Secondary bile acids: an underrecognized cause of colon cancer

Abstract Bile acids were first proposed as carcinogens in 1939. Since then, accumulated evidence has linked exposure of cells of the gastrointestinal tract to repeated high physiologic levels of bile acids as an important risk factor for gastrointestinal cancers. High exposure to bile acids may occu...
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Gespeichert in:

Autor*in:	Ajouz, Hana [verfasserIn] Mukherji, Deborah Shamseddine, Ali

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2014

Schlagwörter:	Bile Acid Cholic Acid Chenodeoxycholic Acid Bile Acid Concentration Secondary Bile Acid

Anmerkung:	© Ajouz et al.; licensee BioMed Central Ltd. 2014. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (

Übergeordnetes Werk:	Enthalten in: World journal of surgical oncology - London : Biomed Central, 2003, 12(2014), 1 vom: 24. Mai
Übergeordnetes Werk:	volume:12 ; year:2014 ; number:1 ; day:24 ; month:05

Links:	Volltext

DOI / URN:	10.1186/1477-7819-12-164

Katalog-ID:	SPR028826655

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spelling	10.1186/1477-7819-12-164 doi (DE-627)SPR028826655 (SPR)1477-7819-12-164-e DE-627 ger DE-627 rakwb eng Ajouz, Hana verfasserin aut Secondary bile acids: an underrecognized cause of colon cancer 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Ajouz et al.; licensee BioMed Central Ltd. 2014. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Abstract Bile acids were first proposed as carcinogens in 1939. Since then, accumulated evidence has linked exposure of cells of the gastrointestinal tract to repeated high physiologic levels of bile acids as an important risk factor for gastrointestinal cancers. High exposure to bile acids may occur in a number of settings, but most importantly, is prevalent among individuals who have a high dietary fat intake. A rapid effect on cells of high bile acid exposure is the generation of reactive oxygen species and reactive nitrogen species, disruption of the cell membrane and mitochondria, induction of DNA damage, mutation and apoptosis, and development of reduced apoptosis capability upon chronic exposure. Here, we review the substantial evidence of the mechanism of secondary bile acids and their role in colon cancer. Bile Acid (dpeaa)DE-He213 Cholic Acid (dpeaa)DE-He213 Chenodeoxycholic Acid (dpeaa)DE-He213 Bile Acid Concentration (dpeaa)DE-He213 Secondary Bile Acid (dpeaa)DE-He213 Mukherji, Deborah aut Shamseddine, Ali aut Enthalten in World journal of surgical oncology London : Biomed Central, 2003 12(2014), 1 vom: 24. Mai (DE-627)369082907 (DE-600)2118383-1 1477-7819 nnns volume:12 year:2014 number:1 day:24 month:05 https://dx.doi.org/10.1186/1477-7819-12-164 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2014 1 24 05
allfields_unstemmed	10.1186/1477-7819-12-164 doi (DE-627)SPR028826655 (SPR)1477-7819-12-164-e DE-627 ger DE-627 rakwb eng Ajouz, Hana verfasserin aut Secondary bile acids: an underrecognized cause of colon cancer 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Ajouz et al.; licensee BioMed Central Ltd. 2014. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Abstract Bile acids were first proposed as carcinogens in 1939. Since then, accumulated evidence has linked exposure of cells of the gastrointestinal tract to repeated high physiologic levels of bile acids as an important risk factor for gastrointestinal cancers. High exposure to bile acids may occur in a number of settings, but most importantly, is prevalent among individuals who have a high dietary fat intake. A rapid effect on cells of high bile acid exposure is the generation of reactive oxygen species and reactive nitrogen species, disruption of the cell membrane and mitochondria, induction of DNA damage, mutation and apoptosis, and development of reduced apoptosis capability upon chronic exposure. Here, we review the substantial evidence of the mechanism of secondary bile acids and their role in colon cancer. Bile Acid (dpeaa)DE-He213 Cholic Acid (dpeaa)DE-He213 Chenodeoxycholic Acid (dpeaa)DE-He213 Bile Acid Concentration (dpeaa)DE-He213 Secondary Bile Acid (dpeaa)DE-He213 Mukherji, Deborah aut Shamseddine, Ali aut Enthalten in World journal of surgical oncology London : Biomed Central, 2003 12(2014), 1 vom: 24. Mai (DE-627)369082907 (DE-600)2118383-1 1477-7819 nnns volume:12 year:2014 number:1 day:24 month:05 https://dx.doi.org/10.1186/1477-7819-12-164 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2014 1 24 05
allfieldsGer	10.1186/1477-7819-12-164 doi (DE-627)SPR028826655 (SPR)1477-7819-12-164-e DE-627 ger DE-627 rakwb eng Ajouz, Hana verfasserin aut Secondary bile acids: an underrecognized cause of colon cancer 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Ajouz et al.; licensee BioMed Central Ltd. 2014. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Abstract Bile acids were first proposed as carcinogens in 1939. Since then, accumulated evidence has linked exposure of cells of the gastrointestinal tract to repeated high physiologic levels of bile acids as an important risk factor for gastrointestinal cancers. High exposure to bile acids may occur in a number of settings, but most importantly, is prevalent among individuals who have a high dietary fat intake. A rapid effect on cells of high bile acid exposure is the generation of reactive oxygen species and reactive nitrogen species, disruption of the cell membrane and mitochondria, induction of DNA damage, mutation and apoptosis, and development of reduced apoptosis capability upon chronic exposure. Here, we review the substantial evidence of the mechanism of secondary bile acids and their role in colon cancer. Bile Acid (dpeaa)DE-He213 Cholic Acid (dpeaa)DE-He213 Chenodeoxycholic Acid (dpeaa)DE-He213 Bile Acid Concentration (dpeaa)DE-He213 Secondary Bile Acid (dpeaa)DE-He213 Mukherji, Deborah aut Shamseddine, Ali aut Enthalten in World journal of surgical oncology London : Biomed Central, 2003 12(2014), 1 vom: 24. Mai (DE-627)369082907 (DE-600)2118383-1 1477-7819 nnns volume:12 year:2014 number:1 day:24 month:05 https://dx.doi.org/10.1186/1477-7819-12-164 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2014 1 24 05
allfieldsSound	10.1186/1477-7819-12-164 doi (DE-627)SPR028826655 (SPR)1477-7819-12-164-e DE-627 ger DE-627 rakwb eng Ajouz, Hana verfasserin aut Secondary bile acids: an underrecognized cause of colon cancer 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Ajouz et al.; licensee BioMed Central Ltd. 2014. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Abstract Bile acids were first proposed as carcinogens in 1939. Since then, accumulated evidence has linked exposure of cells of the gastrointestinal tract to repeated high physiologic levels of bile acids as an important risk factor for gastrointestinal cancers. High exposure to bile acids may occur in a number of settings, but most importantly, is prevalent among individuals who have a high dietary fat intake. A rapid effect on cells of high bile acid exposure is the generation of reactive oxygen species and reactive nitrogen species, disruption of the cell membrane and mitochondria, induction of DNA damage, mutation and apoptosis, and development of reduced apoptosis capability upon chronic exposure. Here, we review the substantial evidence of the mechanism of secondary bile acids and their role in colon cancer. Bile Acid (dpeaa)DE-He213 Cholic Acid (dpeaa)DE-He213 Chenodeoxycholic Acid (dpeaa)DE-He213 Bile Acid Concentration (dpeaa)DE-He213 Secondary Bile Acid (dpeaa)DE-He213 Mukherji, Deborah aut Shamseddine, Ali aut Enthalten in World journal of surgical oncology London : Biomed Central, 2003 12(2014), 1 vom: 24. Mai (DE-627)369082907 (DE-600)2118383-1 1477-7819 nnns volume:12 year:2014 number:1 day:24 month:05 https://dx.doi.org/10.1186/1477-7819-12-164 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2014 1 24 05
language	English
source	Enthalten in World journal of surgical oncology 12(2014), 1 vom: 24. Mai volume:12 year:2014 number:1 day:24 month:05
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topic_facet	Bile Acid Cholic Acid Chenodeoxycholic Acid Bile Acid Concentration Secondary Bile Acid
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authorswithroles_txt_mv	Ajouz, Hana @@aut@@ Mukherji, Deborah @@aut@@ Shamseddine, Ali @@aut@@
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topic_title	Secondary bile acids: an underrecognized cause of colon cancer Bile Acid (dpeaa)DE-He213 Cholic Acid (dpeaa)DE-He213 Chenodeoxycholic Acid (dpeaa)DE-He213 Bile Acid Concentration (dpeaa)DE-He213 Secondary Bile Acid (dpeaa)DE-He213
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topic_unstemmed	misc Bile Acid misc Cholic Acid misc Chenodeoxycholic Acid misc Bile Acid Concentration misc Secondary Bile Acid
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title_sort	secondary bile acids: an underrecognized cause of colon cancer
title_auth	Secondary bile acids: an underrecognized cause of colon cancer
abstract	Abstract Bile acids were first proposed as carcinogens in 1939. Since then, accumulated evidence has linked exposure of cells of the gastrointestinal tract to repeated high physiologic levels of bile acids as an important risk factor for gastrointestinal cancers. High exposure to bile acids may occur in a number of settings, but most importantly, is prevalent among individuals who have a high dietary fat intake. A rapid effect on cells of high bile acid exposure is the generation of reactive oxygen species and reactive nitrogen species, disruption of the cell membrane and mitochondria, induction of DNA damage, mutation and apoptosis, and development of reduced apoptosis capability upon chronic exposure. Here, we review the substantial evidence of the mechanism of secondary bile acids and their role in colon cancer. © Ajouz et al.; licensee BioMed Central Ltd. 2014. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (
abstractGer	Abstract Bile acids were first proposed as carcinogens in 1939. Since then, accumulated evidence has linked exposure of cells of the gastrointestinal tract to repeated high physiologic levels of bile acids as an important risk factor for gastrointestinal cancers. High exposure to bile acids may occur in a number of settings, but most importantly, is prevalent among individuals who have a high dietary fat intake. A rapid effect on cells of high bile acid exposure is the generation of reactive oxygen species and reactive nitrogen species, disruption of the cell membrane and mitochondria, induction of DNA damage, mutation and apoptosis, and development of reduced apoptosis capability upon chronic exposure. Here, we review the substantial evidence of the mechanism of secondary bile acids and their role in colon cancer. © Ajouz et al.; licensee BioMed Central Ltd. 2014. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (
abstract_unstemmed	Abstract Bile acids were first proposed as carcinogens in 1939. Since then, accumulated evidence has linked exposure of cells of the gastrointestinal tract to repeated high physiologic levels of bile acids as an important risk factor for gastrointestinal cancers. High exposure to bile acids may occur in a number of settings, but most importantly, is prevalent among individuals who have a high dietary fat intake. A rapid effect on cells of high bile acid exposure is the generation of reactive oxygen species and reactive nitrogen species, disruption of the cell membrane and mitochondria, induction of DNA damage, mutation and apoptosis, and development of reduced apoptosis capability upon chronic exposure. Here, we review the substantial evidence of the mechanism of secondary bile acids and their role in colon cancer. © Ajouz et al.; licensee BioMed Central Ltd. 2014. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (
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title_short	Secondary bile acids: an underrecognized cause of colon cancer
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