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

Major histocompatibility complex (MHC) antigens and intercellular adhesion molecule-1 (ICAM-1) play important roles in immune response. In order to investigate the association between renal cell cancer (RCC) and host's immune system, expression of MHC antigens and ICAM-1 was examined on RCC. Immunohistochemical analysis revealed a positive correlation between the expression of MHC antigens and ICAM-1. In general, tumor with higher degree of mononuclear cell infiltration expressed MHC antigens and ICAM-1 more frequently and intensely. Among cytokines which were reported to be potent inducers of ICAM-1 on malignant melanoma cell lines, interferon (IFN)-gamma and tumor necrosis factor (TNF)-alpha augmented the expression of ICAM-1 on ACHN cells whereas ICAM-1 and class I antigens on KRC/Y cells. IFN-alpha enhanced MHC class I antigens but not ICAM-1. Class II antigen expression of both cell lines was augmented by only IFN-gamma. These results suggest that cytokines which could be produced by tumor-infiltrating mononuclear cells, especially IFN-gamma and TNF-alpha, might modulate expression of MHC antigens and ICAM-1, and influence host immune response against RCC.
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PMID:[Expression of major histocompatibility complex antigens and intercellular adhesion molecule-1 (ICAM-1) on renal cell cancer. De novo expression and modulation by cytokines on renal cell cancer cell lines]. 167 73

We have previously demonstrated that administration of interferon a/b (IFN) for 4-5 days after challenge with a transplantable Moloney sarcoma virus-induced tumor completely inhibited tumor development. In the present study, we examined the therapeutic effects of IFN on mortality induced by metastatic dissemination of the B16F10L murine melanoma. IFN was administered at various times in relation to the surgical removal of primary tumor: days -5 to -1 prior to tumor excision (neo-adjuvant protocol), or for 5 days after tumor excision, beginning on days 1, 6 or 11 after excision of the primary tumor (adjuvant protocols). The neo-adjuvant protocol was superior to all other protocols, significantly increasing percentage survival (56% vs. 0%) and median survival time (greater than 84 days vs. 33 days) compared to untreated controls, as well as to all adjuvant protocols. In contrast, IFN treatment on days 1 to 5 after excision of the primary tumor decreased median survival time of cases compared to untreated controls (20 days vs. 33 days). Both IFN-induced inhibition and enhancement of metastatic dissemination were dose-dependent, with higher amounts of IFN producing greater inhibition or enhancement. The superior therapeutic efficacy of the neo-adjuvant IFN treatment was associated with increased spleen and lung-derived natural killer cell cytolytic activity (on days -4, 0 and 2) followed by a later (day 13) increase in lung-associated cytolytic T-cell responses.
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PMID:Neoadjuvant immunotherapy with interferon of the spontaneously metastasizing murine B16F10L melanoma. 169 Nov 53

The inhibitory effect of poly(A)poly(U) on the pulmonary metastasis of B16-F10 melanoma was examined in comparison with that of poly(I,C)-L,C and poly(I)poly(C). The correlation between interferon (IFN) level and antimetastatic effect was also investigated. Intraperitoneal injection of poly(A)poly(U) (50 mg/kg) into C57BL/6 mice 24 h before intravenous inoculation of B16-F10 melanoma (1 X 10(5] caused a significant decrease (p less than 0.01) in the number of pulmonary nodules 14 days after tumor challenge. But poly(I,C)-L,C (1 or 0.2 mg/kg) and poly(I)poly(C) (5 mg/kg or 1 mg/kg) did not. From the kinetic study of IFN levels induced by polyribonucleotides, poly(I,C)-L,C showed the most potent IFN-inducing activity, followed by poly(I)poly(C) and poly(A)poly(U), in this order. Plasma IFN reached a peak at 6 h and still continued to be detected at 24 h after intraperitoneal injection of the polyribonucleotides. Against B16-F10 melanoma, the cytotoxicity of spleen cells stimulated by poly(A)poly(U) (50 mg/kg) was significantly (p less than 0.05) higher than that of spleen cells stimulated by poly(I)poly(C) (5 mg/kg) both at 12 and 24 h after intraperitoneal injection of those agents. The above results that there is no correlation between the IFN levels induced by polyribonucleotides and their antimetastatic effect. More extensive study of poly(A)poly(U) might give more fruitful results, which will give valuable information for future clinical trials of this lowly toxic promising agent.
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PMID:Lack of correlation between interferon levels induced by polyribonucleotides and their antimetastatic effect. 169 85

Macrophages derived from in vitro cultured monocytes were infected with herpes simplex virus type 2. A marked impairment in the intrinsic antiviral activity was found in macrophages obtained from patients with breast cancer or melanoma. Moreover, the antiviral activity of macrophages from healthy donors, differentiated in serum from patients with neoplasia, was also impaired. The aim of this work was the evaluation of alpha, beta, gamma exogenous interferon in restoring the intrinsic antiviral activity of macrophages from patients affected by breast cancer or melanoma under different conditions. Pretreatment of macrophages with alpha, beta interferons, but not gamma interferon, restored their impaired intrinsic antiviral activity.
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PMID:Role of exogenous interferons on intrinsic antiviral activity of macrophages from patients affected by neoplasia. 169 41

Both the serum levels of interferon and the activity of lymphocytic (2'-5')-oligoadenylate synthetase (OAS) of 37 patients suffering from malignant melanoma-15 with low (I,I-II,II) and 22 with higher (III,IV,V) Clark levels-were compared with those of a group of healthy controls in order to detect a possible involvement of the interferon system in the pathological process. Previous results obtained in studies on relatively small groups of patients had suggested that melanoma patients with low Clark levels (i.e. biologically early melanoma) show elevated activities of OAS, while those with higher levels show normal values. In our present investigation on a larger sample of patients, we did not find any differences between these two melanoma groups and healthy persons with regard to the OAS activity. Thus we were not able to confirm the provisional results set up by previous studies.
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PMID:[Serum interferon level and (2'-5')-oligo(A) synthetase activity in malignant melanoma]. 169 48

Interferons are proteins with antiviral, antiproliferative, and immune-regulating activity. They are classified as alfa, beta, or gamma on the basis of antigenicity and biologic properties. Alfa interferons as single-agent therapy produce clinical improvement in approximately 90 percent of patients with hairy-cell leukemia, and up to 70 percent of patients with chronic myelogenous leukemia (CML) in early-stage disease. Prolonged suppression or elimination of the leukemic cell clone by interferon may ultimately increase survival of patients with CML. Interferon is not effective single-agent therapy for multiple myeloma, but improves response rate when combined with conventional agents. AIDS-associated Kaposi's sarcoma demonstrates a 40 percent objective response rate to interferon, with less risk of immune system suppression than conventional cytotoxics. Other applications of alfa interferon include malignant melanoma and renal cell carcinoma. Beta interferon is similar to the alfa subtype and may have utility in treatment of brain tumors. Gamma interferon is an important immune regulator with qualitative and quantitative differences in its efficacy and toxicity when compared with alfa interferon.
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PMID:Clinical use of biologic response modifiers in cancer treatment: an overview. Part I. The interferons. 169 95

Recent clinical trials on the systemic application of various forms of interferon in metastatic malignant melanoma showed a moderate response rate of about 11% on an average. Intralesional application of alpha- and beta-interferon, however, resulted in partial or complete regression of the metastases in approx. 50% of the tumors. At present, various combination studies are being carried out in order to enhance the anti-tumor effects of interferon and thus establish a potential therapeutic method in dermato-oncology. In this respect, the combination of alpha-interferon with classic cytostatic drugs (dacarbazine and vindesine) is especially encouraging.
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PMID:[Interferon therapy in malignant melanoma]. 169 48

In this study, we evaluated the effect of a series of peripheral-acting benzodiazepines (BZDs), alone and in combination with recombinant human leukocyte (IFN-alpha A), fibroblast (IFN-beta), or immune (IFN-gamma) interferon (IFN), on the growth of human melanoma cells. Specific peripheral-acting BZDs caused a marked suppression in the proliferation of human melanoma cells. The effect on melanoma cell growth required 72 h exposure to the peripheral-acting BZDs and was not observed if the compounds were removed by 48 h. The relative potency of antiproliferative activity of a series of peripheral-acting BZDs on human melanoma cell growth did not correlate with the reported ability of these agents to bind to peripheral sites on the cell membrane of Friend erythroleukemia cells (FELC), nor did they correlate with the ability of these agents to inhibit [3H]thymidine incorporation in FELC, induce differentiation in FELC, or inhibit neurite outgrowth in nerve growth factor-treated rat pheochromocytoma (PC12) cells. The growth of human melanoma cells was also inhibited by various recombinant human IFNs, with IFN-beta displaying greater antiproliferative activity than IFN-alpha A or IFN-gamma. When the peripheral-acting BZD Ro7-3351, which displays growth inhibitory properties when used alone, was combined with IFN, the antiproliferative activity of the combination was greater than either individual compound exerted independently. The combination of IFN-beta plus Ro7-3351 was more active in suppressing HO-1 melanoma cell growth than other IFN preparations in combination with this peripheral-type BZD. Even when combined with a peripheral-acting BZD, such as Ro5-4608, which displayed only marginal antiproliferative activity against human melanoma cells when applied alone, growth suppression of the combination of this peripheral-type BZD with all three types of IFNs was more than additive. These studies suggest that specific peripheral-acting BZDs, both alone and in combination with recombinant IFNs, display novel antiproliferative activity toward human melanoma cells which may involve a different genetic locus than previously observed in other model cell culture systems.
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PMID:Peripheral-acting benzodiazepines inhibit the growth of human melanoma cells and potentiate the antiproliferative activity of recombinant human interferons. 169 6

Enhancement of the anti-proliferative effect of human interferon (HuIFN) preparations (alpha, beta and gamma) by dipyridamole was detected in a human malignant melanoma cell line, MM-ICB, which we originally established. Cell growth was inhibited by HuIFN alone, but a marked increase in inhibition was noted in vitro and in vivo when dipyrydamole was added. Cellular DNA synthesis, as determined by 3H-deoxythymidine incorporation into the acid-insoluble cellular fraction, was more inhibited by combined treatment than by any of the agents used alone. Two other melanoma cell lines that we established, MM-2CB and MM-3CB, also exhibited sensitivity to combined treatment both in vitro and in vivo. Furthermore, the HMV-I and SEKI melanoma cell lines were susceptible to the combination. Even non-cytotoxic concentrations of dipyridamole could enhance the effect of HuIFN on MM-ICB, MM-2CB, and SEKI cells.
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PMID:Enhancement of an anti-tumor effect of interferon by dipyridamole in established human malignant melanoma cell lines. 169 2

Twenty-five early-passage (less than or equal to 8) melanoma cell lines, isolated from ten patients with metastatic melanoma, were analyzed by a combination of serological, immunochemical, and molecular methods for mRNA levels, synthesis, and surface expression of MHC class I and class II antigens prior to and following exposure to recombinant human leukocyte (IFN-alpha A), fibroblast (IFN-beta), and immune (IFN-gamma) interferon. All the cell lines expressed variable levels of HLA class I gene products that were up-regulated to different extents upon exposure to specific interferons (IFNs). HLA class II antigens were expressed in 22 of the 25 melanoma lines and IFN-gamma increased the levels of class II mRNA, protein synthesis, and surface expression in all cultures displaying baseline expression. A significant up-regulation of class II antigen expression by IFN-alpha or -beta, associated with higher levels of class II transcripts and enhanced synthesis, was found only in two early-passage human melanoma cell lines. In three lesions from the same patient which did not constitutively express class II antigens, no expression of these glycoproteins could be induced with any of the IFNs. These results indicate that IFN-gamma does not act as a de novo inducer of class II antigen expression in early-passage human melanoma cell lines. This hypothesis is further supported by analysis of class II-associated invariant chain (Ii) expression, which is expressed and induced by IFNs in a manner similar to that of class II antigens. The present study also indicates that early-passage metastatic melanoma lesions from the same patient are heterogeneous in their de novo expression of major histocompatibility antigens and in their modulation by IFNs.
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PMID:Effect of recombinant human leukocyte, fibroblast, and immune interferons on expression of class I and II major histocompatibility complex and invariant chain in early passage human melanoma cells. 170 42


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