A bile acid-induced apoptosis assay for colon cancer risk and associated quality control studies
Bile acids are important in the etiology of colorectal cancer. Bile acids induce apoptosis in colonic goblet cells at concentrations comparable to those found in fecal water after high-fat meals. Preliminary evidence indicated that cells of the normal-appearing (nontumorous) portion of the colon epi...
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| Veröffentlicht in: | Cancer research (Chicago, Ill.) Ill.), 1999-05, Vol.59 (10), p.2353-2357 |
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| creator | BERNSTEIN, C BERNSTEIN, H PAYNE, C GAREWAL, H DINNING, P JABI, R SAMPLINER, R. E MCCUSKEY, M. K PANDA, M ROE, D. J L'HEUREUX, L |
| description | Bile acids are important in the etiology of colorectal cancer. Bile acids induce apoptosis in colonic goblet cells at concentrations comparable to those found in fecal water after high-fat meals. Preliminary evidence indicated that cells of the normal-appearing (nontumorous) portion of the colon epithelium of colon cancer patients are more resistant to bile salt-induced apoptosis than are cells from normal individuals. In the present study, 68 patients were examined, and biopsies were taken at 20 cm from the anal verge, cecum, and descending colon. The patients included 17 individuals with a history of colorectal cancer, 37 individuals with adenomas, and 14 individuals who were neoplasia free. The mean bile salt-induced apoptotic index among normal individuals was 57.6 +/- 3.47 (SE), which differed significantly (P < 0.05) from the mean value of 36.41 +/- 3.12 in individuals with a history of colon cancer. The correlation between independent observers was 0.89 (P < 0.001), indicating good interobserver reliability. Components of variance comparing interindividual versus intraindividual sources of variation suggested that site-to-site variability, both between regions of the colon and for adjacent biopsies, was larger than the interpatient variability for individuals with a history of neoplasia. Therefore, there was "patchiness" of the susceptibility of regions of the colon to bile acid-induced apoptosis in individuals with a history of neoplasia (a patchy field effect). There was no obvious correlation of low-apoptotic index regions with regions in which previous neoplasias had been found and removed. On the other hand, for normal, i.e., neoplasia-free, individuals, there was relatively less intraindividual variation compared to interindividual variation. Our assay shows an association between resistance to bile acid-induced apoptosis, measured at 20 cm from the anal verge, and colon cancer risk. Thus, this assay may prove useful as a biomarker of colon cancer risk. |
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E ; MCCUSKEY, M. K ; PANDA, M ; ROE, D. J ; L'HEUREUX, L</creator><creatorcontrib>BERNSTEIN, C ; BERNSTEIN, H ; PAYNE, C ; GAREWAL, H ; DINNING, P ; JABI, R ; SAMPLINER, R. E ; MCCUSKEY, M. K ; PANDA, M ; ROE, D. J ; L'HEUREUX, L</creatorcontrib><description>Bile acids are important in the etiology of colorectal cancer. Bile acids induce apoptosis in colonic goblet cells at concentrations comparable to those found in fecal water after high-fat meals. Preliminary evidence indicated that cells of the normal-appearing (nontumorous) portion of the colon epithelium of colon cancer patients are more resistant to bile salt-induced apoptosis than are cells from normal individuals. In the present study, 68 patients were examined, and biopsies were taken at 20 cm from the anal verge, cecum, and descending colon. The patients included 17 individuals with a history of colorectal cancer, 37 individuals with adenomas, and 14 individuals who were neoplasia free. The mean bile salt-induced apoptotic index among normal individuals was 57.6 +/- 3.47 (SE), which differed significantly (P < 0.05) from the mean value of 36.41 +/- 3.12 in individuals with a history of colon cancer. The correlation between independent observers was 0.89 (P < 0.001), indicating good interobserver reliability. Components of variance comparing interindividual versus intraindividual sources of variation suggested that site-to-site variability, both between regions of the colon and for adjacent biopsies, was larger than the interpatient variability for individuals with a history of neoplasia. Therefore, there was "patchiness" of the susceptibility of regions of the colon to bile acid-induced apoptosis in individuals with a history of neoplasia (a patchy field effect). There was no obvious correlation of low-apoptotic index regions with regions in which previous neoplasias had been found and removed. On the other hand, for normal, i.e., neoplasia-free, individuals, there was relatively less intraindividual variation compared to interindividual variation. Our assay shows an association between resistance to bile acid-induced apoptosis, measured at 20 cm from the anal verge, and colon cancer risk. Thus, this assay may prove useful as a biomarker of colon cancer risk.</description><identifier>ISSN: 0008-5472</identifier><identifier>EISSN: 1538-7445</identifier><identifier>PMID: 10344743</identifier><identifier>CODEN: CNREA8</identifier><language>eng</language><publisher>Philadelphia, PA: American Association for Cancer Research</publisher><subject>Adenoma - metabolism ; Adenoma - pathology ; Anal Canal - cytology ; Anal Canal - drug effects ; Apoptosis - drug effects ; Bile Acids and Salts - pharmacology ; Bile Acids and Salts - secretion ; Biological and medical sciences ; Biological Assay - methods ; Colon, Sigmoid - cytology ; Colon, Sigmoid - drug effects ; Colonic Neoplasms - epidemiology ; Colonic Neoplasms - etiology ; Colonic Neoplasms - metabolism ; Colonic Neoplasms - pathology ; Colonic Polyps - metabolism ; Colonic Polyps - pathology ; Colorectal Neoplasms - metabolism ; Colorectal Neoplasms - pathology ; Deoxycholic Acid - analysis ; Deoxycholic Acid - pharmacology ; Dietary Fats - adverse effects ; Disease Susceptibility ; Drug Resistance ; Feces - chemistry ; Gastroenterology. Liver. Pancreas. Abdomen ; Humans ; Intestinal Mucosa - cytology ; Intestinal Mucosa - drug effects ; Medical sciences ; Observer Variation ; Quality Control ; Rectum - cytology ; Rectum - drug effects ; Risk ; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus ; Tumors</subject><ispartof>Cancer research (Chicago, Ill.), 1999-05, Vol.59 (10), p.2353-2357</ispartof><rights>1999 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1785827$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10344743$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>BERNSTEIN, C</creatorcontrib><creatorcontrib>BERNSTEIN, H</creatorcontrib><creatorcontrib>PAYNE, C</creatorcontrib><creatorcontrib>GAREWAL, H</creatorcontrib><creatorcontrib>DINNING, P</creatorcontrib><creatorcontrib>JABI, R</creatorcontrib><creatorcontrib>SAMPLINER, R. E</creatorcontrib><creatorcontrib>MCCUSKEY, M. K</creatorcontrib><creatorcontrib>PANDA, M</creatorcontrib><creatorcontrib>ROE, D. J</creatorcontrib><creatorcontrib>L'HEUREUX, L</creatorcontrib><title>A bile acid-induced apoptosis assay for colon cancer risk and associated quality control studies</title><title>Cancer research (Chicago, Ill.)</title><addtitle>Cancer Res</addtitle><description>Bile acids are important in the etiology of colorectal cancer. Bile acids induce apoptosis in colonic goblet cells at concentrations comparable to those found in fecal water after high-fat meals. Preliminary evidence indicated that cells of the normal-appearing (nontumorous) portion of the colon epithelium of colon cancer patients are more resistant to bile salt-induced apoptosis than are cells from normal individuals. In the present study, 68 patients were examined, and biopsies were taken at 20 cm from the anal verge, cecum, and descending colon. The patients included 17 individuals with a history of colorectal cancer, 37 individuals with adenomas, and 14 individuals who were neoplasia free. The mean bile salt-induced apoptotic index among normal individuals was 57.6 +/- 3.47 (SE), which differed significantly (P < 0.05) from the mean value of 36.41 +/- 3.12 in individuals with a history of colon cancer. The correlation between independent observers was 0.89 (P < 0.001), indicating good interobserver reliability. Components of variance comparing interindividual versus intraindividual sources of variation suggested that site-to-site variability, both between regions of the colon and for adjacent biopsies, was larger than the interpatient variability for individuals with a history of neoplasia. Therefore, there was "patchiness" of the susceptibility of regions of the colon to bile acid-induced apoptosis in individuals with a history of neoplasia (a patchy field effect). There was no obvious correlation of low-apoptotic index regions with regions in which previous neoplasias had been found and removed. On the other hand, for normal, i.e., neoplasia-free, individuals, there was relatively less intraindividual variation compared to interindividual variation. Our assay shows an association between resistance to bile acid-induced apoptosis, measured at 20 cm from the anal verge, and colon cancer risk. Thus, this assay may prove useful as a biomarker of colon cancer risk.</description><subject>Adenoma - metabolism</subject><subject>Adenoma - pathology</subject><subject>Anal Canal - cytology</subject><subject>Anal Canal - drug effects</subject><subject>Apoptosis - drug effects</subject><subject>Bile Acids and Salts - pharmacology</subject><subject>Bile Acids and Salts - secretion</subject><subject>Biological and medical sciences</subject><subject>Biological Assay - methods</subject><subject>Colon, Sigmoid - cytology</subject><subject>Colon, Sigmoid - drug effects</subject><subject>Colonic Neoplasms - epidemiology</subject><subject>Colonic Neoplasms - etiology</subject><subject>Colonic Neoplasms - metabolism</subject><subject>Colonic Neoplasms - pathology</subject><subject>Colonic Polyps - metabolism</subject><subject>Colonic Polyps - pathology</subject><subject>Colorectal Neoplasms - metabolism</subject><subject>Colorectal Neoplasms - pathology</subject><subject>Deoxycholic Acid - analysis</subject><subject>Deoxycholic Acid - pharmacology</subject><subject>Dietary Fats - adverse effects</subject><subject>Disease Susceptibility</subject><subject>Drug Resistance</subject><subject>Feces - chemistry</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Humans</subject><subject>Intestinal Mucosa - cytology</subject><subject>Intestinal Mucosa - drug effects</subject><subject>Medical sciences</subject><subject>Observer Variation</subject><subject>Quality Control</subject><subject>Rectum - cytology</subject><subject>Rectum - drug effects</subject><subject>Risk</subject><subject>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</subject><subject>Tumors</subject><issn>0008-5472</issn><issn>1538-7445</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpF0EtPwzAMAOAIgdgY_AWUA-JWKc2jyY4T4iVN4gLn4iapCGRNF7eH_XuCGOISK_Jny_YJWdZKmEpLqU7JkjFmKiU1X5ALxM_yVTVT52RRMyGllmJJ3je0C9FTsMFVYXCz9Y7CmMYpYUAKiHCgfcrUppgGamGwPtMc8IvC4H7yyQaYStF-hhimQ4HDlFOkOM0ueLwkZz1E9FfHuCJvD_evd0_V9uXx-W6zrT64ZlOlBGgP0BvWQBmtXptaChBOcAaed0Iy5xqjaieN7nnDbV9eJZpOcANOa7Eit799x5z2s8ep3QW0PkYYfJqxbdba1IqZAq-PcO523rVjDjvIh_bvJgXcHAGghdjnsnPAf6eNMlyLb9H8a00</recordid><startdate>19990515</startdate><enddate>19990515</enddate><creator>BERNSTEIN, C</creator><creator>BERNSTEIN, H</creator><creator>PAYNE, C</creator><creator>GAREWAL, H</creator><creator>DINNING, P</creator><creator>JABI, R</creator><creator>SAMPLINER, R. E</creator><creator>MCCUSKEY, M. K</creator><creator>PANDA, M</creator><creator>ROE, D. J</creator><creator>L'HEUREUX, L</creator><general>American Association for Cancer Research</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>19990515</creationdate><title>A bile acid-induced apoptosis assay for colon cancer risk and associated quality control studies</title><author>BERNSTEIN, C ; BERNSTEIN, H ; PAYNE, C ; GAREWAL, H ; DINNING, P ; JABI, R ; SAMPLINER, R. E ; MCCUSKEY, M. K ; PANDA, M ; ROE, D. J ; L'HEUREUX, L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-h270t-53a7eaaf806a447198143a3d320ae2b340dd6851d487f262cff26536b328ad773</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Adenoma - metabolism</topic><topic>Adenoma - pathology</topic><topic>Anal Canal - cytology</topic><topic>Anal Canal - drug effects</topic><topic>Apoptosis - drug effects</topic><topic>Bile Acids and Salts - pharmacology</topic><topic>Bile Acids and Salts - secretion</topic><topic>Biological and medical sciences</topic><topic>Biological Assay - methods</topic><topic>Colon, Sigmoid - cytology</topic><topic>Colon, Sigmoid - drug effects</topic><topic>Colonic Neoplasms - epidemiology</topic><topic>Colonic Neoplasms - etiology</topic><topic>Colonic Neoplasms - metabolism</topic><topic>Colonic Neoplasms - pathology</topic><topic>Colonic Polyps - metabolism</topic><topic>Colonic Polyps - pathology</topic><topic>Colorectal Neoplasms - metabolism</topic><topic>Colorectal Neoplasms - pathology</topic><topic>Deoxycholic Acid - analysis</topic><topic>Deoxycholic Acid - pharmacology</topic><topic>Dietary Fats - adverse effects</topic><topic>Disease Susceptibility</topic><topic>Drug Resistance</topic><topic>Feces - chemistry</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Humans</topic><topic>Intestinal Mucosa - cytology</topic><topic>Intestinal Mucosa - drug effects</topic><topic>Medical sciences</topic><topic>Observer Variation</topic><topic>Quality Control</topic><topic>Rectum - cytology</topic><topic>Rectum - drug effects</topic><topic>Risk</topic><topic>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>BERNSTEIN, C</creatorcontrib><creatorcontrib>BERNSTEIN, H</creatorcontrib><creatorcontrib>PAYNE, C</creatorcontrib><creatorcontrib>GAREWAL, H</creatorcontrib><creatorcontrib>DINNING, P</creatorcontrib><creatorcontrib>JABI, R</creatorcontrib><creatorcontrib>SAMPLINER, R. E</creatorcontrib><creatorcontrib>MCCUSKEY, M. K</creatorcontrib><creatorcontrib>PANDA, M</creatorcontrib><creatorcontrib>ROE, D. J</creatorcontrib><creatorcontrib>L'HEUREUX, L</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Cancer research (Chicago, Ill.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>BERNSTEIN, C</au><au>BERNSTEIN, H</au><au>PAYNE, C</au><au>GAREWAL, H</au><au>DINNING, P</au><au>JABI, R</au><au>SAMPLINER, R. E</au><au>MCCUSKEY, M. K</au><au>PANDA, M</au><au>ROE, D. J</au><au>L'HEUREUX, L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A bile acid-induced apoptosis assay for colon cancer risk and associated quality control studies</atitle><jtitle>Cancer research (Chicago, Ill.)</jtitle><addtitle>Cancer Res</addtitle><date>1999-05-15</date><risdate>1999</risdate><volume>59</volume><issue>10</issue><spage>2353</spage><epage>2357</epage><pages>2353-2357</pages><issn>0008-5472</issn><eissn>1538-7445</eissn><coden>CNREA8</coden><abstract>Bile acids are important in the etiology of colorectal cancer. Bile acids induce apoptosis in colonic goblet cells at concentrations comparable to those found in fecal water after high-fat meals. Preliminary evidence indicated that cells of the normal-appearing (nontumorous) portion of the colon epithelium of colon cancer patients are more resistant to bile salt-induced apoptosis than are cells from normal individuals. In the present study, 68 patients were examined, and biopsies were taken at 20 cm from the anal verge, cecum, and descending colon. The patients included 17 individuals with a history of colorectal cancer, 37 individuals with adenomas, and 14 individuals who were neoplasia free. The mean bile salt-induced apoptotic index among normal individuals was 57.6 +/- 3.47 (SE), which differed significantly (P < 0.05) from the mean value of 36.41 +/- 3.12 in individuals with a history of colon cancer. The correlation between independent observers was 0.89 (P < 0.001), indicating good interobserver reliability. Components of variance comparing interindividual versus intraindividual sources of variation suggested that site-to-site variability, both between regions of the colon and for adjacent biopsies, was larger than the interpatient variability for individuals with a history of neoplasia. Therefore, there was "patchiness" of the susceptibility of regions of the colon to bile acid-induced apoptosis in individuals with a history of neoplasia (a patchy field effect). There was no obvious correlation of low-apoptotic index regions with regions in which previous neoplasias had been found and removed. On the other hand, for normal, i.e., neoplasia-free, individuals, there was relatively less intraindividual variation compared to interindividual variation. Our assay shows an association between resistance to bile acid-induced apoptosis, measured at 20 cm from the anal verge, and colon cancer risk. Thus, this assay may prove useful as a biomarker of colon cancer risk.</abstract><cop>Philadelphia, PA</cop><pub>American Association for Cancer Research</pub><pmid>10344743</pmid><tpages>5</tpages></addata></record> |
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| subjects | Adenoma - metabolism Adenoma - pathology Anal Canal - cytology Anal Canal - drug effects Apoptosis - drug effects Bile Acids and Salts - pharmacology Bile Acids and Salts - secretion Biological and medical sciences Biological Assay - methods Colon, Sigmoid - cytology Colon, Sigmoid - drug effects Colonic Neoplasms - epidemiology Colonic Neoplasms - etiology Colonic Neoplasms - metabolism Colonic Neoplasms - pathology Colonic Polyps - metabolism Colonic Polyps - pathology Colorectal Neoplasms - metabolism Colorectal Neoplasms - pathology Deoxycholic Acid - analysis Deoxycholic Acid - pharmacology Dietary Fats - adverse effects Disease Susceptibility Drug Resistance Feces - chemistry Gastroenterology. Liver. Pancreas. Abdomen Humans Intestinal Mucosa - cytology Intestinal Mucosa - drug effects Medical sciences Observer Variation Quality Control Rectum - cytology Rectum - drug effects Risk Stomach. Duodenum. Small intestine. Colon. Rectum. Anus Tumors |
| title | A bile acid-induced apoptosis assay for colon cancer risk and associated quality control studies |
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