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Query: UMLS:C0027960 (mole)
 21,279 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We conducted a case-control interview study among 1277 subjects (407 patients, 870 controls selected by using random digit dial) in 11 western United States to determine whether uveal melanoma and cutaneous melanoma shared common risk factors. After adjustment for other factors, the risk of uveal melanoma was increased for those with green, gray, or hazel eyes [relative risk (RR) = 2.5, P less than 0.001] or blue eyes (RR = 2.2, P less than 0.001) when compared to brown. A tendency to sunburn after 0.5 h midday summer sun exposure increased risk for uveal melanoma (burn with tanning RR = 1.5, P = 0.02; burn with little tanning RR = 1.8, P less than 0.001; burn with no tanning RR = 1.7, P = 0.002); as did exposure to UV or black lights (RR = 3.7, P = 0.003); and welding burn, sunburn of the eye, or snow blindness (RR = 7.2, P less than 0.001). An association with uveal melanoma was also noted with an increasing number of large nevi (P = 0.04 for trend), although the individual risk estimates were not remarkable. These data suggest that host factors and exposure to UV light are risk factors for uveal melanoma.
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PMID:Uveal melanoma in relation to ultraviolet light exposure and host factors. 239 51

We report seven examples of pigmented spindle cell naevus (PSCN) and variants, emphasizing their histopathologic differentiation from malignant melanoma (CMM). Confusion with CMM may occur because of upward migration (pagetoid spread) of cells, prominent lateral extension of lentiginous melanocytic hyperplasia, and cytological atypia in spindle cell naevi. However, these proliferations are usually associated with a symmetrical and orderly growth pattern, confinement of the pagetoid spread to the lower epidermis, 'maturation' of the dermal component, and lack of marked cytological atypia.
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PMID:Pigmented spindle cell naevus and its variants: distinction from melanoma. 261 Nov 23

Two hypotheses have been presented. The first states that melanomas commonly evolve from normal melanocytes by a tumor progression pathway from a banal nevus to a nevus with dysplasia, to a micro-invasive, and then to a fully evolved, tumorigenic, primary melanoma which has competence for metastasis. It is important to note that not all melanomas follow this complete pathway. As Foulds noted long ago, tumors may bypass any of the stages of tumor progression. Thus, many melanomas do not, apparently, arise in nevi, and melanomas may evolve "fully formed" as pure tumorigenic nodules. However, from the biological point of view, study of the benign potential precursors (nevi and, especially, dysplastic nevi as well as microinvasive melanomas) may well reveal mechanisms of progression that are applicable to all melanomas, and perhaps to other solid tumors as well. From a clinical viewpoint, follow-up and education of patients at increased risk for melanoma, and early diagnosis of melanomas in their curable, microinvasive stages may result in a reduction of mortality from the disease, even without influencing its overall incidence. The melanomas that occur on plantar and palmar (acral) skin appear to progress through a microinvasive stage similar to that of other cutaneous melanomas. However, the significance of precursor and marker lesions (if any exist) in acral melanoma remains to be elucidated by clinicopathologic and epidemiologic studies. The possibility of etiologic agents other than UV light, such as chemical carcinogens and/or viruses, should be investigated in these cases. The second hypothesis presented here, that UV light is etiologic for the common cutaneous melanoma of white populations, has support from clinical, epidemiologic, and biologic observations. From a biologic viewpoint, ultraviolet light has all of the properties that might enable it to act as a complete carcinogen, and to enhance tumor progression in melanocytic "potential-precursor" lesions. Clinically, it seems appropriate to encourage patients (and members of the general population, as well) to adopt sensible attitudes to sun exposure. By such means, it is possible that some melanomas might be prevented, or that the rate and incidence of progression to more-advanced stages might be inhibited.
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PMID:Human melanocytic neoplasms and their etiologic relationship with sunlight. 265 3

We examined the relationship between self-reported mole counts and cutaneous melanoma with respect to anatomic site in 110 case and 231 control female nurses. Counts of moles on the lower leg were better predictors of melanoma risk than were counts of moles on the arm. The relative risk for the highest quintile of lower leg mole counts versus no lower leg moles was 4.2. Mole counts at each site (arm, thigh, and lower leg) were associated with risk of melanoma of the trunk and lower leg, but none were associated with the risk of melanoma of the upper extremity. The absence of direct site-specificity suggests that mole counts primarily indicate systemic melanoma risk, rather than direct risk from the moles themselves.
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PMID:Moles and site-specific risk of nonfamilial cutaneous malignant melanoma in women. 273 40

The hereditary dysplastic nevus syndrome (DNS) is an autosomal dominant disorder in which affected individuals have increased numbers of dysplastic (premalignant) nevi and a greater than 100-fold increased risk of developing cutaneous melanoma. Epstein-Barr virus-transformed lymphoblastoid cell lines from patients with hereditary DNS have been shown to be hypermutable to UV radiation (M.I.R. Perera et al., Cancer Res., 46: 1005-1009, 1986). To examine the mechanism involved in this UV hypermutability, we used a shuttle vector plasmid, pZ189, which carries a 160-base pair marker gene, supF, and can replicate in human cells. pZ189 was treated with UV radiation and transfected into DNS6BE, a lymphoblastoid cell line from a patient with hereditary DNS. Plasmid survival after UV was similar with the DNS6BE line and with a lymphoblastoid cell line from a normal donor. Plasmid mutation frequency was greater with the DNS line in accord with the DNS cellular hypermutability. Base sequence analysis was performed on 69 mutated plasmids recovered from the DNS line. There were significantly more plasmids with single base substitution mutations (P less than 0.01) in comparison to UV-treated plasmids passed through normal fibroblasts. pZ189 hypermutability and an increased frequency of single base substitutions was previously found with a cell line from a melanoma-prone xeroderma pigmentosum patient. These differences may be related to the increased melanoma susceptibility in both DNS and xeroderma pigmentosum.
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PMID:Ultraviolet mutagenesis in a plasmid vector replicated in lymphoid cells from patient with the melanoma-prone disorder dysplastic nevus syndrome. 279 Aug 6

Patients with xeroderma pigmentosum (XP) have more than a 1000-fold increased risk of cutaneous melanoma. To determine if the XP DNA repair defect is present in cutaneous pigmentary cells, nevus cells and melanocytes from four large, pigmented nevi were cultured from a 12-year-old girl with XP. Cultured melanocytes showed dendritic morphologic features, contained mature melanosomes, and reacted with monoclonal antibody to tyrosinase. Nevus cells were spindle shaped and expressed nevus cell-associated antigens. Melanocytes, nevus cells, and dermal fibroblasts from the patient with XP all had a similar reduction in DNA repair: unscheduled DNA synthesis was 30% to 50% of that in normal fibroblasts following a 30 J/m2 ultraviolet dose. After a 6 J/m2 ultraviolet dose, the proliferative ability of XP nevus cells and fibroblasts was reduced to 10% of that of normal fibroblasts. This study indicates that cultured melanocytes and nevus cells express the characteristic XP DNA repair defect.
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PMID:Reduced DNA repair in cultured melanocytes and nevus cells from a patient with xeroderma pigmentosum. 291 63

The reactivity of 12 surgically removed uveal melanoma lesions with monoclonal antibodies (MoAb) to 14 membrane-bound and 2 cytoplasmic cutaneous melanoma-associated antigens (MAA), to the 2 subunits of HLA Class I antigens and to the gene products of the HLA-D region was compared with that of cutaneous melanoma lesions and correlated with their histiotype. The membrane-bound determinants defined by the anti-Mr 92,000 and 45,000 MAA MoAb TP39.1, anti-Mr 110,000 MAA MoAb M111, anti-Mr 118,000 MAA MoAb TP36.1, anti-Mr 115,000 MAA MoAb 345.134, anti-ICAM-1 MoAb CL203.4 and anti-Mr 31,000 MAA MoAb M2590, and the cytoplasmic determinants defined by the anti-MAA MoAb 465.12 and 2G-10 display a distribution in uveal melanoma lesions similar to that in cutaneous melanoma lesions. On the other hand, membrane-bound determinants defined by the anti-Mr 100,000 MAA MoAb 376.96, anti-9-O-acetyl-GD3 ganglioside MoAb ME311 and anti-GD2-GD3 ganglioside MoAb ME361 were not detected in the uveal melanoma lesions tested. Furthermore, the membrane-bound determinants defined by the anti-GD3 MoAb R24, anti-nerve growth factor receptor MoAb ME20.4, anti-Mr 97,000 MAA MoAb 140.240, anti-carcinoembryonic antigen MoAb B1.1 and anti-HMW-MAA 149.53, 225.28, and 763.74 have a markedly lower expression in uveal than in cutaneous melanoma lesions. Incubation of uveal melanoma lesions with the pool of the MoAb 149.53, 225.28, and 763.74 recognizing distinct and spatially distant determinants of the HMW-MAA increased the intensity of staining of six lesions and stained four lesions which were not stained by the individual monoclonal antibodies. The distribution of HLA Class I antigens in uveal melanoma lesions resembles that in cutaneous melanoma lesions, since they are expressed in all the lesions of the mixed and epithelioid type but were not detected in those of the spindle type, i.e., the counterparts of nevocellular nevi. HLA Class II antigens are expressed with a lower frequency in uveal than in cutaneous melanoma lesions, since they were detected only in 2 of the 12 lesions. One of them is of the mixed type and the other one of the epithelioid type. Besides HLA antigens the determinants defined by the anti-carcinoembryonic MoAb B1.1, anti-ICAM-1 MoAb CL203.4, and anti-GD3 MoAb R24 displayed a differential distribution in the different histiotypes of uveal melanoma, since they are preferentially expressed in lesions of the mixed and epithelioid type.
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PMID:Analysis of the antigenic profile of uveal melanoma lesions with anti-cutaneous melanoma-associated antigen and anti-HLA monoclonal antibodies. 291 56

We examined 2,227 lymph nodes from 100 patients with clinical Stage I cutaneous melanoma for the presence of microscopic deposits of tumor. On examination of hematoxylin-and-eosin-stained sections, none had melanoma. Sixteen nodes from 14 patients had melanoma detectable by an antiserum to S-100 protein in a peroxidase-antiperoxidase (PAP) assay. The melanomatous nature of these cells was confirmed by their reaction with the melanoma-directed monoclonal antibody NKl/C3. The incidence of occult nodal metastases was highest in patients with deeply invasive and micrometrically thick primary tumors. The incidence of occult melanoma was not increased where additional serial sections were cut and semiserial sections examined. Pitfalls in the identification of occult melanoma cells (OMC) include S-100 protein-positive interdigitating dendritic cells, capsular nevus cells, a minority of sinus "macrophages," and the Schwann cells of node-associated nerves. Thus, we conclude that the incidence of early melanoma metastases in the regional lymph nodes of patients with clinical Stage I melanoma is greater than has previously been appreciated on the basis of assessment of routine hematoxylin-and-eosin-stained sections. Six of the 14 patients with OMC died of melanoma (41%), as compared to only 18 of 86 patients without OMC (21%; 0.10 greater than P greater than 0.05).
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PMID:Occult tumor cells in the lymph nodes of patients with pathological stage I malignant melanoma. An immunohistological study. 271 94

Cutaneous malignant melanoma (CMM) rates have been increasing in the United States at an average rate of about 4% per year. In 1987, it was estimated that there would be 25,800 cases and 5,800 deaths from CMM in the United States. The exact cause of the increase in unknown, but there is evidence to suggest that increasing exposure to the ultraviolet B (UVB) radiation present in sunlight may be partly responsible. The evidence includes: 1. the fact that higher CMM incidence rates are observed in people with lesser amounts of skin pigment (which blocks penetration of UV); 2. a correlation of higher CMM rates with decreasing latitude and increasing UVB levels; 3. the observation that freckles and nevi (precursors to CMM) are induced by solar exposure; 4. differences in CMM rates between natives and immigrants to sunny climates; 5. high rates of CMM in patients who cannot repair UVB-induced DNA damage; and 6. the indication that sun exposure at early ages and of an intermittent nature results in higher CMM risks. With the concern that depletion of stratospheric ozone could result in increasing levels of UVB, it has become important to understand the relationship between UVB and CMM in order to estimate the increases in CMM that would be expected with ozone depletion. When empirical relationships between UVB and CMM incidence and mortality rates were derived and used to estimate the impact of stratospheric ozone depletion, a 1% depletion of ozone was predicted to result in increases of 1%-2% in CMM incidence and 0.8%-1.5% in CMM mortality.
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PMID:Cutaneous malignant melanoma and ultraviolet radiation: a review. 306 76

Melanomas are associated with a T-cell predominant infiltrate that may cause their regression. Langerhans cells (LC) are essential for initiation and maintenance of specific T-cell-mediate responses in the skin. Therefore, a change in this antigen-presenting LC population may alter the host response. To determine whether the LC population varies during the evolution of primary cutaneous melanoma 32 melanocytic lesions, nevi, and cutaneous melanomas were studied by quantitative immunohistology. The monoclonal antibody, Leu-6, and the avidin biotin complex immunoperoxidase method were used to identify LC. Compared with histologically normal melanoma-adjacent skin, epidermal LC were depleted above "deeply invasive" melanomas but were relatively unchanged above nevi, "early invasive" melanomas, and cutaneous metastatic melanoma nodules. Dermal LC were significantly increased around in situ and "early invasive" melanomas but not around "deeply invasive" melanomas or cutaneous metastatic nodules. Dermal LC are thus associated with early transformed melanocytes and may present neoantigens to T lymphocytes in situ or after LC maturation in the draining lymph node. Melanoma-associated LC decline in number as melanoma progresses.
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PMID:Quantitative alterations in cutaneous Langerhans cells during the evolution of malignant melanoma of the skin. 326 Sep 30


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