Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027960 (mole)
 21,279 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although neurofibromatosis and cutaneous melanoma are both diseases of neuroectodermal origin, reports of their association are rare. The case history of a patient with histologically documented neurofibromatosis and a nodular melanoma unrelated to a cafe-au-lait spot or congenital nevus is reported, and the literature reviewed. The appearance of only one patient with neurofibromatosis in a series of 900 patients with melanoma suggests that these diseases are probably not associated with greater frequency than that predicted by chance alone.
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PMID:Cutaneous melanoma in a patient with neurofibromatosis. 11 Feb 69

We have identified antibodies against cytoplasmic components of allogeneic uveal melanoma cells in the sera of 16 of 31 patients with proven intraocular melanoma. Similar antibodies were found in 27% of controls and in 24% of patients with uveal nevi. The antibodies in these 3 groups of subjects were absorbed by components of uveal and cutaneous melanoma cells but not by those of normal choroidal melanocytes, normal uvea and retinal pigment epithelium, dermal nevus, pigmented skin or fetal cells. We found that specificity of the antibodies was also demonstrated by absence of reactivity with normal choroidal melanocytes, loss of reactivity after immune blocking, and absence of reactivity of melanoma antigen with conjugated antihuman immunoglobulin alone. Attempted absorption of the conjugated antihuman immunoglobulin by components of uveal melanoma cells did not alter the reactivity of the conjugated antihuman immunoglobulin.
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PMID:Specificity of tumor-associated antibodies in sera of patients with uveal melanoma. 69 90

Doxyribonucleates (DNMe) and deoxyribonucleic acid (DNA) were prepared by the ion-exchange method from Na+-salt from chicken erythrocyte DNA (DNS). (Here Me+ means Rb+, CS+, Na+, or NH4+). It was found that in aqueous solutions of DNMe in which the concentration of nucleic phosphorus was 8-10(5) mole/1 and the supporting electrolyte contained as an impurity only, the secondary structure of DNA was partly restored. This was confirmed by low values of the atomic extinction coefficient (epsilon260(p) = 6800 1/mole-cm and by high values of the hyperchromicity coefficients (1-28). The melting temperatures, as well as the width of the melting transition calculated from the melting curves, did not depend on the nature of Me+. Abnormally high melting temperatures for aqueous solutions of DNMe were noted. It was shown that the DNS - DNA transition was accompanied by spectrum changes that are typical of the denaturation process.
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PMID:[Effect of the nature of a monovalent counterion on the secondary structure of DNA is aqueous solutions]. 84 8

Although sun exposure is believed to be associated causally with cutaneous melanoma, the high incidence on less sun-exposed areas such as the back, as well as on chronically exposed sites such as the face, suggests that the association with sunlight is less straightforward than for other skin cancers. To explain this enigmatic site distribution, a theory of site-dependent susceptibility of melanocytes to malignant transformation is proposed. As possible evidence, all melanomas diagnosed in the state of Queensland, Australia, over a one-year period were surveyed for histologic evidence of benign melanocytic nevus cells adjacent to the melanoma, and analyzed according to anatomic distribution. Results showed a regional variation in the proportion of melanomas with adjacent nevi not explicable by regional variation in nevus density, which suggests that there is a varying susceptibility of nevi to malignant change. Given that nevus cells are equivalent to melanocytes, this finding would support the hypothesis that melanocytes at-large have a differential response to the mitogenic stimulus of sunlight according to anatomic site.
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PMID:A theory of site distribution of melanomas: Queensland, Australia. 142 Aug 53

There has been concern that individuals with nonfamilial melanoma and dysplastic melanocytic nevi (DMN) are not directly comparable to patients with hereditary melanoma and DMN. Because we have conducted a comprehensive study of nonfamilial melanoma over the past several years, we have addressed the above issue by directly comparing the characteristics of 145 nonfamilial patients, 6 patients with familial melanoma and the information available for familial melanoma in the literature. All 6 patients with familial melanoma had at least one first-degree blood relative with cutaneous melanoma. A large number of clinical and histologic variables were compared for both groups. Some pertinent variables included mean age at melanoma diagnosis 46.7 versus 52.3 years, mean Breslow thickness 2.11 versus 1.54 mm, mean total body nevi per patient 20.6 versus 18.3, mean total clinically atypical nevi per patient 2.0 versus 1.7 and total histologically confirmed DMN per group 22 (18.3%) versus 2 (33%), for patients with nonfamilial versus familial melanoma, respectively. No substantial differences were observed between the two groups. A review of the medical literature failed to reveal any quantitative data for melanocytic nevi, either clinical or histologic, at present that would allow distinction of patients with sporadic versus familial melanoma. We conclude that studies concerning the clinical characteristics of patients with DMN and nonfamilial melanoma are relevant to other persons with DMN including familial melanoma.
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PMID:Comparison of nonfamilial and familial melanoma. 155 90

To increase detection of melanoma, medical practitioners and the general public should know the signs of early invasive melanoma. The Scottish Melanoma Group recently presented a revised checklist of the major and minor signs. The validity of the reported clinical and histopathologic criteria for the dysplastic nevus, a precursor to cutaneous melanoma, is not fully established. However, expert pathologists agreed on the use of major and minor criteria. The differential diagnosis between spindle-epitheloid cell nevi and melanoma remains problematic, because the former lesions often show cellular atypia. Other lesions that can cause considerable diagnostic difficulties are melanoma in situ and minimal-deviation melanoma. Immunohistochemical studies of human melanocytic lesions have contributed to the diagnosis of poorly differentiated tumors but, so far, have not helped in the discrimination among benign, premalignant, and malignant lesions. They have provided additional prognostic information in cases of primary melanoma and locoregional melanoma metastasis. Quality control of antibody reagents continues to be a problem. Microstaging of primary melanoma using Breslow depth and Clark's level of invasion may be subject to considerable intra- and interobserver variation. To improve the accuracy of the measurements, using a vernier scale is recommended. The type of melanoma is relevant in considering clinicopathologic prognostic factors. Acral melanoma (for example, that arise from glabrous skin) has been reported to carry a grave prognosis. Polypoid melanoma may have a less unfavorable outlook than previously thought. DNA cytophotometry provides prognostic information in case of primary melanoma but loses significance when stratified for tumor thickness. In patients with lymph node-positive melanoma, however, DNA ploidy analysis appears to yield additional prognostic information. In the management of primary disease, the width of the surgical excision and whether to approach the regional lymph nodes remain the main issues. A multicenter study conducted by the World Health Organization Melanoma Programme has found that a "narrow" excision is a safe procedure for primary melanomas not thicker than 1 mm. Several investigators underline the need for continued annual follow-up for all melanoma patients; recurrence may occur late. Currently, elective lymph node dissection is not recommended in the management of "thick" primary melanoma. Because data from randomized trials conducted in patients with a tumor of intermediate thickness are not yet available, only guidelines on management offered by experienced surgeons can be given. Patients with the dysplastic nevus syndrome should be closely followed so that melanomas can be diagnosed as early as possible.
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PMID:Clinical and pathologic diagnosis, staging and prognostic factors of melanoma and management of primary disease. 159 9

In a 26-year-old patient there have been benign enlargements of the lymphatic nodes and a splenomegaly since the end of the adolescence. In the 21st year of age the diagnosis of a Tangier disease was made. Allogenic HDL-rich serum fraction (COHN IV/1-fraction, prepared according to the modified method 6) infused under therapeutic aspect led to a prolonged increase of the serum total cholesterol and of the thrombocytes. The results pled for an activation of the reverse cholesterol transport. Excessively high malonic dialdehyde concentrations in the serum were relating to a "free radical"-associated metabolic defect, which was caused by the hypocholesterolaemia, the reduced transport capacity of vitamin E in the plasma and the nutrition poor in selenium and cholesterol, respectively. Under a nutritive antioxidant supplementation with sodium selenite and D-alpha-tocopherol a slight increase of the total cholesterol, of the thrombocytes as well as a normalization of the MDA values could be reached. The chronic oxidative stress appeared in the patient in a distinct lipofuscinosis of the skin and formations of naevus-cell naevi as an expression of massive denaturations of protein-lipids. In the Tangier disease we must reckon with an increased mutagenic effect of free radicals with an additional DNS repair capacity as well as an increased sensitivity to radical-generating cancerogenic xenobiotics.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Tangier disease--a "free radical"-associated disease. Results of HDL and anti-oxidant therapy with selenium and D-alpha tocopherol]. 166 43

To investigate the UV effect on epidermal melanocytes, 21 volunteers and 11 patients with dysplastic nevus syndrome (DNS) received UVB irradiation three times weekly during 17 days. Skin biopsies were taken before and three weeks after the last irradiation (on day 37) from exposed and covered buttock skin. The epidermal melanocyte population density was estimated in dopa-stained split skin preparations. The biopsies taken on day 37 revealed that repeated UVB irradiation induces an increase in the number of melanocytes not only in exposed but also in covered skin. This increased mitotic activity might be a link between sun exposure and melanoma development in covered skin. The size of the proliferative response was inversely correlated to the basal melanocyte number. The larger population increase in skin with few melanocytes might amplify the propagation of DNA damage and increase the likelihood of tumor development. The pigment metabolite 5-S-cysteinyldopa (5-S-CD) was measured in urine before the irradiation and twice weekly until day 38. No correlation was found between the basal 5-S-CD excretion and the size or activity of the melanocyte organ, suggesting that the basal 5-S-CD excretion is mainly of non-melanocytic origin. Despite numerous nevi, DNS-patients did not differ from controls in their 5-S-CD excretion. The normal upper range for the tumor maker 5-S-CD is therefore valid in these melanoma-prone subjects. During the irradiation, subjects with a low tanning ability developed a more pronounced erythema and excreted more 5-S-CD than those with a good tanning ability. This suggests that the UVB-induced 5-S-CD excretion is rather due to melanocyte damage than to an increased melanin synthesis. To investigate the influence of sun exposure on the development of nevi and melanoma (CMM), the distribution over the body surface of CMM, common nevi (CN) greater than or equal to 2 mm and dysplastic nevi (DN) was registered in 121 melanoma patients and 310 controls. Four times as many nevi were found in a sun-exposed area than in a comparable sun-protected area, demonstrating that sun exposure plays an important role in nevus development. Subjects with DNA had a larger difference in nevus counts between the two areas than subjects without DN, indicating a different UV-dose and/or a higher sensitivity to the "nevogenic" effect of UV-light than subjects without DN.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Melanocytes, moles and melanoma--a study on UV effects. 181 38

Nerve growth factor (NGF) stimulates growth and differentiation of sensory and sympathetic neurons. It is not known what role NGF plays in melanoma development, but nevus and malignant melanoma cells express NGF-receptor (NGF-R). We counted nerve fibers within melanocytic nevi, primary cutaneous melanomas, and cutaneous melanoma metastases using a monoclonal antibody (MoAb) as marker against a 200-kD glycoprotein that is expressed on human nerves. The expression of NGF-R was studied in serial cryostat sections using a MoAb against the NGF-R. Compared to normal skin, increased numbers of nerve fibers were found in 72 melanocytic nevi. In congenital nevi their number significantly increased with age. In 47 primary cutaneous melanomas the number of nerve fibers decreased in proportion to tumor thickness. In 33 cutaneous melanoma metastases no accumulation of nerve fibers was found. NGF-R was not expressed in normal skin melanocytes and in the majority of nevus cells in melanocytic nevi. Considerable numbers of NGF-R-positive nervus cells were found only in some congenital nevi and few acquired nevi with dysplastic features. By contrast, in primary and metastatic melanomas higher expression of NGF-R was observed. The increased number of nerve fibers in melanocytic nevi suggests that neurite-promoting factors are produced in situ. Production of such factors appears to be lost in malignant melanoma cells. The finding of an inverse correlation between an abundance of nerve fibers in NGF-R-poor nevi and a high expression of NGF-R in melanomas that show no evidence of nerve growth suggest a role of NGF and its receptor in malignant melanocytic tumors.
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PMID:Nerve growth and expression of receptors for nerve growth factor in tumors of melanocyte origin. 185 Jul 72

We examined the role of UVR (UV radiation) (UVA, 320-400 nm; UVB, 290-320 nm; and the combination of UVA and UVB) as a promoter in the induction of cutaneous melanoma. One hundred and seventy hairless mice (Skh-hr2), 6-8 weeks old, were treated in 8 groups: group I, DMBA [7,12-dimethylbenz(a)anthracene] plus UVA; group II, DMBA plus UVA plus UVB; group III, DMBA plus UVB; group IV, DMBA; group V, UVA; group VI, UVA plus UVB; group VII, UVB; group VIII, control. DMBA (0.5% solution) was applied once to promote the formation of dermal melanocytic nevus-like lesions while UVR treatments were conducted 3 times/week for 30 weeks. The mice were examined periodically for the development of multiple pigmented lesions, papillomas, squamous cell carcinomas, melanomas, and lymphomas. Treatment with DMBA plus UVA, DMBA plus UVB, and DMBA plus UVA plus UVB stimulated the development of multiple pigmented nevus-like lesions (85-100%) in mice of groups I, II, III, and IV. Upon necroscopy, 27-33% of animals in groups I, II, and III receiving UVR treatments developed clinically and histologically characterized melanomas. Treatment with DMBA alone did not produce melanomas. DMBA-treated animals in groups I, II, and III which received UVR treatments also developed lymphomas (21-50%). Animals treated with DMBA alone or those that received UVB or the combination of UVB plus UVA (without DMBA) developed only papillomas and squamous cell carcinomas (25-47%). Skin tumors were analyzed for the presence of point mutations in the ras gene. Polymerase chain reaction amplification of DNA and selective oligonucleotide hybridization revealed mutations in the 61st codon of the N-ras gene in the precursor nevus-like lesions and melanoma samples studied. This study suggests that UVR (both UVA and UVB) plays a role as a promoter in the stimulation of melanoma and lymphoma development in hairless mice.
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PMID:Role of ultraviolet radiation in the induction of melanocytic tumors in hairless mice following 7,12-dimethylbenz(a)anthracene application and ultraviolet irradiation. 190 31


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