Document Detail


In Lynch syndrome adenomas, loss of mismatch repair proteins is related to an enhanced lymphocytic response.
MedLine Citation:
PMID:  19817892     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Tineke W H Meijer; Nicoline Hoogerbrugge; Fokko M Nagengast; Marjolein J L Ligtenberg; J Han J M van Krieken
Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Histopathology     Volume:  55     ISSN:  1365-2559     ISO Abbreviation:  Histopathology     Publication Date:  2009 Oct 
Date Detail:
Created Date:  2009-10-12     Completed Date:  2010-01-28     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7704136     Medline TA:  Histopathology     Country:  England    
Other Details:
Languages:  eng     Pagination:  414-22     Citation Subset:  IM    
Affiliation:
Department of Pathology, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands.
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MeSH Terms
Descriptor/Qualifier:
Adaptor Proteins, Signal Transducing / 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:
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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