytes, for as mentioned previously, they are small cells tucked along
the basal layers of the epithelium. Although they are scattered throughout the entire skin
surface they are most numerous along the basal portions of the rete pegs of the epidennis.
In many melanocytic disorders the number, distribution, and localization of melanocytic
cells within the epidennis may be of considerable help in arriving at the correct diagnosis
and can be of assistance in the understanding of the malignant potential of the lesion.
Meianocytic lesions, therefore, may be viewed in tenns of the numerical, positional,
and morphological and/or cytological abnonnalities which may be present. Generally
speaking, the presence of a numerical increase in the number of cells in the absence of a
positional or cytological aberration is the least significant perturbation, the positional and
cytological abnonnalities generally being associated with dysplasias and malignancy
(Fig. 1). In the most innocuous lesions, such as freckles and lentigines, the prominence of