Comparison of the significance of three histopathological thresholds of malignancy in experimental colorectal tumours
The purpose of this experiment was to study sequential histogenesis of colonic epithelial tumours in the dimethylhydrazine (DMH) induced rat colon cancer model. Seventy outbred female Wistar rats treated with DMH (40 mg/kg, subcutaneously weekly for five weeks) were killed and autopsied in batches o...
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| Veröffentlicht in: | Gut 1989-06, Vol.30 (6), p.845-853 |
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| creator | Rowlatt, C Cruse, J P Barton, T Sadrudin, A A Lewin, M R |
| description | The purpose of this experiment was to study sequential histogenesis of colonic epithelial tumours in the dimethylhydrazine (DMH) induced rat colon cancer model. Seventy outbred female Wistar rats treated with DMH (40 mg/kg, subcutaneously weekly for five weeks) were killed and autopsied in batches of 10 every five weeks from the 10th to 40th weeks from first treatment. The resulting 378 colonic lesions were assigned to benign or malignant categories using each of three standard histopathological thresholds of malignancy: alpha, the transition from dysplasia to intraepithelial carcinoma; beta, invasion through the crypt basement membrane; and gamma, invasion through the muscularis mucosae. These comprised 79 'benign' and 299 'malignant' or 273 'benign' and 141 'malignant' lesions depending on the threshold (alpha or gamma) assigned (p less than 0.001). Decreasing ratios of pre-threshold to post-threshold lesions between 15 and 40 weeks (alpha, 2.0 to 0.051; beta, 3.5 to 0.57; gamma, 8.0 to 0.87) provide some support for an 'adenoma-carcinoma' progression for each. Comparison of time-dependent prevalence curves confirms that the alpha threshold (cyto-architecture) is qualitatively different from the beta and gamma thresholds (invasion), showing that the adenoma-carcinoma and de novo hypotheses need not be mutually exclusive. The time-dependent prevalence data support de novo origin of some carcinomas, as well as at least two other modes of accrual for neoplastic lesions. |
| doi_str_mv | 10.1136/gut.30.6.845 |
| format | Article |
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Seventy outbred female Wistar rats treated with DMH (40 mg/kg, subcutaneously weekly for five weeks) were killed and autopsied in batches of 10 every five weeks from the 10th to 40th weeks from first treatment. The resulting 378 colonic lesions were assigned to benign or malignant categories using each of three standard histopathological thresholds of malignancy: alpha, the transition from dysplasia to intraepithelial carcinoma; beta, invasion through the crypt basement membrane; and gamma, invasion through the muscularis mucosae. These comprised 79 'benign' and 299 'malignant' or 273 'benign' and 141 'malignant' lesions depending on the threshold (alpha or gamma) assigned (p less than 0.001). Decreasing ratios of pre-threshold to post-threshold lesions between 15 and 40 weeks (alpha, 2.0 to 0.051; beta, 3.5 to 0.57; gamma, 8.0 to 0.87) provide some support for an 'adenoma-carcinoma' progression for each. Comparison of time-dependent prevalence curves confirms that the alpha threshold (cyto-architecture) is qualitatively different from the beta and gamma thresholds (invasion), showing that the adenoma-carcinoma and de novo hypotheses need not be mutually exclusive. The time-dependent prevalence data support de novo origin of some carcinomas, as well as at least two other modes of accrual for neoplastic lesions.</description><identifier>ISSN: 0017-5749</identifier><identifier>EISSN: 1468-3288</identifier><identifier>EISSN: 1458-3288</identifier><identifier>DOI: 10.1136/gut.30.6.845</identifier><identifier>PMID: 2753408</identifier><identifier>CODEN: GUTTAK</identifier><language>eng</language><publisher>London: BMJ Publishing Group Ltd and British Society of Gastroenterology</publisher><subject>1,2-Dimethylhydrazine ; Adenoma - pathology ; Animal tumors. Experimental tumors ; Animals ; Biological and medical sciences ; Carcinogens ; Carcinoma in Situ - pathology ; Colonic Neoplasms - chemically induced ; Colonic Neoplasms - pathology ; Dimethylhydrazines ; Experimental digestive system and abdominal tumors ; Female ; Intestinal Mucosa - pathology ; Medical sciences ; Neoplasm Invasiveness ; Rats ; Rectal Neoplasms - chemically induced ; Rectal Neoplasms - pathology ; Tumors</subject><ispartof>Gut, 1989-06, Vol.30 (6), p.845-853</ispartof><rights>1989 INIST-CNRS</rights><rights>Copyright BMJ Publishing Group LTD Jun 1989</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b4215-294bf88d977ef18c25e1d6e2e3d81ce4f3b3e2e2ddcbd634527ef7eecb56f9dc3</citedby><cites>FETCH-LOGICAL-b4215-294bf88d977ef18c25e1d6e2e3d81ce4f3b3e2e2ddcbd634527ef7eecb56f9dc3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1434141/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1434141/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27923,27924,53790,53792</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=7269628$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/2753408$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rowlatt, C</creatorcontrib><creatorcontrib>Cruse, J P</creatorcontrib><creatorcontrib>Barton, T</creatorcontrib><creatorcontrib>Sadrudin, A A</creatorcontrib><creatorcontrib>Lewin, M R</creatorcontrib><title>Comparison of the significance of three histopathological thresholds of malignancy in experimental colorectal tumours</title><title>Gut</title><addtitle>Gut</addtitle><description>The purpose of this experiment was to study sequential histogenesis of colonic epithelial tumours in the dimethylhydrazine (DMH) induced rat colon cancer model. Seventy outbred female Wistar rats treated with DMH (40 mg/kg, subcutaneously weekly for five weeks) were killed and autopsied in batches of 10 every five weeks from the 10th to 40th weeks from first treatment. The resulting 378 colonic lesions were assigned to benign or malignant categories using each of three standard histopathological thresholds of malignancy: alpha, the transition from dysplasia to intraepithelial carcinoma; beta, invasion through the crypt basement membrane; and gamma, invasion through the muscularis mucosae. These comprised 79 'benign' and 299 'malignant' or 273 'benign' and 141 'malignant' lesions depending on the threshold (alpha or gamma) assigned (p less than 0.001). Decreasing ratios of pre-threshold to post-threshold lesions between 15 and 40 weeks (alpha, 2.0 to 0.051; beta, 3.5 to 0.57; gamma, 8.0 to 0.87) provide some support for an 'adenoma-carcinoma' progression for each. Comparison of time-dependent prevalence curves confirms that the alpha threshold (cyto-architecture) is qualitatively different from the beta and gamma thresholds (invasion), showing that the adenoma-carcinoma and de novo hypotheses need not be mutually exclusive. The time-dependent prevalence data support de novo origin of some carcinomas, as well as at least two other modes of accrual for neoplastic lesions.</description><subject>1,2-Dimethylhydrazine</subject><subject>Adenoma - pathology</subject><subject>Animal tumors. Experimental tumors</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Carcinogens</subject><subject>Carcinoma in Situ - pathology</subject><subject>Colonic Neoplasms - chemically induced</subject><subject>Colonic Neoplasms - pathology</subject><subject>Dimethylhydrazines</subject><subject>Experimental digestive system and abdominal tumors</subject><subject>Female</subject><subject>Intestinal Mucosa - pathology</subject><subject>Medical sciences</subject><subject>Neoplasm Invasiveness</subject><subject>Rats</subject><subject>Rectal Neoplasms - chemically induced</subject><subject>Rectal Neoplasms - pathology</subject><subject>Tumors</subject><issn>0017-5749</issn><issn>1468-3288</issn><issn>1458-3288</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1989</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kc2P0zAQxS0EWroLN65IkUDaCyn-iu1cVkIVX6ICIZZF4mI5zqRNaeJgJ2j3v2dKqgounGzP-834aR4hTxhdMibUy800LgVdqqWRxT2yYFKZXHBj7pMFpUznhZblQ3Ke0o5SakzJzsgZ14WQ1CzItArd4GKbQp-FJhu3kKV207dN613vYa5FgGzbpjEMbtyGfdiguP9TT_is04Hq3B77sOcua_sMbgeIbQf9iKDHlgj-cB2nLkwxPSIPGrdP8Ph4XpCvb15fr97l609v369erfNKclbkvJRVY0xdag0NM54XwGoFHERtmAfZiErgi9e1r2olZMGR0wC-KlRT1l5ckKt57jBVHdQe_US3twNac_HOBtfaf5W-3dpN-GWZFJJJhgOeHQfE8HOCNNod-u_Rs2VaU6q4EgVSL2bKx5BShOb0A6P2kJHFjKygVlnMCPGnf7s6wcdQUH9-1F3CRTcRt9qmE6a5KhU_YPmMYTJwe5Jd_GGVFrqwH29W9sv3zzfrD9-YvUb-cuarbvd_g78Btda67w</recordid><startdate>19890601</startdate><enddate>19890601</enddate><creator>Rowlatt, C</creator><creator>Cruse, J P</creator><creator>Barton, T</creator><creator>Sadrudin, A A</creator><creator>Lewin, M R</creator><general>BMJ Publishing Group Ltd and British Society of Gastroenterology</general><general>BMJ</general><general>BMJ Publishing Group LTD</general><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>BTHHO</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>5PM</scope></search><sort><creationdate>19890601</creationdate><title>Comparison of the significance of three histopathological thresholds of malignancy in experimental colorectal tumours</title><author>Rowlatt, C ; Cruse, J P ; Barton, T ; Sadrudin, A A ; Lewin, M R</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b4215-294bf88d977ef18c25e1d6e2e3d81ce4f3b3e2e2ddcbd634527ef7eecb56f9dc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1989</creationdate><topic>1,2-Dimethylhydrazine</topic><topic>Adenoma - pathology</topic><topic>Animal tumors. Experimental tumors</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Carcinogens</topic><topic>Carcinoma in Situ - pathology</topic><topic>Colonic Neoplasms - chemically induced</topic><topic>Colonic Neoplasms - pathology</topic><topic>Dimethylhydrazines</topic><topic>Experimental digestive system and abdominal tumors</topic><topic>Female</topic><topic>Intestinal Mucosa - pathology</topic><topic>Medical sciences</topic><topic>Neoplasm Invasiveness</topic><topic>Rats</topic><topic>Rectal Neoplasms - chemically induced</topic><topic>Rectal Neoplasms - pathology</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rowlatt, C</creatorcontrib><creatorcontrib>Cruse, J P</creatorcontrib><creatorcontrib>Barton, T</creatorcontrib><creatorcontrib>Sadrudin, A A</creatorcontrib><creatorcontrib>Lewin, M R</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>BMJ Journals</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Gut</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Rowlatt, C</au><au>Cruse, J P</au><au>Barton, T</au><au>Sadrudin, A A</au><au>Lewin, M R</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Comparison of the significance of three histopathological thresholds of malignancy in experimental colorectal tumours</atitle><jtitle>Gut</jtitle><addtitle>Gut</addtitle><date>1989-06-01</date><risdate>1989</risdate><volume>30</volume><issue>6</issue><spage>845</spage><epage>853</epage><pages>845-853</pages><issn>0017-5749</issn><eissn>1468-3288</eissn><eissn>1458-3288</eissn><coden>GUTTAK</coden><abstract>The purpose of this experiment was to study sequential histogenesis of colonic epithelial tumours in the dimethylhydrazine (DMH) induced rat colon cancer model. Seventy outbred female Wistar rats treated with DMH (40 mg/kg, subcutaneously weekly for five weeks) were killed and autopsied in batches of 10 every five weeks from the 10th to 40th weeks from first treatment. The resulting 378 colonic lesions were assigned to benign or malignant categories using each of three standard histopathological thresholds of malignancy: alpha, the transition from dysplasia to intraepithelial carcinoma; beta, invasion through the crypt basement membrane; and gamma, invasion through the muscularis mucosae. These comprised 79 'benign' and 299 'malignant' or 273 'benign' and 141 'malignant' lesions depending on the threshold (alpha or gamma) assigned (p less than 0.001). Decreasing ratios of pre-threshold to post-threshold lesions between 15 and 40 weeks (alpha, 2.0 to 0.051; beta, 3.5 to 0.57; gamma, 8.0 to 0.87) provide some support for an 'adenoma-carcinoma' progression for each. Comparison of time-dependent prevalence curves confirms that the alpha threshold (cyto-architecture) is qualitatively different from the beta and gamma thresholds (invasion), showing that the adenoma-carcinoma and de novo hypotheses need not be mutually exclusive. The time-dependent prevalence data support de novo origin of some carcinomas, as well as at least two other modes of accrual for neoplastic lesions.</abstract><cop>London</cop><pub>BMJ Publishing Group Ltd and British Society of Gastroenterology</pub><pmid>2753408</pmid><doi>10.1136/gut.30.6.845</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Gut, 1989-06, Vol.30 (6), p.845-853 |
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| subjects | 1,2-Dimethylhydrazine Adenoma - pathology Animal tumors. Experimental tumors Animals Biological and medical sciences Carcinogens Carcinoma in Situ - pathology Colonic Neoplasms - chemically induced Colonic Neoplasms - pathology Dimethylhydrazines Experimental digestive system and abdominal tumors Female Intestinal Mucosa - pathology Medical sciences Neoplasm Invasiveness Rats Rectal Neoplasms - chemically induced Rectal Neoplasms - pathology Tumors |
| title | Comparison of the significance of three histopathological thresholds of malignancy in experimental colorectal tumours |
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