Source:http://linkedlifedata.com/resource/pubmed/id/21412023
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1
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| pubmed:dateCreated |
2011-6-9
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| pubmed:abstractText |
The transcription factor Krüppel-like factor 4 (KLF4) may act both as an oncogene and a tumor suppressor in a tissue-dependent manner, and further studies on its role in pancreatic ductal adenocarcinoma (PDAC) progression and clinical outcome are warranted. Therefore, we investigated the loss of heterozygosity (LOH) in the 9q22.3-32 region and loss of KFL4 gene expression in epithelial cells from 35 PDAC, 6 pancreatic intraductal neoplasias (PanINs) and 6 normal ducts, isolated by laser microdissection, as well as their correlation with overall survival (OS) in patients treated with gemcitabine in the adjuvant setting. LOH was evaluated with 4 microsatellite markers and in situ hybridization, while KLF4 expression was studied by reverse transcription-PCR and immunohistochemistry. LOH in at least 1 locus was observed in 25 of 35 PDAC cases and in 5 of 6 PanINs, respectively. In particular, the loss of the D9S105 marker was present in 46.9% of PDAC and 83.3% of PanINs, becoming the most deleted marker, while no LOH in D9S105 was observed in normal Wirsung pancreatic duct. Lack of KLF4 mRNA expression was significantly associated with: (1) genomic deletion flanking KLF4 in PDAC and in PanINs (with LOH of D9S105), (2) low-grade PDAC-associated PanIN, (3) lack of KLF4 protein expression, and (4) shorter OS. These results strongly suggest a relationship between D9S105 deletion and downregulation of KLF4 gene expression as an early event in PDAC progression, as well as a possible role of KLF4 as a prognostic biomarker in gemcitabine-treated patients. and IAP.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:issn |
1424-3911
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| pubmed:author | |
| pubmed:copyrightInfo |
Copyright © 2011 S. Karger AG, Basel.
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| pubmed:issnType |
Electronic
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| pubmed:volume |
11
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
30-42
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| pubmed:meshHeading |
pubmed-meshheading:21412023-Adult,
pubmed-meshheading:21412023-Aged,
pubmed-meshheading:21412023-Aged, 80 and over,
pubmed-meshheading:21412023-Carcinoma, Pancreatic Ductal,
pubmed-meshheading:21412023-Carcinoma in Situ,
pubmed-meshheading:21412023-Down-Regulation,
pubmed-meshheading:21412023-Female,
pubmed-meshheading:21412023-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:21412023-Humans,
pubmed-meshheading:21412023-Immunohistochemistry,
pubmed-meshheading:21412023-In Situ Hybridization,
pubmed-meshheading:21412023-Kruppel-Like Transcription Factors,
pubmed-meshheading:21412023-Loss of Heterozygosity,
pubmed-meshheading:21412023-Male,
pubmed-meshheading:21412023-Microsatellite Repeats,
pubmed-meshheading:21412023-Middle Aged,
pubmed-meshheading:21412023-Pancreatic Neoplasms,
pubmed-meshheading:21412023-RNA, Messenger,
pubmed-meshheading:21412023-Retrospective Studies,
pubmed-meshheading:21412023-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:21412023-Tumor Markers, Biological
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| pubmed:year |
2011
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| pubmed:articleTitle |
Loss of heterozygosity status of D9S105 marker is associated with downregulation of Krüppel-like factor 4 expression in pancreatic ductal adenocarcinoma and pancreatic intraepithelial lesions.
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| pubmed:affiliation |
Division of General and Transplantation Surgery, University of Pisa, Pisa, Italy.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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