rdf:type |
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lifeskim:mentions |
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pubmed:issue |
23
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pubmed:dateCreated |
2001-11-7
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pubmed:abstractText |
The functional role and specificity of tumor infiltrating lymphocytes (TIL) is generally not well characterized. Prominent lymphocyte infiltration is the hallmark of the most common form of hereditary colon cancer, hereditary nonpolyposis colon cancer (HNPCC) and the corresponding spontaneous colon cancers with the microsatellite instability (MSI) phenotype. These cancers are caused by inherited or acquired defects in the DNA mismatch-repair machinery. The molecular mechanism behind the MSI phenotype provides a clue to understanding the lymphocyte reaction by allowing reliable prediction of potential T cell epitopes created by frameshift mutations in candidate genes carrying nucleotide repeat sequences, such as TGF beta RII and BAX. These tumors therefore represent an interesting human system for studying TIL and characterizing tumor-specific T cells. We here describe T cell reactivity against several T helper cell epitopes, representing a common frameshift mutation in TGF beta RII, in TIL and peripheral blood lymphocytes from patients with MSI(+) tumors. The peptide SLVRLSSCVPVALMSAMTTSSSQ was recognized by T cells from two of three patients with spontaneous MSI(+) colon cancers and from all three patients with HNPCC. Because such mutations are present in 90% of cancers within this patient group, these newly characterized epitopes provide attractive targets for cancer vaccines, including a prophylactic vaccine for individuals carrying a genetic disposition for developing HNPCC.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/11687624-10074914,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11687624-10362805,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11687624-11041376,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/11687624-1639630,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11687624-1840703,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11687624-7585596,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11687624-7585632,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11687624-7691613,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11687624-7761852,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/11687624-8505985,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11687624-8841452,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11687624-8861899,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/11687624-9495251
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Neoplasm,
http://linkedlifedata.com/resource/pubmed/chemical/BAX protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/DNA Primers,
http://linkedlifedata.com/resource/pubmed/chemical/Peptides,
http://linkedlifedata.com/resource/pubmed/chemical/Protein-Serine-Threonine Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-bcl-2,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Transforming Growth...,
http://linkedlifedata.com/resource/pubmed/chemical/bcl-2-Associated X Protein,
http://linkedlifedata.com/resource/pubmed/chemical/transforming growth factor-beta...
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0027-8424
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pubmed:author |
pubmed-author:BjørheimJJ,
pubmed-author:BukholmI KIK,
pubmed-author:EriksenJ AJA,
pubmed-author:GaudernackGG,
pubmed-author:GjertsenM KMK,
pubmed-author:LindblomAA,
pubmed-author:LislerudKK,
pubmed-author:MøllerMM,
pubmed-author:NeslandJ MJM,
pubmed-author:OlsenO COC,
pubmed-author:SaeterdalII
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pubmed:issnType |
Print
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pubmed:day |
6
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pubmed:volume |
98
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
13255-60
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:11687624-Adenocarcinoma,
pubmed-meshheading:11687624-Amino Acid Sequence,
pubmed-meshheading:11687624-Antigens, Neoplasm,
pubmed-meshheading:11687624-Base Sequence,
pubmed-meshheading:11687624-Colorectal Neoplasms,
pubmed-meshheading:11687624-DNA Primers,
pubmed-meshheading:11687624-Female,
pubmed-meshheading:11687624-Frameshift Mutation,
pubmed-meshheading:11687624-Humans,
pubmed-meshheading:11687624-Immunohistochemistry,
pubmed-meshheading:11687624-Immunologic Memory,
pubmed-meshheading:11687624-Molecular Sequence Data,
pubmed-meshheading:11687624-Mutation,
pubmed-meshheading:11687624-Peptides,
pubmed-meshheading:11687624-Protein-Serine-Threonine Kinases,
pubmed-meshheading:11687624-Proto-Oncogene Proteins,
pubmed-meshheading:11687624-Proto-Oncogene Proteins c-bcl-2,
pubmed-meshheading:11687624-Receptors, Transforming Growth Factor beta,
pubmed-meshheading:11687624-T-Lymphocytes,
pubmed-meshheading:11687624-bcl-2-Associated X Protein
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pubmed:year |
2001
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pubmed:articleTitle |
Frameshift-mutation-derived peptides as tumor-specific antigens in inherited and spontaneous colorectal cancer.
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pubmed:affiliation |
The Norwegian Radium Hospital, Department of Immunology, Section for Immunotherapy, University of Oslo, 0310 Oslo, Norway.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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