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

Pieces of amelanotic Greene melanoma were transplanted onto the iris surface of rabbit eyes, where they started to grow rapidly after a dormant period of four to five days. Light microscopically, the melanoma cells appeared round or polygonal and contained large, lightly staining nuclei and prominent nucleoli. Electron microscopy revealed rather electron translucent nuclei containing only a small rim of heterochromatin immediately subjacent to the nuclear envelope. The very prominent, reticulated nucleoli frequently lay close to the nuclear surface. The cytoplasm of the cells showed a well developed Golgi field which contained myriad vesicles of different shape and density and cross-striated, membrane-bound organelles of early melanin synthesis. The mitochondria were short and the smooth-surfaced endoplasmic reticulum was inconspicuous. The rough-surface endoplasmic reticulum was sparse and exhibited predominantly short segments. Like other very active cells, the melanoma cells contained a multitude of ribosomes. Melanoma cells which were not completely surrounded by other cells exhibited numerous processes at the free cell surface and, directly subjacent to these, a layer of very electron dense cytoplasm, indicating that these cells may possess a certain amount of motility. Many light and electron microscopical aspects of the amelanotic Greene melanoma are identical or similar to human uveal melanomas, especially of the epithelioid variety. On morphological grounds it is therefore possible to suspect a close biological relationship of these tumors. Thus, the use of the Greene amelanotic melanoma as a model for study of diagnostic and therapeutic problems in ophthalmology may be considered adequate.
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PMID:The morphology of the amelanotic Greene melanoma. 690 21

Sera from a patient with systemic lupus erythematosus (SLE), tested by indirect immunofluorescence on frozen tissue sections, gave granular cytoplasmic staining of hepatocytes, gastric chief cells, exocrine cells of the pancreas and submandibular glands, and cerebellar Purkinje cells. In acetone-fixed monolayers of rat embryonic fibroblasts, 3T3 cells, mouse neuroblastoma cells, and cells from a human melanoma and colon carcinoma cell line, the sera stained perinuclear cytoplasmic granules which radiated out towards the cell periphery. More mature and differentiated fibroblasts from rat of human foetal lung showed staining of reticular cytoplasmic structures corresponding to phase-dense rough endoplasmic reticulum (RER). Nucleoli were prominently stained in all cultured cells. Serum absorption with ribosomes inhibited all antibody activity but absorption with RNA or with RNase-treated ribosomes resulted only in partial inhibition. Monolayers of RNase-treated fibroblasts gave weaker staining reactions compared to control untreated cultures. These observations suggest that the autoantibody is directed against ribosomal RNA and ribosomal protein present in cytoplasmic polyribosomes, in RER and in nucleoli.
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PMID:Autoantibody to ribosomes and systemic lupus erythematosus. 700 92

This report describes a transmission electron microscopic study on hybrids between subhexaploid mouse melanoma cells and subtetraploid mouse fibroblasts. The melanoma cell line was heterogeneous in terms of pigment production, but all cells contained melanosomes, although in different stages of development. Characteristic features of the fibroblasts included the cytoskeleton, endocytic vesicles, and occurrence of dilated cisternae of granular endoplasmic reticulum. Despite the gene dosage in favour of the melanoma parent cell, the hybrids were devoid of melanosomes, and their phenotype was typically fibroblastic in character.
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PMID:Ultrastructural characterization of a mouse melanoma cell line, a mouse fibroblastic cell line, and hybrids between them. 723 33

The degree of differentiation of two types of hereditary melanomas of interspecific hybrids between the spotted variety of the platyfish (Xiphophorus maculatus) and the swordtail (Xiphophorus helleri) was examined electron microscopically. Melanomas of the fry consisted mainly of pigmented cells containing intermediately matured melanosomes and few other cytoplasmic structures. Melanomas of the adult consisted of lightly pigmented cells having a small number of immature melanosomes; numerous polysomes; well-developed, rough-surfaced endoplasmic reticulum (RER) and Golgi systems; and irregularly shaped nuclei. Thus the fry and adult melanomas appear to represent relatively well- and poorly differentiated states of fish melanophores, respectively. Amelanotic melanomas in the adult melanotic F1 generation were also characterized. Virus-like particle were often found in the nuclei of both melanotic and amelanotic melanoma cells in the adult fish.
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PMID:Differentiation of melanomas occurring in platyfish-swordtail hybrids of different ages: an ultrastructural study. 727 87

Cultivated mouse melanocytes with the genotype of D/- and d/d obtained from dorsal skin of infants, and the variant melanoma cells (subline agm) in which melanosomes were aggregated around the nucleus were characterized by means of electron microscopy. In D/- melanocytes, dendrites contained a number of microtubules and 10-nm filaments, mitochondria, endoplasmic reticulum, and peripherally distributed melanosomes. On the other hand, in d/d melanocytes and agm cells, melanosomes were aggregated in the perinuclear region of the cell body. Their fibrous dendrites contained numerous microtubules and 10-nm filaments, mitochondria, and endoplasmic reticulum. It is suggested that the interactive process of melanosomes with cytoskeletal elements is defective in d/d melanocytes, and that a similar defect is present in agm cells.
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PMID:Ultrastructural observations on melanosome aggregation in genetically defective melanocytes of the mouse. 734 May 65

Mouse B16 melanoma cells in cultures were treated with 2 microgram/ml cytochalasin B. Melanosomes, localized in dendrites as well as those in the peripheral cell body, formed aggregates which then showed centripetal migration. After 24 hr of treatment, melanosomes were found as large aggregates near the nucleus. However, cytochalasim B showed no effect on the distribution of mitochondria and endoplasmic reticulum. When cells were released from the 24 hr-treatment with cytochalasin B, each melanosome began centrifugal migration. In this process, melanosomes were situated in the periphery, and were in close association with microtubules. Side arm-like structures were observed between microtubules and melanosomes, or mitochondria. These results seem to indicate the presence of mechanism(s) specific to melanosome migration, and possible participation of microtubules in this melanosome migration.
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PMID:Differential effect of cytochalasin B on the aggregation of melanosomes in cultured mouse melanoma cells. 739 34

Presentation of exogenous protein antigens to T lymphocytes is based on the intersection of two complex pathways: (a) synthesis, assembly, and transport of major histocompatibility complex (MHC) class II-invariant chain complexes from the endoplasmic reticulum to a specialized endosomal compartment, and (b) endocytosis, denaturation, and proteolysis of antigens followed by loading of antigenic peptides onto newly synthesized MHC class II molecules. It is believed that expression of MHC class II heterodimers, invariant chain and human leukocyte antigen-DM is both necessary and sufficient to reconstitute a functional MHC class II loading compartment in antigen-presenting cells. Expression of each of these essential molecules is under the control of the MHC class II transactivator CIITA. Unexpectedly, however, whereas interferon gamma stimulation does confer effective antigen-processing function to nonprofessional antigen presenting cells, such as melanoma cells, expression of the CIITA transactivator alone is not sufficient. Activation of antigen-specific T cells thus requires additional CIITA-independent factor(s), and such factor(s) can be induced by interferon gamma.
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PMID:A novel antigen-processing-defective phenotype in major histocompatibility complex class II-positive CIITA transfectants is corrected by interferon-gamma. 750 24

Induction of apoptosis by diverse exogenous signals is dependent on elevation of intracellular Ca2+. This process of cell death can be blocked by actinomycin D, indicating that it requires gene transcription events. To identify genes that are required for apoptosis, we used thapsigargin (TG), which inhibits endoplasmic reticulum-dependent Ca(2+)-ATPase and thereby increases cytosolic Ca2+. Exposure to TG led to induction of the zinc finger transcription factor, EGR-1, and apoptosis in human melanoma cells, A375-C6. To determine the functional relevance of EGR-1 expression in TG-inducible apoptosis, we employed a dominant negative mutant which functionally competes with EGR-1 in these cells. Interestingly, the dominant negative mutant inhibited TG-inducible apoptosis. Consistent with this observation, an antisense oligomer directed against Egr-1 also led to a diminution of the number of cells that undergo TG-inducible apoptosis. These results suggest a novel regulatory role for EGR-1 in mediating apoptosis that is induced by intracellular Ca2+ elevation. We have previously shown that in these melanoma cells, EGR-1 acts to inhibit the growth arresting action of interleukin-1. Together, these results imply that EGR-1 plays inducer-specific roles in growth control.
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PMID:Role of EGR-1 in thapsigargin-inducible apoptosis in the melanoma cell line A375-C6. 756 79

The pathway of envelopment and egress of the varicella-zoster virus (VZV) and the primary site of viral production within the epidermal layer of the skin are not fully understood. There are several hypotheses to explain how the virus may receive an envelope as it travels to the surface of the monolayer. In this study, we expand earlier reports and provide a more detailed explanation of the growth of VZV in human melanoma cells. Human melanoma cells were selected because they are a malignant derivative of the melanocyte, the melanin-producing cell which originates in the neural crest. We were able to observe the cytopathic effects of syncytial formation and the pattern of egress of virions at the surfaces of infected monolayers by scanning electron microscopy and laser-scanning confocal microscopy. The egressed virions did not appear uniformly over the syncytial surface, rather they were present in elongated patterns which were designated viral highways. In order to document the pathway by which VZV travels from the host cell nucleus to the outer cell membrane, melanoma cells were infected and then processed for examination by transmission electron microscopy (TEM) at increasing intervals postinfection. At the early time points, within minutes to hours postinfection, it was not possible to localize the input virus by TEM. Thus, viral particles first observed at 24 h postinfection were considered progeny virus. On the basis of the TEM observations, the following sequence of events was considered most likely. Nucleocapsids passed through the inner nuclear membrane and acquired an envelope, after which they were seen in the endoplasmic reticulum. Enveloped virions within vacuoles derived from the endoplasmic reticulum passed into the cytoplasm. Thereafter, vacuoles containing nascent enveloped particles acquired viral glycoproteins by fusion with vesicles derived from the Golgi. The vacuoles containing virions fused with the outer plasma membrane and the particles appeared on the surface of the infected cell. Late in infection, enveloped virions were also present within the nuclei of infected cells; the most likely mechanism was retrograde flow from the perinuclear space back into the nucleus. Thus, this study suggests a role for the melanocyte in the pathogenesis of VZV infection, because all steps in viral egress can be accounted for if VZV subsumes the cellular pathways required for melanogenesis.
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PMID:Egress of varicella-zoster virus from the melanoma cell: a tropism for the melanocyte. 760 70

An established human melanoma cell line was treated with several concentrations of three antineoplastic drugs: melphalan (0.016, 0.032, 0.16 microns), CCNU (1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea) (0.04, 0.21, 0.42 microM), and 4-OHA (4-hydroxyanisole) (4.01 x 10(-4), 1.20 x 10(-3), 2.4 x 10(-3) microM), and the effects on cell growth and viability were compared. 24 hours after treatment, 4-OHA (ID50 = 2.4 x 10(-3) microM) was more cytotoxic than melphalan (ID50 = 0.016 microM) and CCNU (ID50 = 0.21 microM). However, after 96 hours exposure, the most effective drug was CCNU (growth rate = -1.277), which caused the death of the culture. This was followed by melphalan (growth rate = -1.024) and finally 4-OHA (growth rate = -0.69). Similar ultrastructural cell injuries were observed after the use of the three drugs: the dilation of endoplasmic reticulum vesicles and the nuclear membrane; mitochondria swelling; and the existence of lamellar structures and cytoplasmic vacuoles.
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PMID:Effects of various antineoplastic agents on an established human melanoma cell line (G-361). 775 47


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