Linked Life Data

10582700

Source:http://linkedlifedata.com/resource/pubmed/id/10582700

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
22
pubmed:dateCreated
1999-12-14
pubmed:databankReference
pubmed:abstractText
We have pursued our analysis of antigens recognized by autologous cytolytic T lymphocytes (CTLs) on the melanoma cells of patient LB33. This patient enjoys an unusually favorable evolution, which is associated with a strong and sustained antitumor CTL response. We reported previously the analysis of two melanoma cell lines, MEL.A and MEL.B, which were derived from metastases removed from the patient at 5 years' distance. Autologous CTL clones derived from blood lymphocytes recognized several antigens presented by different HLA class I molecules on MEL.A. The MEL.B cells resisted lysis by these CTLs because they have lost expression of most HLA molecules, suggesting that they were selected in vivo by the anti-MEL.A CTL response. One of the MEL.A antigens was shown to result from a point mutation in the tumor. Here we report the cloning of a gene that encodes two other MEL.A antigens. This new gene, MUM-2, is expressed ubiquitously. In the melanoma cells of patient LB33, it contains a point mutation that changes one amino acid in the translated protein. Two different antigenic peptides, one presented to CTL by HLA-B44 molecules and another by HLA-C6 molecules, overlap and contain the mutated residue. Gene MUM-2 is homologous to an essential yeast gene, bet5, that was recently shown to be implicated in the vesicular transport of proteins from the endoplasmic reticulum to the Golgi. In a mutant yeast with a disrupted bet5 gene, both the wild-type and the mutated MUM-2 genes could complement for bet5 function. These results indicate that the antigenic mutation does not destroy the function of the protein, a function that is conserved in eukaryotic cells. The identification of these antigens suggests that point mutations could be the major cause of the strong immunogenicity of MEL.A cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0008-5472
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
59
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
5785-92
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:10582700-Amino Acid Sequence, pubmed-meshheading:10582700-Antigens, Neoplasm, pubmed-meshheading:10582700-Base Sequence, pubmed-meshheading:10582700-DNA, Complementary, pubmed-meshheading:10582700-Genetic Complementation Test, pubmed-meshheading:10582700-HLA-B Antigens, pubmed-meshheading:10582700-HLA-B44 Antigen, pubmed-meshheading:10582700-Humans, pubmed-meshheading:10582700-Melanoma, pubmed-meshheading:10582700-Membrane Transport Proteins, pubmed-meshheading:10582700-Molecular Sequence Data, pubmed-meshheading:10582700-Point Mutation, pubmed-meshheading:10582700-Polymerase Chain Reaction, pubmed-meshheading:10582700-RNA, Messenger, pubmed-meshheading:10582700-Skin Neoplasms, pubmed-meshheading:10582700-T-Lymphocytes, Cytotoxic, pubmed-meshheading:10582700-Tumor Cells, Cultured, pubmed-meshheading:10582700-Vesicular Transport Proteins, pubmed-meshheading:10582700-Yeasts
pubmed:year
1999
pubmed:articleTitle
Two antigens recognized by autologous cytolytic T lymphocytes on a melanoma result from a single point mutation in an essential housekeeping gene.
pubmed:affiliation
Cellular Genetics Unit, Université Catholique de Louvain, Brussels, Belgium.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't