Cytochrome P450 1B1 expression in rat esophageal tumorigenesis promoted by gastric and duodenal reflux

Cytochrome P450 1B1 (CYP1B1) mRNA is constitutively expressed in most normal extra‐hepatic tissues; however the protein is not detectable in these tissues but is expressed in a wide variety of tumors. CYP1B1 is responsible for the activation of a number of carcinogens present in tobacco smoke and fo...

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Published in:	Molecular carcinogenesis Vol. 48; no. 2; pp. 110 - 117
Main Authors:	Devlin, Andrea H., McIlroy, Marie, McKeen, Hayley D., Bonde, Pramode, Menezes, A.A. Carlos, Swarbrick, Christine J., Robson, Tracy, Hirst, David G., Campbell, F. Charles, McGuigan, James A., McKeown, Stephanie R.
Format:	Journal Article
Language:	English
Published:	Hoboken Wiley Subscription Services, Inc., A Wiley Company 01-02-2009
Subjects:	Animals Antibody Specificity Aryl Hydrocarbon Hydroxylases - genetics Aryl Hydrocarbon Hydroxylases - immunology Blotting, Western CYP1B1 Cytochrome P-450 CYP1B1 Duodenogastric Reflux - complications Duodenogastric Reflux - enzymology Esophageal Neoplasms - enzymology Esophageal Neoplasms - etiology esophagus Female Gastroesophageal Reflux - complications Gastroesophageal Reflux - enzymology Immunohistochemistry Mice Mice, Knockout Rats Rats, Sprague-Dawley RNA, Messenger - genetics rodent tumorigenesis
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Abstract	Cytochrome P450 1B1 (CYP1B1) mRNA is constitutively expressed in most normal extra‐hepatic tissues; however the protein is not detectable in these tissues but is expressed in a wide variety of tumors. CYP1B1 is responsible for the activation of a number of carcinogens present in tobacco smoke and food. A surgical model of rat esophageal tumorigenesis, promoted by gastric or duodenal reflux was used to determine CYP1B1 expression in premalignant esophageal tissue. Immunohistochemistry was performed using a modified amplified fluorescein tyramide protocol. CYP1B1 was not observed in normal esophageal mucosa, submucosa, or muscularis mucosa. Animals exposed to gastric reflux developed mild hyperplasia. Varying degrees of hyperplasia were observed in the duodenal reflux group. All regions of hyperplasia showed moderate or strong CYP1B1 immunoreactivity. Duodenal reflux induced a small number of premalignant changes: immunoreactivity was absent from the epithelium of squamous dysplasia (0/10), Barrett's esophagus (0/7), and majority of dysplastic Barrett's esophagus (1/4). Moderate or strong immunoreactivity was observed in the majority (7/8) of squamous cell carcinomas (SCCs) in situ. Immunoreactivity was also observed in the lamina propria and submucosa in association with inflammation, regardless of the severity of inflammation. The expression of CYP1B1 in hyperplasia, SCCs in situ, or in association with inflammation may increase the production of carcinogenic metabolites, which may promote esophageal tumorigenesis. © 2008 Wiley‐Liss, Inc.
AbstractList	Cytochrome P450 1B1 (CYP1B1) mRNA is constitutively expressed in most normal extra‐hepatic tissues; however the protein is not detectable in these tissues but is expressed in a wide variety of tumors. CYP1B1 is responsible for the activation of a number of carcinogens present in tobacco smoke and food. A surgical model of rat esophageal tumorigenesis, promoted by gastric or duodenal reflux was used to determine CYP1B1 expression in premalignant esophageal tissue. Immunohistochemistry was performed using a modified amplified fluorescein tyramide protocol. CYP1B1 was not observed in normal esophageal mucosa, submucosa, or muscularis mucosa. Animals exposed to gastric reflux developed mild hyperplasia. Varying degrees of hyperplasia were observed in the duodenal reflux group. All regions of hyperplasia showed moderate or strong CYP1B1 immunoreactivity. Duodenal reflux induced a small number of premalignant changes: immunoreactivity was absent from the epithelium of squamous dysplasia (0/10), Barrett's esophagus (0/7), and majority of dysplastic Barrett's esophagus (1/4). Moderate or strong immunoreactivity was observed in the majority (7/8) of squamous cell carcinomas (SCCs) in situ. Immunoreactivity was also observed in the lamina propria and submucosa in association with inflammation, regardless of the severity of inflammation. The expression of CYP1B1 in hyperplasia, SCCs in situ, or in association with inflammation may increase the production of carcinogenic metabolites, which may promote esophageal tumorigenesis. © 2008 Wiley‐Liss, Inc. Cytochrome P450 1B1 (CYP1B1) mRNA is constitutively expressed in most normal extra-hepatic tissues; however the protein is not detectable in these tissues but is expressed in a wide variety of tumors. CYP1B1 is responsible for the activation of a number of carcinogens present in tobacco smoke and food. A surgical model of rat esophageal tumorigenesis, promoted by gastric or duodenal reflux was used to determine CYP1B1 expression in premalignant esophageal tissue. Immunohistochemistry was performed using a modified amplified fluorescein tyramide protocol. CYP1B1 was not observed in normal esophageal mucosa, submucosa, or muscularis mucosa. Animals exposed to gastric reflux developed mild hyperplasia. Varying degrees of hyperplasia were observed in the duodenal reflux group. All regions of hyperplasia showed moderate or strong CYP1B1 immunoreactivity. Duodenal reflux induced a small number of premalignant changes: immunoreactivity was absent from the epithelium of squamous dysplasia (0/10), Barrett's esophagus (0/7), and majority of dysplastic Barrett's esophagus (1/4). Moderate or strong immunoreactivity was observed in the majority (7/8) of squamous cell carcinomas (SCCs) in situ. Immunoreactivity was also observed in the lamina propria and submucosa in association with inflammation, regardless of the severity of inflammation. The expression of CYP1B1 in hyperplasia, SCCs in situ, or in association with inflammation may increase the production of carcinogenic metabolites, which may promote esophageal tumorigenesis.
Author	Robson, Tracy McKeown, Stephanie R. Hirst, David G. Campbell, F. Charles McIlroy, Marie Menezes, A.A. Carlos McGuigan, James A. Devlin, Andrea H. Bonde, Pramode McKeen, Hayley D. Swarbrick, Christine J.
Author_xml	– sequence: 1 givenname: Andrea H. surname: Devlin fullname: Devlin, Andrea H. organization: Biomedical Sciences Research Institute, University of Ulster, Coleraine, Northern Ireland, UK – sequence: 2 givenname: Marie surname: McIlroy fullname: McIlroy, Marie organization: Biomedical Sciences Research Institute, University of Ulster, Coleraine, Northern Ireland, UK – sequence: 3 givenname: Hayley D. surname: McKeen fullname: McKeen, Hayley D. organization: School of Pharmacy, Queen's University, Belfast, Northern Ireland, UK – sequence: 4 givenname: Pramode surname: Bonde fullname: Bonde, Pramode organization: Department of Cardiothoracic Surgery, Royal Victoria Hospital, Belfast, Northern Ireland, UK – sequence: 5 givenname: A.A. Carlos surname: Menezes fullname: Menezes, A.A. Carlos organization: Department of Surgery, Queen's University, Belfast, Northern Ireland, UK – sequence: 6 givenname: Christine J. surname: Swarbrick fullname: Swarbrick, Christine J. organization: Department of Pathology, Royal Victoria Hospital, Belfast, Northern Ireland, UK – sequence: 7 givenname: Tracy surname: Robson fullname: Robson, Tracy organization: School of Pharmacy, Queen's University, Belfast, Northern Ireland, UK – sequence: 8 givenname: David G. surname: Hirst fullname: Hirst, David G. organization: School of Pharmacy, Queen's University, Belfast, Northern Ireland, UK – sequence: 9 givenname: F. Charles surname: Campbell fullname: Campbell, F. Charles organization: Department of Surgery, Queen's University, Belfast, Northern Ireland, UK – sequence: 10 givenname: James A. surname: McGuigan fullname: McGuigan, James A. organization: Department of Cardiothoracic Surgery, Royal Victoria Hospital, Belfast, Northern Ireland, UK – sequence: 11 givenname: Stephanie R. surname: McKeown fullname: McKeown, Stephanie R. organization: Biomedical Sciences Research Institute, University of Ulster, Coleraine, Northern Ireland, UK
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/18618592$$D View this record in MEDLINE/PubMed
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CitedBy_id	crossref_primary_10_1089_ten_tea_2009_0217 crossref_primary_10_1093_carcin_bgu190 crossref_primary_10_1002_mc_20589 crossref_primary_10_2217_pgs_2018_0197
Cites_doi	10.1093/carcin/24.2.327 10.1074/jbc.270.19.11595 10.1073/pnas.93.18.9776 10.1016/S0006-291X(02)02004-1 10.1158/1078-0432.CCR-07-0483 10.1080/00365520701452209 10.1093/jnci/92.16.1316 10.1016/S0021-9258(17)36551-1 10.1081/DMR-100101929 10.1002/jemt.1070310303 10.1093/mutage/12.2.83 10.1182/blood-2003-05-1374 10.1177/002215549904701111 10.1016/j.taap.2006.06.004 10.1093/carcin/bgh039 10.1124/dmd.32.8.840 10.1016/j.abb.2005.02.001 10.1093/hmg/6.4.641 10.1038/nature01322 10.1073/pnas.96.5.1977 10.1016/j.canlet.2006.02.003 10.1097/00008571-200012000-00001 10.1054/bjoc.2001.1907 10.1016/S0378-4274(02)00417-4 10.1093/carcin/20.8.1607 10.1093/hmg/11.10.1185 10.1124/dmd.104.002410 10.1001/archsurg.137.11.1238 10.1016/S0003-9861(03)00174-7 10.1016/S0021-9258(17)36803-5 10.1158/1078-0432.CCR-03-0166 10.1016/j.ijrobp.2003.09.064
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Snippet	Cytochrome P450 1B1 (CYP1B1) mRNA is constitutively expressed in most normal extra‐hepatic tissues; however the protein is not detectable in these tissues but... Cytochrome P450 1B1 (CYP1B1) mRNA is constitutively expressed in most normal extra-hepatic tissues; however the protein is not detectable in these tissues but...
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SubjectTerms	Animals Antibody Specificity Aryl Hydrocarbon Hydroxylases - genetics Aryl Hydrocarbon Hydroxylases - immunology Blotting, Western CYP1B1 Cytochrome P-450 CYP1B1 Duodenogastric Reflux - complications Duodenogastric Reflux - enzymology Esophageal Neoplasms - enzymology Esophageal Neoplasms - etiology esophagus Female Gastroesophageal Reflux - complications Gastroesophageal Reflux - enzymology Immunohistochemistry Mice Mice, Knockout Rats Rats, Sprague-Dawley RNA, Messenger - genetics rodent tumorigenesis
Title	Cytochrome P450 1B1 expression in rat esophageal tumorigenesis promoted by gastric and duodenal reflux
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