Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2001-12-14
pubmed:abstractText
Loss of human mismatch repair (hMSH2) gene function has been linked to hereditary non-polyposis colorectal cancer (HNPCC), Muir-Torre syndrome (MTS), and sporadic cancers, excluding skin cancers unrelated to MTS. We immunohistochemically examined 125 squamous cell carcinomas (SCCs) using a monoclonal antibody to the hMSH2 protein and compared the results with those for 106 precursor lesions of SCC, consisting of actinic keratosis (AK), Bowenoid type of actinic keratosis (BAK), and Bowen's disease (BOD). In contrast to the homogeneous immunoreactivity of proliferating cells composed of AK, BAK, and BOD, heterogeneous and diminished immunostaining to hMSH2 was observed in tumor cells of SCCs examined. In addition, two SCCs (2 of 125; 1.6%) at multiple loci exhibited a complete lack of immunoreaction to hMSH2. Immunohistochemical staining of hMSH2 was semiquantitatively scored as 0 (0% of total cells examined), 1 (less than 10%), 2 (10-50%), or 3 (more than 50%). Percentage preservation of and average score for hMSH2 expression in normal, AK, BAK, BOD, and SCC were 56% and 2.06, 100% and 2.80, 94% and 2.88, 83% and 2.78, 63% and 2.36, respectively. The percentage preservation of and average scores for hMSH2 in AK, BAK, and BOD were significantly higher than those in presumably normal skin (P<0.01). There were no significant differences in the percentage preservation of and average scores for hMSH2 between presumably normal skin and SCC. The score for hMSH2 expression was significantly correlated with score for sun exposure in presumably normal skin of each lesion (R=0.70). These findings for hMSH2 expression in precursor lesions and SCC suggest that promotion or activation of hMSH2 expression may be induced by the increased DNA damage caused by sun exposure and that diminished expression of it might occur according to the transformation from precancerous lesions to SCC.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0945-6317
pubmed:author
pubmed:issnType
Print
pubmed:volume
439
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
622-7
pubmed:dateRevised
2005-11-17
pubmed:meshHeading
pubmed-meshheading:11764381-Adult, pubmed-meshheading:11764381-Aged, pubmed-meshheading:11764381-Aged, 80 and over, pubmed-meshheading:11764381-Base Pair Mismatch, pubmed-meshheading:11764381-Bowen's Disease, pubmed-meshheading:11764381-Carcinoma, Squamous Cell, pubmed-meshheading:11764381-Cell Count, pubmed-meshheading:11764381-DNA Repair, pubmed-meshheading:11764381-DNA-Binding Proteins, pubmed-meshheading:11764381-Female, pubmed-meshheading:11764381-Humans, pubmed-meshheading:11764381-Immunohistochemistry, pubmed-meshheading:11764381-Keratosis, pubmed-meshheading:11764381-Male, pubmed-meshheading:11764381-Middle Aged, pubmed-meshheading:11764381-MutS Homolog 2 Protein, pubmed-meshheading:11764381-Neoplasms, Radiation-Induced, pubmed-meshheading:11764381-Precancerous Conditions, pubmed-meshheading:11764381-Proto-Oncogene Proteins, pubmed-meshheading:11764381-Skin Neoplasms, pubmed-meshheading:11764381-Sunlight
pubmed:year
2001
pubmed:articleTitle
Reduced human mismatch repair protein expression in the development of precancerous skin lesions to squamous cell carcinoma.
pubmed:affiliation
Department of Pathology II, Kochi Medical School, Japan.
pubmed:publicationType
Journal Article