Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0025202 (melanoma)
 69,561 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Oral mucosa from six sites in 95 autopsies was tested for melanin using the Masson-Fontana silver reduction method. Melanin was detected in 51.6% of labial, 46.3% of palatal, 45.3% of buccal, 28.4% of mandibular gingival, 25.3% of lingual and 21.1% of maxillary gingival samples. 93.7% of epidermal samples from the same population were positive. In 24.2% of the subjects there was no detectable melanin at any intraoral site and 4.2% showed activity in all six sites. The mean number of positive oral sites per individual was 2.2. There are thus regional differences in oral epithelial melanocyte activity, but no parallel with the known regional incidence of primary oral melanoma.
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PMID:A histochemical study on the distribution of melanin in human oral epithelium at six regional sites. 174 76

The paper gives a case report of the primary malignant melanoma of the trachea in a 61 years old patient with micrometastasis in the right upper lobe of the lung. The diagnosis was made after autopsy. Macroscopically, a polypoid, greyish, partly dark brown tumor was found 6 cm above the tracheal bifurcation on the site of connection between the membranous and cartilaginous part. The tumor was fixed to the trachea wall with a very narrow long stalk, causing long dispnoic attacks worsening in a back lying position particularly. Histologically, both the primary tumor and its secondary deposit in the right lobe were found to have similar appearance as a malignant melanoma elsewhere. Melanin pigment was found in abundance here and there and easily detected already in preparations stained by the hematoxylin--eosin method. The large polypoid tumor caused an obstruction of the trachea and finally suffocation.
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PMID:[Primary malignant melanoma of the trachea]. 176 92

Effects of dexamethasone on melanogenesis and tyrosinase mRNA levels were determined in B16/F10 melanoma cells. Melanin content of B16 cells increased in a dose-dependent manner by the addition of dexamethasone to the culture medium. After 72 hr exposure, dexamethasone (10(-6) M) produced a 2.4-fold increase in melanin content. Northern blot analysis revealed that tyrosinase mRNA level also increased by the addition of dexamethasone to the culture medium. After 24 hr exposure, dexamethasone (10(-6) M) caused a 1.8-fold increase in tyrosinase mRNA levels. A tumor promoter, 12-O-tetradecanoyl phorbol-13-acetate (TPA) decreased tyrosinase mRNA level at 30 nM concentration. Dexamethasone antagonized this TPA-mediated decrease in tyrosinase mRNA. It is suggested that glucocorticoids are involved in the regulation of tyrosinase activity at the transcriptional level.
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PMID:Glucocorticoid stimulates melanogenesis and tyrosinase gene expression in B16 melanoma cells. 182 29

Melanin is a widely-distributed pigment in the biosphere. In the human adult, the enzymatically-catalysed process of melanin generation is the exclusive prerogative of melanocytes. Melanogenesis generates a number of reactive intermediates including orthoquinones and has been recognised as a potential hazard to melanocytes. Amplification of this cytotoxic hazard to selectively damage malignant melanogenic cells has been investigated as a rational therapeutic strategy for melanoma. A number of surrogate substrates for tyrosinase have been studied, including a range of phenols and catechols. Initial attempts to use these agents for the treatment of disseminated melanoma have foundered on problems due to unfavourable pharmacokinetics, primary toxicity or pharmacological actions of the analogue substrates, and the toxicity of hepatic metabolites. Successful exploitation of the undoubted potential of the metabolic targeting strategy presented by the subversion of melanogenesis depends on the development of prodrugs with minimal primary toxicity and improved pharmacokinetics. The range of possible novel approaches is being extended by the emergent understanding of the complexities of melanogenesis which are outlined.
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PMID:Melanogenesis: a realistic target for antimelanoma therapy? 183 32

Malignant melanomas of the mucous membranes are rare tumors. They make up about 10% of all malignant melanomas of the head and neck; 15 of the authors' cases are reviewed in this article. Six of these had neck lymph node metastasis when first diagnosed. The tumors were surgically removed in all patients. Thirteen patients developed at least one tumor recurrence, ten patients distant metastasis. Eight patients died of the tumor condition; the mean survival time of all patients was 33.4 months. While the tumors could be classified histologically into four types, this had no bearing on the course of the disease. In many cases, primary tumor and metastasis or recurrent tumor differed histologically. Melanin pigment was found in 13 tumors. Mucosal melanomas can be regarded as a discrete tumor entity because their biological behavior differs from that of malignant melanomas of the skin. However there are no morphological differences between the two tumor entities. Ophthalmological and dermatological examinations must be performed in all patients with mucosal melanoma to exclude metastasis of the skin or choroid melanoma.
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PMID:[Malignant melanoma of the mucous membranes of the upper aerodigestive tract. Clinical, histological and immunohistochemical characteristics]. 187 32

We tried to culture melanoma cells from a Mongolian gerbil's (Meriones unguiculatus) malignant tumor. In primary culture, most of cells have abundant melanin granules in their cytoplasm. Melanin granules decreased through 5 to 15 serial passages and disappeared after 15 th passage. The morphology of the cells varied from spindle to large polydendritic cells. Although typical melanin granules were not seen when the cells were stained by Masson-Fontana method, the cells were positive for DOPA reaction. Electron microscopically, most of the cells have well-developed Golgi apparatus and rough-surfaced endoplasmic reticulum with dilated cistern, and premelanosome-like granules were frequently observed in their cytoplasm.
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PMID:Tissue culture study on Mongolian gerbil's (Meriones unguiculatus) malignant melanoma. 191 6

Melanin contains melanin-free radicals and can both absorb and produce additional free radicals and active oxygen species on exposure to various stimuli. Yet its role in the radiation responses of malignant melanoma has been little studied. In this report, three subclones of Cloudman S91 mouse melanoma clone PC1A varying in constitutive melanin content were compared with respect to killing by gamma irradiation. Radiation responses correlated with melanin content. The least melanotic line, S91/amel, was most sensitive and the most melanotic line, S91/I3, was most resistant. Curve fitting using the linear-quadratic model suggests that S91/amel is killed only by single event inactivations; S91/I3, only by double event inactivations; and S91/M1B, with intermediate melanin and radiation response, by both types of inactivations. Split dose experiments confirmed a lack of immediate split dose recovery in S91/amel and its existence in S91/I3. Potentially lethal damage and its repair could be demonstrated in both S91/amel and S91/I3. Double strand break (DSB) induction was evaluated as a function of gamma ray dose in DNA of S91/I3 and S91/amel, as well as in EMT6, a mouse mammary cancer line that lacks tyrosinase and melanin. The rates of induction were proportional to cellular melanization, i.e., the rate of DSB induction was greatest in S91/I3, least in EMT6. Levels of thioredoxin reductase (TR), glutathione reductase (GR), superoxide dismutase (SOD), and catalase (CAT) were determined in S91/amel and S91/I3. TR was the same in both cell lines, while the other three enzymes were 3- to 4-fold lower in S91/amel.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Does melanin affect the low LET radiation response of Cloudman S91 mouse melanoma cell lines? 194 13

A case of amelanotic malignant melanoma of the esophagus in a 76-year-old woman is reported. A whitish polypoid tumor, measuring 3 x 2 x 2.7 cm, surrounded by black pigmented mucosa, was detected in the middle intrathoracic esophagus. The tumor showed a lobulated surface lined by squamous cell layer, and had epithelioid and polyhedral cells forming alveolar clusters. Melanin pigments or stainability for the dihydroxyphenylalanine (DOPA) reaction were only observed in a few tumor cells. Junctional changes and mucosal melanosis, however, were found freely in the mucosa around the tumor. Many tumor cells showed a strongly positive immunohistochemical reaction for neuron specific enolase (NSE) and S100 protein. The patient died of widespread metastases six months after surgery. Further, a review of 106 reported cases of primary esophageal malignant melanoma, including 29 autopsies, was made; the melanomas were found to include 10 of amelanotic type, eight of which had been misdiagnosed at biopsy. Junctional changes could be found in the mucosa over or around the tumor, in four cases, and mucosal melanosis in one. Lymph node metastasis was the most frequently observed development at autopsy regardless of whether the tumor was amelanotic or melanotic. For correct diagnoses of melanomas of the amelanotic type, peripheral mucosal findings, such as junctional changes or melanosis, should be helpful; and, in order to obtain a good prognosis, a careful resection of the regional lymph nodes could prove valuable.
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PMID:Amelanotic malignant melanoma of the esophagus: case report and review of the literature. 225 5

Photokilling of pigmented mouse melanoma cells (B-16) was investigated using pulsed high intensity visible radiation. Melanin acts as an endogenous chromophore, and 694 nm radiation with 40 nsec pulse duration and 0.5-3 X 10(7)w/cm2 intensity causes cell death. Irradiation of non-pigmented human melanoma cells (U1) or human squamous carcinoma cells (FaDu) under similar conditions did not kill the cells. Also, irradiation of B-16 cells with 300 microsec laser pulses (10(3)W/cm2) or with continuous wave (CW) radiation (10(-3)W/cm2) did not kill the cells. These data indicate that pigmented cell killing is due to absorption of radiation by melanin and that the pulsewidth and intensity of radiation play important roles in cell killing. The generation of acoustic waves due to absorption of the pulsed radiation by pigmented cells and by isolated melanosomes was demonstrated at 532 and 625 nm and 8.5 nsec pulse duration (10(7)-10(8) W/cm2); the amplitudes of the acoustic signals were approximately 2.5-3.0-fold higher at 532 nm compared with 625 nm, and they increased with increasing fluence. In contrast, irradiation of U1 or FaDu cells with comparable fluences and intensities did not generate acoustic waves. A possible correlation between the generation of photoacoustic waves and pigment cell death is proposed. Since the thermal relaxation time of melanosomes is 0.5-1.0 microsec, the mechanism proposed is that thermal confinement of high intensity, short-pulse visible radiation generates acoustic waves by thermal expansion, leading to mechanical damage to the cells.
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PMID:Irradiation of pigmented melanoma cells with high intensity pulsed radiation generates acoustic waves and kills cells. 230 65

Cytologic specimens of neuroendocrine tumors metastatic to the liver were examined with regard to their silver staining properties after the application of argentaffin and argyrophil staining techniques (Masson, Grimelius and Sevier-Munger). In tumors with a content of serotonin (small intestine carcinoids), the presence of this substance was demonstrated cytologically as an argentaffin reaction in individual tumor cells; however, formalin fixation was a prerequisite for positive staining. Melanin in malignant melanoma cells displayed a positive argentaffin reaction, irrespective of the fixation used (air drying, formalin, Bouin's fluid or acetone-alcohol). Thus, serotonin and melanin can be distinguished in cytologic samples of neuroendocrine tumors by the use of the Masson argentaffin reaction with different fixatives. The nonargentaffin-positive neuroendocrine tumor cells were weakly stained or unreactive with the Grimelius argyrophil technique. The Sevier-Munger argyrophil technique was negative or gave a disturbing nonspecific background staining reaction that was difficult to interpret in the cytologic samples. Thus, the Grimelius method appears to be the most useful silver stain for identifying neuroendocrine tumor cells in cytologic material, irrespective of their hormone content, since both argentaffin-positive and argentaffin-negative cell samples were stained at least to some degree.
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PMID:Application of silver stains to cytologic specimens of neuroendocrine tumors metastatic to the liver. 241 33


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