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)

Recently, we have described a monoclonal antibody, named MS-1, which identifies a novel high-molecular-weight protein expressed by noncontinuous, sinusoidal endothelia and by interstitial dendritic cells in certain normal human organs (S Goerdt, LJ Walsh, GF Murphy, JS Pober, J Cell Biol 1991, 113:1425-1437; and LJ Walsh, S Goerdt, JS Pober, H Sueki, GF Murphy, Lab Invest 1991, 65: 732-741). In this report, we demonstrate in studying a variety of skin lesions that MS-1 antigen can also be expressed by endothelia of continuous origin under certain pathological conditions. Among the skin lesions tested, MS-1 antigen expression by endothelial cells of continuous origin is frequently observed in wound healing tissue, in cutaneous T-cell lymphoma, in psoriasis, and in melanoma metastasis, ie, in 100%, 80%, 71%, and 71% of cases, respectively. In contrast, endothelial MS-1 antigen expression rarely occurred in other skin lesions, including vascular tumors, six of which were Kaposi's sarcomas (13% and 0% of cases with vascular MS-1 expression, respectively). The percentage of cases with MS-1+ vessels is only marginally different in malignant versus benign lesions (55% versus 31%); when melanocytic nevi, primary melanomas, and melanoma metastases are compared, however, an increase in the percentage of cases with MS-1+ vessels is seen (31%, 50%, and 71%, respectively). Apart from wound healing, the relative number of MS-1+ vessels in a given lesion amounts to less than 5% compared with the number of continuous type vessels stained by monoclonal antibody 1F10 (S Goerdt, F Steckel, K Schulze-Osthoff, H-H Hagemeier, E Macher, C Sorg, Exp Cell Biol 1989, 57: 185-192). In addition, the occurrence of MS-1+ vessels is not related to the overall vascularity of a given lesion. Thus, the conditions for MS-1 antigen expression by endothelia of continuous origin cannot as yet be exactly defined. Furthermore, we have noticed that the number of MS-1+ dendritic cells varies considerably in skin lesions; in the early patch lesions of Kaposi's sarcoma and in juvenile xanthogranuloma MS-1+ cells even constitute the major cell type. This prompted us to investigate MS-1 antigen expression and its regulation in cultured human monocytes/macrophages. Expression of MS-1 antigen by these cells regularly starts at day 3 of culture and reaches its maximal value at day 9, after which it declines.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Inducible expression of MS-1 high-molecular-weight protein by endothelial cells of continuous origin and by dendritic cells/macrophages in vivo and in vitro. 849 45

To determine the risk of cutaneous neoplasia following photochemotherapy (PUVA), we reviewed patients with psoriasis treated at our unit between 1979 and 1991. Two hundred and forty-five patients were assessed, with a median duration of follow-up of 9.5 years. Fifty-nine per cent were male, and 41% female. The median number of exposures was 59, and the median total dose was 133 J/cm2 for the group as a whole. Non-melanoma skin cancers (NMSC) occurred in six individuals (2.4%). Basal cell carcinoma occurred in all six and one individual also developed four squamous cell carcinomas and Bowen's disease of the penis. No cases of malignant melanoma were recorded. Patients who developed NMSC received a median number of 225 exposures and a median cumulative dose of 654 J/cm2. Compared with a control study population in West Glamorgan, Wales, there was a 1.4 (95% confidence limits (CL) 0.5 and 3.1) times increased risk of NMSC. A statistically significant increased incidence of NMSC was found for patients who had received 100 or more exposures, and 250 or more J/cm2, with risks of 3.7 (95% CL 1.0 and 9.5), and 4.0 (95% CL 1.1 and 10), respectively. A PUVA dose of < 250 J/cm2 or < 100 exposures conferred a minimal increase in risk of NMSC in our study population.
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PMID:Cutaneous neoplasia following PUVA therapy for psoriasis. 873 63

The expression of SPRR (small proline-rich protein) was investigated in normal human skin and in diseased skin from patients with psoriasis, squamous cell carcinoma, basal cell epithelioma, naevus pigmentosus, ichthyosis vulgaris and several inflammatory skin diseases, by immunohistochemical staining. A polyclonal antibody was raised against a synthetic peptide for a C-terminal common region for SPRR1 and SPRR3. In immunoblot analysis, a positive band of 18 kDa was detected, which showed the presence of SPRR1 in human epidermal keratinocytes. In normal epidermis, positive staining for SPRR was observed in keratinocytes in the granular layer and the uppermost or two spinous cell layers, with no staining of the other spinous or basal layers. The staining was obvious at the cell periphery, weak at the cytoplasm, and absent in the nucleus. Staining was observed in several outer layers of the follicular infundibulum to the isthmus. No staining was detected in the inner root sheath of the hair follicles, hair matrix, sebaceous gland, eccrine gland, eccrine duct, melanocytes, Langerhans cells or fibroblasts. The arrectores pilorum, striated muscles, muscle layers of vessels, and myoepithelia of eccrine gland, were weakly stained. In psoriatic skin, stained keratinocytes were distributed in the spinous cell layers except for the basal layer. In ichthyosis vulgaris, SPRR was barely expressed in the uppermost living cell layers of the epidermis. In epidermolytic hyperkeratosis, degenerated squamous cells widely expressed SPRR. In Darier's disease, dyskeratotic cells were clearly stained. In squamous cell carcinoma, staining was observed in keratotic cells around horny pearls. In basal cell epithelioma, naevus pigmentosus, and malignant melanoma, the tumour cells or naevus cells were not stained. The distribution of SPRR was similar to that of involucrin in normal and several diseased skin, except for ichthyosis vulgaris. We conclude that SPRR is expressed in close association with epidermal differentiation in normal skin and skin diseases. The alteration of the expression of the proteins correlated to terminal differentiation, and differs from disease to disease.
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PMID:Differentiation-associated localization of small proline-rich protein in normal and diseased human skin. 873 72

In the past, interleukin-8 (IL-8) could be demonstrated within keratinocytes in normal epidermis and inflammatory skin diseases, like psoriasis and eczema. Using monoclonal antibodies, the distribution of IL-8 immunoreactivity was inversely related to the density of inflammatory infiltrate. Other in vitro observations indicated IL-8 to be a growth factor for keratinocytes. These results prompted an immunohistochemical examination of IL-8 immunoreactivity in malignant and semimalignant epithelial tumours of human skin. Whereas IL-8 could not be detected within the transformed cells of epithelial tumours or melanoma, some tumour cells within well differentiated squamous cell carcinoma and Bowen's disease showed IL-8 immunoreactivity. Thus, loss of IL-8 immunoreactivity can be a sign of malignant transformation. This indicates an important role in growth regulation as well as terminal differentiation of human keratinocytes.
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PMID:Interleukin-8 immunoreactivity in malignant tumours of the skin. 880 Mar 1

In recent years, interferon-alpha has become widely used for systemic therapy of tumours and infectious diseases. Well-known cutaneous side effects include dry skin, pruritus and hair loss. Since 1986, 17 patients with renal cell carcinoma, malignant melanoma, hepatitis B and C, carcinoid syndrome and hairy cell leukemia have been reported in whom psoriasis with or without psoratic B joint involvement was induced or exacerbated by systemic interferon-alpha therapy. In these patients, the drug was discontinued because of the severity of the psoriatic symptoms induced. The psoriatic lesions then resolved in nearly all patients within 2 weeks to 6 months, but in 10 of 22 patients treated with interferon-alpha specifically for psoriasis exacerbation was reported. We report three new cases of interferon-alpha-induced psoriasis. The patients were treated with the drug for HIV-associated Kaposi's sarcoma, renal cell carcinoma, and hepatitis C. We conclude that interferon-alpha can provoke psoriatic skin and joint symptoms, especially when additional precipitating factors are involved. In patients in whom such risks are present careful consideration of the benefit/risk ratio and concomitant antipsoriatic treatment are essential if interferon-alpha therapy is to be continued.
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PMID:[Interferon-alpha-induced psoriasis vulgaris]. 886 56

The expression pattern of epithelial (E)- and placental (P)-calcium-dependent cell-cell adhesion molecules was examined immunohistochemically in various skin tumors. E- and P-cadherin expression was preserved in nodular and superficial types of basal cell carcinoma (BCC). In well-differentiated squamous cell carcinoma (SCC), E-cadherin on the cell surface of the tumor was reduced but expression of P-cadherin was preserved more frequently at the peripheral sites of the tumor than in the central sites of the tumor. Paget's cells and melanoma cells did not express E- or P-cadherins in the nest of the epidermis. Immunoreactive E-cadherin levels in sera were significantly elevated in patients with invasive Paget's disease, metastatic malignant melanoma and severe types of psoriasis and atopic dermatitis when compared with those of normal controls. Reduced or loss of cadherin in localized tumor cells may be correlated with the proliferation, and the level of soluble E-cadherin in circulation may be a marker in the extent of damaged skin by tumor and/or inflammation.
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PMID:E- and P-cadherin expression in tumor tissues and soluble E-cadherin levels in sera of patients with skin cancer. 890 51

Although photodynamic therapy (PDT) was first used in the treatment of skin diseases, phase-III-clinical trials were primarily conducted for the treatment of bladder cancer, endobronchial and oesophageal carcinoma. In dermatology PDT has most extensively been used for the treatment of malignant cutaneous lesions. Up to now those patients have been treated systemically with first-generation photosensitizers. However, prolonged skin photosensitivity is a major disadvantage of this form of therapy. Topical PDT utilizing a variety of sensitizers bypass this unwanted effect. Of strong interest is 5-aminolevulinic acid (ALA), first introduced in the topical PDT of skin disorders in 1990 by Kennedy and co-workers. ALA serves as a pro-drug, i.e. the active photosensitizing compound is protoporphyrin IX which is synthesized in vivo after exogenous application of ALA. In several oncologic and non-oncologic skin conditions including non-melanoma skin cancer, premalignant conditions like actinic keratoses and in psoriasis, topical ALA-PDT showed it's effectiveness. Besides ALA, new sensitizers like benzoporphyrines and porphycenes may play a role in topical PDT. However, at the moment, there is still a need for comparative studies and standardized therapeutic protocols to define the place of topical PDT in Dermatology.
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PMID:Topical photodynamic therapy in dermatology. 900 64

The Ca(2+)-dependent cell-cell adhesion molecules, termed cadherins, are subdivided into several subclasses. E (epithelial)- and P (placental)-cadherins are involved in the selective adhesion of epidermal cells. E-cadherin is expressed on the cell surfaces of all epidermal layers and P-cadherin is expressed only on the surfaces of basal cells. Ultrastructural studies have shown that E-cadherin is distributed on the plasma membranes of keratinocytes with a condensation in the intercellular space of the desmosomes. During human skin development P-cadherin expression is spatiotemporally controlled and closely related to the segregation of basal layers as well as to the arrangement of epidermal cells into eccrine ducts. In human skin diseases E-cadherin expression is markedly reduced on the acantholytic cells of tissues in pemphigus and Darier's disease. Cell adhesion molecules are now considered to play a significant role in the cellular connections of cancer and metastatic cells. Reduced expression of E-cadherin on invasive neoplastic cells has been demonstrated for cancers of the stomach, liver, breast, and several other organs. This reduced or unstable expression of E- and P-cadherin is observed in squamous cell carcinoma, malignant melanoma, and Paget's disease, but cadherin expression is conserved in basal cell carcinoma. Keratinocytes cultured in high calcium produce much more intense immunofluorescence of intercellular E- and P-cadherin than those cells grown in low calcium. E-cadherins on the plasma membrane of the keratinocytes are shifted to desmosomes under physiological conditions, and therein may express an adhesion function in association with other desmosomal cadherins. Soluble E-cadherins in sera are elevated in various skin diseases including bullous pemphigoid, pemphigus vulgaris, and psoriasis, but not in patients with burns. Markedly high levels in soluble E-cadherin are demonstrated in patients with metastatic cancers.
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PMID:Roles of E- and P-cadherin in the human skin. 929 84

In 1974 a new photobiologic principle i.e. light + drug, called photochemotherapy was discovered in Boston and immediately confirmed in Vienna. Psoralen + UVA (PUVA) photochemotherapy has now been applied to the treatment of more than 24 heterogeneous groups of diseases, especially psoriasis and mycosis fungoides. After 24 years of experience in thousands of patients with psoriasis and 23 other skin disorders, virtually the only risk is the development of squamous-cell carcinomas. This risk is low with two exceptions: previous history of treatment with ionizing radiation or inorganic trivalent arsenic, and patients with recalcitrant psoriasis who require continuous treatment for many years. In a recent report from a large USA clinical trial, melanoma developed in a few patients with psoriasis treated with PUVA. This prospective clinical trial did not have a control population, and therefore, the conclusion that PUVA can cause melanoma is tentative.
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PMID:The benefits and risks of long-term PUVA photochemotherapy. 958 96

The possibility that there is an increased risk of melanoma in patients with psoriasis treated with psoralen-UV-A (PUVA) therapy has raised concern on the part of physicians and patients about the long-term safety of this treatment. In response to this concern, the National Psoriasis Foundation sponsored a workshop at which invited participants with expertise in PUVA therapy, psoriasis treatment, melanoma and nonmelanoma skin cancer, and epidemiological and clinical trials were asked to develop a consensus on the following 3 issues: the risk of long-term adverse effects of PUVA therapy with emphasis on nonmelanoma and melanoma skin cancer; the guidelines for physicians and patients for selection and use of PUVA therapy with consideration of the risk-benefit ratio of this treatment compared with the risk-benefit ratios of alternative treatments; and the directions for further evaluation of the long-term effects Of PUVA therapy.
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PMID:Consensus workshop on the toxic effects of long-term PUVA therapy. 960 29


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