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dc.contributor.authorHour, Tzyh-Chyuan
dc.contributor.authorPu, Yeong-Shiau
dc.contributor.authorLin, Chia-Chi
dc.contributor.authorHuang, Shi-Wei
dc.contributor.authorChen, Jun
dc.contributor.authorChiu, Allen W.
dc.contributor.authorChen, Chien-Jen
dc.contributor.authorHuang, Chao-Yuan
dc.date.accessioned2009-05-15T08:03:13Z
dc.date.available2009-05-15T08:03:13Z
dc.date.issued2009-05-15T08:03:13Z
dc.identifier.citationAnticancer Res. 2006, 26 (1A):375-8en
dc.identifier.issn0250-7005
dc.identifier.pmid16475721
dc.identifier.urihttp://hdl.handle.net/10146/68254
dc.descriptionKEYWORDS - CLASSIFICATION: Arsenic Poisoning;biosynthesis;chemically induced;complications;Environmental Exposure;Glutathione;Glutathione S-Transferase pi;Humans;metabolism;mechanisms of carcinogenesis;Proteins;Proto-Oncogene Proteins;Proto-Oncogene Proteins c-bcl-2;Research;Taiwan;Tumor Markers,Biological;Tumor Suppressor Protein p53;Urinary Bladder Neoplasms.en
dc.description.abstractBACKGROUND: Little is known about the mechanisms of arsenic-related urothelial cancer (AsUC). The aim of this study was to reveal the differential expression of molecular markers between AsUC and non-arsenic-related UC (non-AsUC). MATERIALS AND METHODS: Tissues of AsUC (n=33), non-AsUC (n=20) and normal bladder urothelia from patients with benign diseases (n=4) were examined for multiple selected molecular markers responsible for various cellular functions, includingglutathione, GST-pi, Bcl-2, p53 and c-Fos. RESULTS: The mean cellular glutathione content of normal mucosal samples (33.4 +/- 7.2 microM/mg protein) was significantly higher than either non-AsUC (22.8 +/- 1.8, p = 0.04) or AsUC (16.4 +/- 1.6, p = 0.002). The glutathione content of non-AsUC was higher than that of AsUC (p = 0.012). The expressions of Bcl-2 and c-Fos in AsUC were significantly higher than those in non-AsUC (p = 0.004 and p = 0.02, respectively). CONCLUSION: The carcinogenic pathway for AsUC is different, in part, from that of non-AsUC. Cellular glutathione contents may be down-regulated during urothelial carcinogenesis. Bcl-2 and c-Fos may play important roles in arsenic-mediated carcinogenesis of the urothelium.
dc.language.isoenen
dc.relation.urlhttp://ar.iiarjournals.org/content/26/1A/375.longen
dc.subject.meshArsenic Poisoning
dc.subject.meshEnvironmental Exposure
dc.subject.meshGlutathione
dc.subject.meshGlutathione S-Transferase pi
dc.subject.meshHumans
dc.subject.meshProto-Oncogene Proteins c-bcl-2
dc.subject.meshTumor Markers, Biological
dc.subject.meshTumor Suppressor Protein p53
dc.subject.meshUrinary Bladder Neoplasms
dc.titleDifferential expression of molecular markers in arsenic- and non-arsenic-related urothelial cancer.en
dc.typeArticleen
dc.identifier.journalAnticancer researchen
html.description.abstractBACKGROUND: Little is known about the mechanisms of arsenic-related urothelial cancer (AsUC). The aim of this study was to reveal the differential expression of molecular markers between AsUC and non-arsenic-related UC (non-AsUC). MATERIALS AND METHODS: Tissues of AsUC (n=33), non-AsUC (n=20) and normal bladder urothelia from patients with benign diseases (n=4) were examined for multiple selected molecular markers responsible for various cellular functions, includingglutathione, GST-pi, Bcl-2, p53 and c-Fos. RESULTS: The mean cellular glutathione content of normal mucosal samples (33.4 +/- 7.2 microM/mg protein) was significantly higher than either non-AsUC (22.8 +/- 1.8, p = 0.04) or AsUC (16.4 +/- 1.6, p = 0.002). The glutathione content of non-AsUC was higher than that of AsUC (p = 0.012). The expressions of Bcl-2 and c-Fos in AsUC were significantly higher than those in non-AsUC (p = 0.004 and p = 0.02, respectively). CONCLUSION: The carcinogenic pathway for AsUC is different, in part, from that of non-AsUC. Cellular glutathione contents may be down-regulated during urothelial carcinogenesis. Bcl-2 and c-Fos may play important roles in arsenic-mediated carcinogenesis of the urothelium.


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