Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1990-3-28
pubmed:abstractText
The experiments reported here describe the derivation of an immunogenic melanoma cell line from B16 melanoma by sequential in vitro mutagenization with two chemical mutagens: n-methyl n-nitro n-nitrosoguanine (MNNG) and ethane methyl sulfonate (EMS). Following in vivo screening of over 100 mutant melanoma clones, a single clone was selected for further study. When transplanted to the anterior segment of the mouse eye, the mutant melanoma (D5.1G4) underwent spontaneous resolution in 20% of the immunologically intact hosts. Tumor rejection involved extensive necrosis and culminated in phthisis of the tumor-containing eye. Histologic analysis revealed a prominent mononuclear cellular infiltrate in contrast to the parental progressor B16 melanoma. Immunologic analysis of tumor-bearing hosts showed variable cytotoxic T lymphocyte (CTL) responses but potent delayed-type hypersensitivity (DTH) responses directed against the melanoma cells. Fluorescent activated cell sorter (FACS) analysis of tumor-infiltrating cells from ocular tumors revealed a cellular response consisting mainly of CD8+ CTLs and macrophages. Cultured D5.1G4 melanoma cells demonstrated: 1) enhanced expression of class I major histocompatibility complex (MHC) antigens; 2) increased susceptibility to CTL-mediated killing; and 3) increased susceptibility to tumor necrosis factor (TNF)-mediated cytolysis. Therefore, the intraocular D5.1G4 mutant melanoma model provides important insights into the immunology and immunopathology of intraocular tumor rejection. More intensive analysis of this intraocular melanoma may yield strategies for directing the immune response toward tumor rejection while minimizing damage to normal ocular components.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0146-0404
pubmed:author
pubmed:issnType
Print
pubmed:volume
31
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
247-57
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:2154414-Animals, pubmed-meshheading:2154414-Anterior Eye Segment, pubmed-meshheading:2154414-Cell Separation, pubmed-meshheading:2154414-Disease Models, Animal, pubmed-meshheading:2154414-Eye Neoplasms, pubmed-meshheading:2154414-Female, pubmed-meshheading:2154414-Flow Cytometry, pubmed-meshheading:2154414-Histocompatibility Antigens Class I, pubmed-meshheading:2154414-Hypersensitivity, Delayed, pubmed-meshheading:2154414-Killer Cells, Natural, pubmed-meshheading:2154414-Melanoma, Experimental, pubmed-meshheading:2154414-Mesylates, pubmed-meshheading:2154414-Methylnitronitrosoguanidine, pubmed-meshheading:2154414-Mice, pubmed-meshheading:2154414-Mice, Inbred C57BL, pubmed-meshheading:2154414-Mutation, pubmed-meshheading:2154414-Neoplasm Regression, Spontaneous, pubmed-meshheading:2154414-Neoplasm Transplantation, pubmed-meshheading:2154414-T-Lymphocytes, Cytotoxic, pubmed-meshheading:2154414-T-Lymphocytes, Regulatory, pubmed-meshheading:2154414-Tumor Cells, Cultured
pubmed:year
1990
pubmed:articleTitle
Immunologic evaluation of spontaneous regression of an intraocular murine melanoma.
pubmed:affiliation
Graduate Program in Immunology, University of Texas Southwestern Medical School, Dallas.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't