| In Lynch syndrome adenomas, loss of mismatch repair proteins is related to an enhanced lymphocytic response. | |
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MedLine Citation:
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PMID: 19817892 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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AIMS: Lynch syndrome-associated tumours are characterized by the presence of an increased number of tumour-infiltrating lymphocytes. This enhanced lymphocytic response may be elicited by genetically altered proteins that may arise as a result of a defective DNA mismatch repair system. The aim was to investigate this hypothesis by correlating loss of mismatch repair proteins and infiltration of lymphocytes in Lynch syndrome-associated adenomas and hyperplastic polyps. METHODS AND RESULTS: Mismatch repair protein expression and the number of tumour-infiltrating lymphocytes were assessed in Lynch syndrome (41 adenomas and nine hyperplastic polyps) and in familial colorectal cancer (nine adenomas and one hyperplastic polyp). Nineteen sporadic adenomas were included as a control group. Twenty of 32 (63%) adenomas with loss of mismatch repair protein expression showed an increase in tumour-infiltrating lymphocytes. Eight adenomas (8/32; 25%) displayed many tumour-infiltrating lymphocytes, whereas most adenomas (12/32; 38%) showed a minor increase. In adenomas with mismatch repair protein expression, both sporadic and Lynch syndrome associated, not one showed an increased number of tumour-infiltrating lymphocytes. Hyperplastic polyps in Lynch syndrome patients showed neither loss of mismatch repair expression nor an increase in tumour-infiltrating lymphocytes. CONCLUSIONS: There is a correlation between the loss of mismatch repair proteins and the infiltration of lymphocytes in Lynch syndrome-associated adenomas. |
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Authors:
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Tineke W H Meijer; Nicoline Hoogerbrugge; Fokko M Nagengast; Marjolein J L Ligtenberg; J Han J M van Krieken |
Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Histopathology Volume: 55 ISSN: 1365-2559 ISO Abbreviation: Histopathology Publication Date: 2009 Oct |
Date Detail:
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Created Date: 2009-10-12 Completed Date: 2010-01-28 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 7704136 Medline TA: Histopathology Country: England |
Other Details:
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Languages: eng Pagination: 414-22 Citation Subset: IM |
Affiliation:
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Department of Pathology, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adaptor Proteins, Signal Transducing
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genetics,
metabolism Adenoma / genetics, metabolism*, pathology* Adenosine Triphosphatases / genetics, metabolism Case-Control Studies Colonic Neoplasms / genetics, metabolism*, pathology* Colonic Polyps / genetics, metabolism, pathology Colorectal Neoplasms, Hereditary Nonpolyposis / genetics, metabolism*, pathology* DNA Mismatch Repair / genetics DNA Repair Enzymes / genetics, metabolism* DNA, Neoplasm / genetics, metabolism DNA-Binding Proteins / genetics, metabolism Germ-Line Mutation / genetics Humans Lymphocytes, Tumor-Infiltrating / pathology* MutS Homolog 2 Protein / genetics, metabolism Nuclear Proteins / genetics, metabolism |
| Chemical | |
Reg. No./Substance:
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0/Adaptor Proteins, Signal Transducing; 0/DNA, Neoplasm; 0/DNA-Binding Proteins; 0/G-T mismatch-binding protein; 0/MLH1 protein, human; 0/Nuclear Proteins; EC 3.6.1.-/Adenosine Triphosphatases; EC 3.6.1.-/PMS2 protein, human; EC 3.6.1.3/MSH2 protein, human; EC 3.6.1.3/MutS Homolog 2 Protein; EC 6.5.1.-/DNA Repair Enzymes |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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