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)

The malignant transformation of a plantar nevus is presented. Perilesional vitiligo developed concurrently with the onset of malignancy. The primary lesion was controlled surgically, but the patient succumbed to metastiatic melanoma within a year. The relation of perilesional vitiligo in malignant melanoma to the so-called halo nevus, and the immunologic significance of these discolorations is reviewed.
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PMID:Perilesional vitiligo in melanoma. 83 17

Three patients with malignant melanoma and coexisting vitiligo are described. All three appear to exhibit at least partial spontaneous control of the melanoma. The hypothesis is made that there may be a significant association between vitiligo and regressing melanoma. The basis for this is the fact that there may be an association between vitiligo and the production of an antimelanoma antibody, promoting rejection of the melanoma.
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PMID:Vitiligo and malignant melanoma: a significant association? 97 63

In 1975, 117 patients with malignant melanoma attented the Department of Dermatology at the University of Cologne, and three of these had had a superficial spreading melanoma (SSM) over a long period-one patient most probably for more than 25 years. With these patients another primary malignant melanoma developed, though not a metastasis. It appears that SSM gives no protection against other melanomas of the superficial or nodular type. In comparison, a 70-year-old patient had had a pigmented tumour for about 40 years and this suddenly spread five years ago; however, at least some of the metastases regressed to form vitiligo-like lesions surrounding deposits of melanin in macrophages. In this case the spontaneous regression did not protect the patient against new metastases in the lymph nodes and probably in the liver as well.
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PMID:[Primary multiple malignant melanomas of unusually long duration]. 100 59

In four patients with superficial spreading melanoma, partial spontaneous regression and/or leukodermas of different appearance occurred. In two patients leukoderma appeared within the central area of the primary tumor; one of whom developed, in addition, vitiligo elsewhere on the body. In a further case the melanoma exhibited a depigmented halo resembling Sutton's nevus. Presumably, these leukodermas represent an epiphenomenon of the specific immunological reaction between the host and the melanoma.
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PMID:[Spontaneous regression and leukoderma in malignant melanoma]. 112 45

Anti-tumour antibody was sought in the sera of three groups of patients; idiopathic vitiligo, malignant melanoma and miscellaneous skin disorders. No precipitating antibody to a series of prepared pigmented tumour antigens was demonstrated. All sera were tested for a number of auto-antibodies. No significant differences were detected between the groups. The evidence for an immunological factor in the causation of vitiligo remains circumstantial only.
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PMID:Serum anti-tumour antibodies and auto-antibodies in vitiligo. 115 53

Six patients with vitiligo and malignant melanoma are reported. The relationship between vitiligo and melanoma seems to be a firm one. This process is supposed to represent an expression of induced autoimmunity.
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PMID:Vitiligo and malignant melanoma. 119 28

The therapeutic uses of naturally occurring psoralens in modern-day medicine (8-methoxypsoralen (8-MOP), 5-methoxypsoralen (5-MOP), 4,5',8-trimethylpsoralen, and a few other synthetic psoralens) have evolved through five stages of development. (1) In the historical period (2000 BC to 1930 AD), the pigment-stimulating properties of naturally occurring plants containing psoralens were described anecdotally. (2) The second period (1930-1960) dealing with the chemistry of psoralens involved extraction, identification of their structure, synthesis, and the relationship between chemical structure and their photoreactivity and pigment-stimulating properties. The treatment of vitiligo with oral and topical 8-MOP became popular. (3) In the third period (1960-1974), we witnessed a new beginning and the growth of basic science studies and clinical investigations into various biological properties of psoralens including action spectrum studies, mutagenesis and carcinogenesis studies, in vitro and in vivo photoreactivity studies of various psoralens with DNA, RNA, proteins, and pharmacological and toxicological studies in vitiligo patients undergoing long-term therapy for repigmentation. (4) The fourth period (1974-1988) is recognized as the period of photochemotherapy and the development of the science of photomedicine which established the therapeutic effectiveness of psoralens in combination with newly developed UV irradiation systems that emitted high-intensity UVA radiation in the treatment of severe psoriasis, mycosis fungoides, and over 16 other skin diseases. The effectiveness of PUVA (psoralen + UVA) was confirmed by well controlled clinical trials in thousands of patients, both in the USA and in European countries. Combination therapy with oral retinoids and PUVA contributed to greater effectiveness and long-term safety of psoralen photochemotherapy. (5) In the fifth period (1989 and beyond), psoralens are now emerging as photochemoprotective agents against non-melanoma skin cancers and as immunologic modifiers in the management of certain patients with disorders of circulating T-cells using new techniques of photopheresis. In the final analysis, perhaps the application of pharmacological and therapeutic concepts and principles of using psoralens in combination with UVA has contributed to the development of a new science of photomedicine in which the interaction between basic scientists, photobiologists, and physicians has produced both basic and new clinical knowledge for the care and control of human suffering.
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PMID:The evolution of photochemotherapy with psoralens and UVA (PUVA): 2000 BC to 1992 AD. 143 83

We report the case of a patient with stage 2 malignant melanoma (MM), who received a specific immunotherapy consisting of intralymphatic injections of irradiated MM cells. She developed subsequently vitiligo-like leukoderma and several plaques of localized scleroderma. Simultaneously an increase in the patient's cytotoxic activity against MM cells was detected in vitro. The responsibility of immune phenomena and specific immunotherapy for the appearance of depigmentation and morpheas is discussed.
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PMID:Vitiligo-like depigmentation and morpheas after specific intralymphatic immunotherapy for malignant melanoma. 149 95

We have tested the diagnostic value in malignant melanoma of HMB45, a monoclonal antibody available for use on paraffin-embedded tissue. MATERIAL AND METHOD. Tissues tested. The following pathological tissues were tested: 10 intradermal and 11 compound naevi; 6 spitz naevi; 20 dysplastic naevi; 10 blue naevi; 2 Bednar's tumours; 6 Sutton naevi; 15 melanonychias; 21 cutaneous and 11 ocular malignant melanomas (MM), and 3 achromic metastases. Control tissues were: vitiligo (20), carcinoma (5), malignant schwannoma of the orbit (1), soft tissue sarcoma (5) and malignant lymphoma (5). Antibodies. The antibodies used were antiprotein S100, antivimentin, anticytokeratin (KL1), monoclonal antileucocyte (CD45) antibodies and HMB45, a monoclonal antibody of the IgG 1 type obtained from lymph node metastases from pigmented malignant melanomas. RESULTS. None of the control tissues were stained by the HMB Ab. Intradermal naevi did not react positively. Compound naevi: the juntional cells were stained by HMB45 in 2/10 cases. Dysplastic naevi: HMB45 showed heterogeneous reactivity of junctional cells in 15/20 cases, and this correlated with the degree of atypia. Blue naevi: HMB45 stained the superficial and deep cells in 3/10 cases. Bednar's tumour: no cell was stained by HMB45. Spitz naevi: HMB45 gave an intensely positive reaction of junctional cells in 4/5 cases and a weaker reaction of dermal cells. Sutton naevi: the naevus cells were not stained by HMB45 in 5/6 cases. In simple melanocytic hyperplasia of the nail bed, only a few atypical cells were stained. In superficially spreading melanoma (SSM) all neoplastic cells were stained by HMB45 in proportion to their degree of atypia. Residual naevus cells were negative. The anti S100 and the antivimentin antibodies stained all neoplastic and naevus cells. In nodular melanoma (NM), HMB45 stained all neoplastic cells in proportion to their degree of atypia. The antivimentin Ab stained the neoplastic cells, and so did the anti-S100 Ab which also stained inflammatory cells. In acral-lentiginous melanoma (ALM), HMB stained the dermal tumoral cells moderately and the junctional cells more strongly. In ocular melanoma, HMB45 strongly stained the fusiform cells and less strongly the epithelioid cells. In achromic metastases from cutaneous malignant melanomas, HMB45 strongly stained the neoplastic cells but did not stain the peritumoral cells. DISCUSSION. The purpose of this study was to compare the value of HMB45 with that of other immunohistochemical staining methods A. Main data from the literature. (ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Contribution of monoclonal antibody HMB45 in the histopathologic diagnosis of melanoma]. 170 64

Melanogenesis is an important biochemical process for the production of skin pigments which protect many animals from the damage of solar radiation. The abnormalities in melanogenesis are associated with albinism, vitiligo, as well as malignant melanoma in humans. In the lower forms of animals viz., insects, the exoskeleton is hardened to protect their soft bodies by a process called sclerotization, which is often accompanied by melanization. Recent advances in the biochemistry of sclerotization and melanization reveal remarkable similarity between these two processes. The seven stages of sclerotization are: (a) enzymatic oxidation of N-acyldopamine, (b) Michael-1,4-addition reactions of N-acyldopamine quinone, (c) tautomerization of quinone to quinone methide, (d) Michael-1,6-addition of quinone methides, (e) tautomerization of N-acyldopamine quinone methide to 1,2-dehydro-N-acyldopamine, (f) enzymatic oxidation of 1,2-dehydro-N-acyldopamine, and (g) the reactions of resultant quinonoid compounds. Amazingly, striking similarities in the reaction sequences are found in the melanization process starting from dopa. These comparisons predict a central role for quinone methides as reactive intermediates during melanization. Accordingly, recent studies provide increasing evidence in favor of this proposition.
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PMID:Molecular mechanisms for mammalian melanogenesis. Comparison with insect cuticular sclerotization. 176 60


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