Different Types Of Melanoma Research Articles

Immunocytochemical and immunoelectron microscopic demonstration of cathepsin B in human malignant melanoma.

Proteases are known to enhance the spread of tumour cells. Possible sources of these proteases are the tumour cells themselves or fibroblasts in the tumour tissue. Immunological staining with anticathepsin B antibody indicates that the subcellular distribution of cathepsin B in tumour cell lines differs from that in normal liver. The aims of this study were: (i) to show whether different types of melanoma differ in their production of cathepsin B; (ii) to identify the cathepsin B-producing cells; and (iii) to determine the subcellular distribution of cathepsin B in melanoma cells. All types of melanomas contained cell regions stained with anticathepsin B antibody. The intensity of the stain and the number of cells reacting with anticathepsin B antibody depended on the size of the tumour but not on the type of melanoma. Epithelioid cells stained more intensely with anticathepsin B antibody than spindle-shaped cells. Cells staining with anticathepsin B antibody were almost exclusively tumour cells. Anticathepsin B stain was located mainly in vesicular structures which did not contain a filamentous matrix. Additional anticathepsin B stain was detected at the extracellular spaces. Hypomelanotic melanoma cells, mainly of the epithelioid type, produced most of the cathepsin B. Cathepsin B may be involved in both the degradation of possibly abnormal melanosomes and the focal degradation of the extracellular matrix.

New Therapies Targeting the Genetic Mutations Responsible for Different Types of Melanoma

A number of molecular alterations have been described for melanoma. Melanomas with BRAF mutations tend to be located in areas of intermittent sun exposure, whereas melanomas with KIT mutations mostly appear in acral areas, the mucosa, and areas of chronic sun exposure. Sorafenib, a BRAF inhibitor, has a cytostatic effect on most melanomas with mutations affecting the mitogen-activated protein kinase (MAPK) pathway, and is also capable of triggering apoptosis in a small subgroup of these melanomas. By inhibiting KIT, imatinib has a cytostatic and cytotoxic effect on melanomas with KIT mutations, and probably has the same effect on another subgroup of melanomas with other as yet imperfectly understood KIT mutations. For therapy to be effective, agents should be selected according to the pathways associated with the genetic mutations present in the melanoma.

Short German guidelines: Malignant melanoma

Malignant melanoma is a malignant tu-mor which arises from melanocytic cellsand primarily involves the skin. For thebalance of these guidelines, the termsmalignant melanoma and melanoma willbe used interchangeably, because thereare no benign melanomas. Melanomascan also arise in the eye (conjunctiva anduvea), meninges and on various mucosalsurfaces. While melanomas are usuallyheavily pigmented, there are also amela-notic tumors. Even small tumors have atendency towards metastasis and thus arelatively unfavorable prognosis. Melan-omas account for 90% of the deaths as-sociated with cutaneous tumors. The incidence of melanoma is increasingworldwide in white populations, especi-ally where fair-skinned peoples receiveexcessive sun exposure. In central Europethe incidence is 10 – 12 / 100,000yearly; in the USA, 10-25 / 100,000yearly; and in Australia the highest inci-dence, 50-60 / 100,000 yearly. In indivi-duals with more pigmentation (Asians,Africans) melanomas are uncommonand almost always found on either acralor mucosal surface. Individuals withlarge numbers of melanocytic nevi andthose with melanoma precursors (dyspla-stic nevi, congenital nevi) are at greaterrisk. The inheritance of melanoma is po-lygenic; 5-10% of melanomas appear inmelanoma-prone families. In addition tothese genetic and constitutional factors,the most important exogenous factor isexposure to UV irradiation. The relativeroles of toxic substances, medicationsand hormones (pregnancy, oral contra-ceptives) are controversial. The immunestatus of the patient plays a major role indetermining the course of melanoma, asnumerous examples of spontaneous re-gression or of rapid progression in im-munosuppressed individuals bear testi-mony.A number of different types of melano-mas can be identified clinically and hi-stologically. Some tumors either repre-sent mixed forms or are not classifiable.Examples of special forms are amelanoticmelanomas, mucosal melanomas, andother extracutaneous melanomas, whichtogether account for about 5% of allmelanomas.

Trends in melanoma epidemiology suggest three different types of melanoma

Trends in melanoma epidemiology suggest three different types of melanoma

Trends in melanoma epidemiology suggest three different types of melanoma

It has been suggested that the incidence of thin melanomas but not of thick tumours is rising in fair-skinned populations, although the reason for this discrepancy is not understood. To describe temporal trends in melanoma epidemiology in a limited part of France in order to confirm this observation and to provide an explanation. This is a retrospective population- and academic centre-based study in which all melanomas diagnosed in the department of the Bas-Rhin, France between January 1980 and December 2004 were included. The study included 2094 melanomas diagnosed in 2020 patients. There was a steady increase in incidence of thin (< 1 mm) melanomas, mainly located on the trunk, and to a lesser extent in the head and neck region, in both sexes, and of intermediate (1-2 mm) melanomas in men. The incidence of intermediate melanomas in women and of thick (> 2 mm) melanomas, as well as mortality related to melanoma, remained stable. There was a steady decline of mean and median Breslow thickness. The 12 months median delay to diagnosis of thick tumours was significantly shorter than the 24 months delay to diagnosis of thin tumours. Temporal trends suggest the existence of three unrelated types of melanoma: type I, thick melanomas, with stable incidence; type II, thin melanoma with a steady and important increase in incidence, mainly located on the trunk; and type III, melanoma with a slower increase in incidence, mainly located on the head and neck region.

Classification of cutaneous malignant melanoma: a reassessment of histopathologic criteria for the distinction of different types.

Human cutaneous malignant melanoma currently is classified into four principle types: nodular, superficial spreading, lentigo maligna, and acral lentiginous. The criteria for the histopathologic diagnosis of these types are not applied consistently. Nevertheless, the classification has become the foundation of many clinical, histopathologic, epidemiologic, and molecular studies. The results of those studies can have validity only if the classification itself is valid. For this reason, the authors reassessed histopathologic criteria advocated for the distinction of the different types of melanoma and searched for other repeatable constellations of findings that may serve to define distinct subsets of the neoplasm. Nine hundred fifteen melanomas were examined with regard to 72 parameters that are considered to be important for histopathologic diagnosis. The results were analyzed statistically with special attention to findings that have been reported to be characteristic of the four principle types of melanoma. The histopathologic criteria advocated for the distinction of different types of melanoma were found not to correlate with one another. A logistic regression analysis did not detect any other repeatable constellation of morphologic findings that may reflect a distinct biologic subgroup. The validity of the current classification of cutaneous malignant melanoma into four principle types could not be substantiated. Malignant melanoma may present with many different forms, but these forms appear to be part of a continuous spectrum rather than examples of distinct biologic entities.