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dc.contributor.authorWang, Xiao-Ping
dc.contributor.authorLi, Zhi-Jun
dc.contributor.authorMagnusson, Jonas
dc.contributor.authorBrunicardi, F Charles
dc.date.accessioned2006-05-16T13:32:50Z
dc.date.available2006-05-16T13:32:50Z
dc.date.issued2005-03-01
dc.identifier.citationWorld J Surg 2005, 29(3):334-8en
dc.identifier.issn0364-2313
dc.identifier.pmid15706433
dc.identifier.doi10.1007/s00268-004-7823-4
dc.identifier.otherSAG12en
dc.identifier.urihttp://hdl.handle.net/2336/2691
dc.descriptionTo access publisher full text version of this article. Please click on the hyperlink in Additional Links fielden
dc.description.abstractIn previous studies, we demonstrated that rat insulin promoter (RIP)-driven gene therapy successfully targeted human pancreatic tumor PANC-1 cells and mouse insulinoma NIT-1 cells, which are both pancreatic duodenal homeobox-1 (PDX-1)-positive. The purpose of this study was to perform a human tissue array analysis to determine potential targets for RIP-driven gene therapy. A custom-designed tissue MicroArray analysis of various human cancer specimens was performed using a PDX-1 polyclonal antibody generated in our laboratory. The custom-designed Tissue MicroArray of human tumor specimens consists of human cancer specimens from different origins, such as the pancreas, breast, colon, prostate, kidney, liver, lung, and ovary. A panel of normal human specimens from 20 organs or tissues was used as a control. All tissues were fixed in formalin and embedded in paraffin. The immunohistochemistry studies of the cytoplasm and the nuclear expression levels were compared using the Loda method and blind reviews. Data are presented as the mean +/- SEM (p < 0.05 was considered significant by the unpaired student t-test). PDX-1 expression intensity was elevated in both benign and malignant tissues from the same patient with pancreas, breast, colon, prostate, and kidney cancers, whereas normal human tissues from control subjects without cancer did not express PDX-1. These results suggest that PDX-1 is an early marker for these cancers and could be potentially used as a diagnostic parameter and perhaps could be targeted by PDX-1-activated gene therapies, such as RIP-TK.
dc.language.isoenen
dc.publisherSpringer Verlagen
dc.relation.urlhttp://www.springerlink.com/content/p5egepmxdmqedqk6en
dc.subjectHomeodomain Proteinsen
dc.subjectAdenocarcinomaen
dc.subjectOligonucleotide Array Sequence Analysisen
dc.subjectPancreatic Neoplasmsen
dc.subjectTrans-Activatorsen
dc.subjectPancreatitisen
dc.subjectRNA, Messengeren
dc.subjectGene Therapyen
dc.subjectFemaleen
dc.subjectMaleen
dc.titleTissue MicroArray analyses of pancreatic duodenal homeobox-1 in human cancersen
dc.typeArticleen
dc.identifier.journalWorld journal of surgeryen
dc.identifier.journalWorld journal of surgeryen
dc.format.digYES
html.description.abstractIn previous studies, we demonstrated that rat insulin promoter (RIP)-driven gene therapy successfully targeted human pancreatic tumor PANC-1 cells and mouse insulinoma NIT-1 cells, which are both pancreatic duodenal homeobox-1 (PDX-1)-positive. The purpose of this study was to perform a human tissue array analysis to determine potential targets for RIP-driven gene therapy. A custom-designed tissue MicroArray analysis of various human cancer specimens was performed using a PDX-1 polyclonal antibody generated in our laboratory. The custom-designed Tissue MicroArray of human tumor specimens consists of human cancer specimens from different origins, such as the pancreas, breast, colon, prostate, kidney, liver, lung, and ovary. A panel of normal human specimens from 20 organs or tissues was used as a control. All tissues were fixed in formalin and embedded in paraffin. The immunohistochemistry studies of the cytoplasm and the nuclear expression levels were compared using the Loda method and blind reviews. Data are presented as the mean +/- SEM (p < 0.05 was considered significant by the unpaired student t-test). PDX-1 expression intensity was elevated in both benign and malignant tissues from the same patient with pancreas, breast, colon, prostate, and kidney cancers, whereas normal human tissues from control subjects without cancer did not express PDX-1. These results suggest that PDX-1 is an early marker for these cancers and could be potentially used as a diagnostic parameter and perhaps could be targeted by PDX-1-activated gene therapies, such as RIP-TK.


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