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Query: UMLS:C0025202 (melanoma)
 69,561 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In certain experimental tumor models, tumor growth is less pronounced in immune deficient animals. Characteristically, tumors such as the murine B16 melanoma and Lewis lung carcinoma (3LL) are weakly antigenic. We proposed that with such tumors that are weakly antigenic, growth is enhanced by T-cell factors. Young mice were inoculated with irradiated B16 cells in complete Freunds adjuvant (CFA) on three occasions, each separated by 2 weeks. Specific antibody (IgG) to B16 membrane antigens was detected by an enzyme-linked immunosorbent assay (ELISA) after the first injection, and it continued to rise for 6 weeks. B16 growth was compared in 20 mice that had received irradiated B16 in CFA or CFA alone by the same schedule previously. Despite the previous sensitization, the rates of tumor appearance and growth were similar. In an additional experiment involving 23 mice that had received B16 immunization, the period of time in which a palpable tumor developed after the injection of viable B16 cells did not correlate with anti-B16 antibody level. It appeared that detectable antibody to B16 antigens was of little consequence. To explain why B16 primary growth and metastases were reduced in immune deficient hosts, we proposed that lymphocytes might enhance tumor growth. To demonstrate this, splenic lymphocytes from tumor-bearing (B16 or 3LL) or control mice were injected with B16 cells into young, immune competent hosts. Tumors (B16) developed earlier and growth was more rapid in mice that received spleen cells from tumor-bearing (B16) mice. Subsequent cell depletion experiments to determine the mediator of tumor enhancement implicated a T-cell fraction that was neither of T-helper nor T-suppressor cell type phenotypically. Immune deficiency states that are associated with dysfunction of those cells that account for tumor enhancement might explain the reduced tumor aggressiveness that is observed frequently in these conditions.
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PMID:Immunologic enhancement of B16 melanoma growth. 325 40

We describe a gene, NM23, that is associated with the tumor metastatic process. NM23 RNA levels were highest in cells and tumors of relatively low metastatic potential in two experimental systems: (1) murine K-1735 melanoma cell lines, in which the gene was identified, and (2) N-nitroso-N-methylurea-induced rat mammary carcinomas. NM23 RNA levels did not correlate with cell sensitivity to host immunological responses and may, therefore, be associated with intrinsic aggressiveness. The predicted carboxy-terminal protein sequence encoded by the pNM23 cDNA clone is novel compared with Genebank animal, bacterial, and viral sequences.
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PMID:Evidence for a novel gene associated with low tumor metastatic potential. 334 12

A 62 yo man presented with an enlargement of the parotid gland that had accentuated over the past ten months. Results of a needle aspiration cytology were interpreted as consistent with an adenocarcinoma. A surgical investigation was decided. Frozen and paraffin sections of superficial parotidectomy specimen disclosed a malignant melanoma. This specimen also contained an intraparotid lymph node which was free of tumor. Cervical lymph node dissection yielded 4 metastatic adenopathies among 15 lymph nodes. A retrospective search for an anterior melanocytic lesion was negative. The final diagnosis was primary malignant melanoma of the parotid gland. Cervical radiotherapy was applied. 7 months later, the patient died of diffuse metastatic involvement in the skin, brain, lungs and liver. No local recurrence occurred. Review of the medical literature revealed the rarity of malignant melanomas of the parotid gland (0.68%). No significant differences concerning clinical data and pathological aspects were noted in so called primary malignant melanoma and secondary malignant melanoma of the parotid gland. Nevertheless, primary malignant melanoma of the parotid gland is a controversial entity. Pathogenesis is discussed on the light of modern concepts of diffuse neuro-endocrine system. Prognosis remains poor, due to a late diagnosis and to an inherent aggressiveness of this type of tumor.
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PMID:[Primary malignant melanoma of the parotid gland: anatomico-clinical study. Apropos of a case and review of the medical literature]. 351 76

The induction of new vasculature is essential for tumor growth and survival. Through studies of the angiogenic properties of human breast cancer and melanoma cell lines by implantation in rabbit cornea, results show that both breast tumor and melanoma cells produce an angiogenic factor. Melanoma cells had approximately twice the activity compared to breast tumor cells. Initiation of angiogenesis by 1 X 10(6) melanoma cells occurred in 3 days, reached maximum at 7 days, and resolved in 21 days. Implantation of 2 X 10(6) breast tumor cells initiated angiogenesis in 6 days, reached maximum in 10 days and resolved in 24 days. The difference in the time of angiogenic induction may be related to the aggressiveness of each tumor type.
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PMID:Angiogenesis by human melanoma and breast cancer cells. 616 83

The matter of sex differences in survival from melanoma is more complex than generally recognized, and at least 6 factors, some of which appear to be interrelated, must be conisdered: location of the primary melanoma; stage of disease at presentation; endocrine factors; immunologic factors; pattern of metastatic spread (i.e., lymphogenic versus hematogenic), and environmental and behavioral characteristics. Extremity melanomas have a more favorable prognosis than axial melanomas, but, after allowance for tumor site, women still fare better than men. There appears to be a stage-by-stage difference in favor of women for survival. This applies to clinical stages (stage 1, local disease; stage 2, regional spread; and stage 3, distant metastases), as well as to pathologic microstages. Some authors have inferred that female advantage disappears once the disease has metastasized. No valid explanation for this observation has ever been advanced, and careful review of the literature reveals a female superiority in survival at stage 2 or stage 3 disease as well as stage 1. Many recent studies have confirmed the ancient impression that the incidence of metastatic disease at the time of diagnosis is higher in men. Men tend to have an equal or shorter history before treatment, yet they have more advanced disease at the time of diagnosis. They have an unfavorable outcome irrespective of lesion site, tumor thickness, histogenetic subtype, and clinical stage of disease. These data suggest that the disease develops more rapidly in men. Thus, the aggressiveness and metastatic potential of cutaneous melanoma is more distinct in the male sex. The exacerbation of melanoma during pregnancy may be due to the increase of estrogens or to the elevated androgen levels. The first possibility is unlikely. The elevation of follicle stimulating hormone, luteinizing hormone, and MSH levels may play a role. Several case-controlled studies have failed to reveal any overall relationship between prior history of oral contraceptive use and the development of melanoma. Because the role of estrogens (and hormones in general) in the course of melanoma is not yet satisfactorily established, oral contraceptives are best avoided. It is concluded that malignant melanoma may be a hormone-responsive tumor, despite the fact that the exact nature of such endocrine factors remains nebulous.
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PMID:Sex differences in survival from cutaneous melanoma. 638 12

Melanoma is an especially important malignant disease for surgeons to know about, since it can be cured with surgical treatment if diagnosed at an early stage. In the American College of Surgeons Melanoma Survey of 4,545 melanoma patients diagnosed during 1980, the typical melanoma was relatively thin (less than 1.5 millimeters), not ulcerated (except in 9 per cent) and did not invade into the reticular dermis or beyond (level IV or V). The melanomas were most commonly located on the trunk in men and on the lower extremities in women. Eighty-eight per cent of the patients had no clinical evidence of metastases to regional nodes or to distant sites at the time of initial diagnosis. Only a small proportion (1 per cent) of patients in the survey were black and in most of these patients, their melanoma were located on the feet or hands. The treatment of melanoma was surgical in 92.5 per cent of the patients, with the majority of patients undergoing a wide excision of the melanoma as the initial form of treatment. Only one-fifth of the patients underwent elective regional node dissection for suspected micrometastases, and most of these patients had a tumor thickness exceeding 1.5 millimeters or a lesion invading to the reticular dermis (level III, IV or V). While the Breslow Microstaging Method is now recognized as the most important parameter that predicts the clinical course of the patient, this parameter was reported in only 45 per cent of the patients in the survey. The natural history of melanoma is changing, since the disease is increasing in frequency and becoming more curable. Surgical treatment should be tailored to the biologic aggressiveness of each individual patient's melanoma. This can be estimated by integrating such prognostic factors as the melanoma thickness, the presence or absence of ulceration, the level of invasion, the anatomic site and the gender of the patient.
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PMID:Management of cutaneous melanoma in the United States. 671 Feb 91

Previous studies have demonstrated pathologic similarities between human melanoma and the spontaneous melanoma in the Sinclair miniature swine (SMS) with respect to cutaneous histologic features and patterns of metastasis. The current biopsy series, correlating growth curves and histopathologic features of cutaneous melanomas, was undertaken for documentation of the histologic events associated with the successful regression of melanoma in the SMS. Cutaneous growth and regression was characterized by a series of cellular events that eventually led to depigmentation and scar formation. Mononuclear inflammatory infiltrates, seen in over half of the 104 biopsies, showed several temporal and topographic distribution patterns, similar to that described in human melanoma. Histopathologic observations in the SMS confirm clinical observations that the host can, with consistent effectiveness, react with the tumors to modify their biologic aggressiveness. Although regression is associated with lymphocytic and macrophage infiltration, the exact role of the immune response in the regression of the cutaneous melanoma remains to be elucidated.
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PMID:Growth and regression of cutaneous melanomas in Sinclair miniature swine. 675 3

We studied 101 Malignant Melanomas (MM) in the files of Department of Pathology of the National Medical Center of El Salvador. The incidence was 0,20 per 100.000, 54.5% in females and 45.5% in males. The mean age was 53.9% years (range 16 days-115 years). Highest frequency there occurred among 41 and 50 years. 42.5% were placed in lower limbs, 17.8% in the face, 14.8% in thorax, 7.9% in upper limbs, and 4.95 in the eye. In 18.8% it was found the antecedent of "mole" previous in the site of the tumor. 43% of the patients consulted before 6 months of evolution. In 53.8% metastasis were detected at the time of consultation. Microscopically 98.1% were of the nodular type and 1.9% lentigo maligna melanoma. Amont the nodulars, 38.5% were predominantly to epitheloid cells, 8% to fusiform cells, and 53.5% to mixed cells. 63% were placed at Clark's level V, 32% at level IV, and 5% at level III. All of them were more than 1.5 mm. in depth. 52% were medium thickness and 48% were more thant 4 mm. It is worth to emphasize: the highest frequency among females, the highest incidence in lower limbs and the microscopic aggressiveness of these tumors, almost all being of nodular type.
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PMID:[Malignant melanoma in El Salvador. Study of 101 cases]. 676 54

Melanomas of the skin and mucous membranes of the head and neck region are an uncommon problem for most clinicians. The article emphasizes the differences in terms of biological aggressiveness and treatment between lentigo maligna (LM) and lentigo maligna melanoma (LMM), superficial spreading melanoma (SSM), and nodular melanoma de novo. The results of radiotherapy in the treatment of melanoma of the head and neck are reviewed, and indications are suggested for the use of irradiation in the management of patients with this tumor. A brief discussion of the results of treatment of mucosal melanomas is given.
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PMID:Melanomas of the head and neck. 684 53

The growth of solid tumors to a clinically relevant size is dependent upon an adequate blood supply. This is achieved by the process of tumor stroma generation where the formation of new capillaries is a central event. Progressive recruitment of blood vessels to the tumor site and reciprocal support of tumor expansion by the resulting neovasculature are thought to result in a self-perpetuating loop helping to drive the growth of solid tumors. The development of new vasculature also allows an 'evacuation route' for metastatically-competent tumor cells, enabling them to depart from the primary site and colonize initially unaffected organs. Several molecular and cellular mechanisms have been identified by which tumor parenchyma may exert its angiogenic effect on host endothelial cells. As a result of this paracrine influence, tumor-associated endothelial cells acquire an 'immature' phenotype manifested by rapid proliferation, migration, release of proteases and expression of cytokines, endothelial-specific tyrosine kinases (e.g. flk-1, tek and others) as well as numerous other molecular alterations. Consequently a network of structurally and functionally aberrant blood vessels is formed within the tumor mass. There is also evidence that endothelial cells themselves, and likewise other stromal cells, may act reciprocally to alter the behavior of adjacent tumor cells in a paracrine or cell contact mediated fashion. For example, production of interleukin 6(IL-6) by endothelial cells may have a differential effect on human melanoma cells expressing different degrees of aggressiveness. In this manner endothelial derived cytokines could conceivably contribute to tumor progression by suppressing the growth of the less aggressive tumor cells and promoting dominance of their malignant counterparts in 'strategic' perivascular zones. Distinct biological features expressed by tumor-associated vasculature may serve as potential prognostic markers of disease progression as well as novel targets for therapeutic intervention.
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PMID:Consequences of angiogenesis for tumor progression, metastasis and cancer therapy. 753 29


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