Source:http://linkedlifedata.com/resource/pubmed/id/10752476
Switch to
| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
12
|
| pubmed:dateCreated |
2000-4-19
|
| pubmed:abstractText |
Down-regulation of the expression of major histocompatibility complex molecules is a frequent event that is associated with the poor immunogenicity of tumor cells. Acquired resistance to T-cell-based immunotherapy has been associated with loss of functional beta2-microglobulin expression. This anomaly appears to be particularly relevant in tumors exhibiting a defect in DNA-mismatch repair, and induces structural abnormalities in HLA cell-surface expression that are not reversible by cytokine treatment. We examined HLA expression in 118 melanoma, colon or larynx tumors to identify total loss of HLA class I expression with or without somatic beta2-microglobulin gene mutation. Microsatellite instability was investigated in these tumors to determine whether a replication error phenotype (RER+) implied a particular alteration in HLA phenotype. A total of 7.6% of the tumors showed the RER+ phenotype, and 12.7% were HLA-ABC-negative. In the RER+ group, only one tumor was HLA-ABC-negative and no beta2-microglobulin mutation was identified. In contrast, in the HLA-ABC-negative group, only one tumor showed microsatellite instability. None of the three melanomas that contained beta2-microglobulin mutation exhibited the mutator phenotype. These findings suggest that beta2-microglobulin mutation in human melanoma tumors may arise through a mechanism that does not necessarily involve microsatellite instability. Our results also indicate that somatic mutations of the beta2-microglobulin gene are not the main mechanism of total loss of HLA expression.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Mar
|
| pubmed:issn |
0340-7004
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
48
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
684-90
|
| pubmed:dateRevised |
2006-11-15
|
| pubmed:meshHeading |
pubmed-meshheading:10752476-Adenocarcinoma,
pubmed-meshheading:10752476-Antigens, Neoplasm,
pubmed-meshheading:10752476-Carcinoma, Squamous Cell,
pubmed-meshheading:10752476-Colorectal Neoplasms,
pubmed-meshheading:10752476-Colorectal Neoplasms, Hereditary Nonpolyposis,
pubmed-meshheading:10752476-DNA, Neoplasm,
pubmed-meshheading:10752476-DNA Repair,
pubmed-meshheading:10752476-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:10752476-Genes, MHC Class I,
pubmed-meshheading:10752476-HLA Antigens,
pubmed-meshheading:10752476-Humans,
pubmed-meshheading:10752476-Laryngeal Neoplasms,
pubmed-meshheading:10752476-Loss of Heterozygosity,
pubmed-meshheading:10752476-Melanoma,
pubmed-meshheading:10752476-Microsatellite Repeats,
pubmed-meshheading:10752476-Mutagenesis,
pubmed-meshheading:10752476-Mutation,
pubmed-meshheading:10752476-Neoplasms,
pubmed-meshheading:10752476-Phenotype,
pubmed-meshheading:10752476-beta 2-Microglobulin
|
| pubmed:year |
2000
|
| pubmed:articleTitle |
Microsatellite instability analysis in tumors with different mechanisms for total loss of HLA expression.
|
| pubmed:affiliation |
Departamento de Análisis Clínicos, Hospital Universitario Virgen de las Nieves, Universidad de Granada, Spain.
|
| pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
|