Failure to detect colonic mucosal hyperproliferation in mutation positive members of a family with hereditary non-polyposis colorectal cancer
Mucosal proliferation was studied in biopsies obtained from the ascending colon from four mutation positive members of a hereditary non-polyposis colorectal cancer family (group I) and compared to subjects with some positive family history of colorectal cancer but lacking the clinical and pathologic...
Ausführliche Beschreibung
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| Autor*in: |
JASS, J.R. [verfasserIn] AJIOKA, Y. [verfasserIn] RADOJKOVIC, M. [verfasserIn] |
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E-Artikel |
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| Erschienen: |
Oxford, U.K. and Cambridge, USA: Blackwell Science Ltd ; 1997 |
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Online-Ressource |
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2003 ; Blackwell Publishing Journal Backfiles 1879-2005 |
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In: Histopathology - Oxford [u.a.] : Wiley-Blackwell, 1977, 30(1997), 3, Seite 0 |
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volume:30 ; year:1997 ; number:3 ; pages:0 |
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| DOI / URN: |
10.1046/j.1365-2559.1997.d01-589.x |
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| 520 | |a Mucosal proliferation was studied in biopsies obtained from the ascending colon from four mutation positive members of a hereditary non-polyposis colorectal cancer family (group I) and compared to subjects with some positive family history of colorectal cancer but lacking the clinical and pathological features of hereditary non-polyposis colorectal cancer (group II). Labelling indices were derived through immunohistochemical staining of the cell cycle associated nuclear proteins proliferating cell nuclear antigen (PCNA) and Ki–67. Only perfectly longitudinally sectioned crypts were assessed and good intra- and interobserver reproducibility was demonstrated. The labelling indices and proliferative compartment locations were similar in both groups. The mean Ki-67 derived labelling indices (group I 18.0% and group II 17.5%) were similar to values obtained for normal subjects in other studies. PCNA derived labelling indices (group I 58.5% and group II 57.0%) were high, but probably reflect optimization of staining through methacarn fixation. The negative findings do not fit with most published data but critical appraisal of the literature indicates that they are likely to be correct. | ||
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10.1046/j.1365-2559.1997.d01-589.x doi (DE-627)NLEJ242777147 DE-627 ger DE-627 rakwb JASS, J.R. verfasserin aut Failure to detect colonic mucosal hyperproliferation in mutation positive members of a family with hereditary non-polyposis colorectal cancer Oxford, U.K. and Cambridge, USA Blackwell Science Ltd 1997 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Mucosal proliferation was studied in biopsies obtained from the ascending colon from four mutation positive members of a hereditary non-polyposis colorectal cancer family (group I) and compared to subjects with some positive family history of colorectal cancer but lacking the clinical and pathological features of hereditary non-polyposis colorectal cancer (group II). Labelling indices were derived through immunohistochemical staining of the cell cycle associated nuclear proteins proliferating cell nuclear antigen (PCNA) and Ki–67. Only perfectly longitudinally sectioned crypts were assessed and good intra- and interobserver reproducibility was demonstrated. The labelling indices and proliferative compartment locations were similar in both groups. The mean Ki-67 derived labelling indices (group I 18.0% and group II 17.5%) were similar to values obtained for normal subjects in other studies. PCNA derived labelling indices (group I 58.5% and group II 57.0%) were high, but probably reflect optimization of staining through methacarn fixation. The negative findings do not fit with most published data but critical appraisal of the literature indicates that they are likely to be correct. 2003 Blackwell Publishing Journal Backfiles 1879-2005 |2003|||||||||| colon AJIOKA, Y. verfasserin aut RADOJKOVIC, M. verfasserin aut ALLISON, L.J. oth LANE, M.R. oth In Histopathology Oxford [u.a.] : Wiley-Blackwell, 1977 30(1997), 3, Seite 0 Online-Ressource (DE-627)NLEJ243927045 (DE-600)2006447-0 1365-2559 nnns volume:30 year:1997 number:3 pages:0 http://dx.doi.org/10.1046/j.1365-2559.1997.d01-589.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 30 1997 3 0 |
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10.1046/j.1365-2559.1997.d01-589.x doi (DE-627)NLEJ242777147 DE-627 ger DE-627 rakwb JASS, J.R. verfasserin aut Failure to detect colonic mucosal hyperproliferation in mutation positive members of a family with hereditary non-polyposis colorectal cancer Oxford, U.K. and Cambridge, USA Blackwell Science Ltd 1997 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Mucosal proliferation was studied in biopsies obtained from the ascending colon from four mutation positive members of a hereditary non-polyposis colorectal cancer family (group I) and compared to subjects with some positive family history of colorectal cancer but lacking the clinical and pathological features of hereditary non-polyposis colorectal cancer (group II). Labelling indices were derived through immunohistochemical staining of the cell cycle associated nuclear proteins proliferating cell nuclear antigen (PCNA) and Ki–67. Only perfectly longitudinally sectioned crypts were assessed and good intra- and interobserver reproducibility was demonstrated. The labelling indices and proliferative compartment locations were similar in both groups. The mean Ki-67 derived labelling indices (group I 18.0% and group II 17.5%) were similar to values obtained for normal subjects in other studies. PCNA derived labelling indices (group I 58.5% and group II 57.0%) were high, but probably reflect optimization of staining through methacarn fixation. The negative findings do not fit with most published data but critical appraisal of the literature indicates that they are likely to be correct. 2003 Blackwell Publishing Journal Backfiles 1879-2005 |2003|||||||||| colon AJIOKA, Y. verfasserin aut RADOJKOVIC, M. verfasserin aut ALLISON, L.J. oth LANE, M.R. oth In Histopathology Oxford [u.a.] : Wiley-Blackwell, 1977 30(1997), 3, Seite 0 Online-Ressource (DE-627)NLEJ243927045 (DE-600)2006447-0 1365-2559 nnns volume:30 year:1997 number:3 pages:0 http://dx.doi.org/10.1046/j.1365-2559.1997.d01-589.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 30 1997 3 0 |
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10.1046/j.1365-2559.1997.d01-589.x doi (DE-627)NLEJ242777147 DE-627 ger DE-627 rakwb JASS, J.R. verfasserin aut Failure to detect colonic mucosal hyperproliferation in mutation positive members of a family with hereditary non-polyposis colorectal cancer Oxford, U.K. and Cambridge, USA Blackwell Science Ltd 1997 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Mucosal proliferation was studied in biopsies obtained from the ascending colon from four mutation positive members of a hereditary non-polyposis colorectal cancer family (group I) and compared to subjects with some positive family history of colorectal cancer but lacking the clinical and pathological features of hereditary non-polyposis colorectal cancer (group II). Labelling indices were derived through immunohistochemical staining of the cell cycle associated nuclear proteins proliferating cell nuclear antigen (PCNA) and Ki–67. Only perfectly longitudinally sectioned crypts were assessed and good intra- and interobserver reproducibility was demonstrated. The labelling indices and proliferative compartment locations were similar in both groups. The mean Ki-67 derived labelling indices (group I 18.0% and group II 17.5%) were similar to values obtained for normal subjects in other studies. PCNA derived labelling indices (group I 58.5% and group II 57.0%) were high, but probably reflect optimization of staining through methacarn fixation. The negative findings do not fit with most published data but critical appraisal of the literature indicates that they are likely to be correct. 2003 Blackwell Publishing Journal Backfiles 1879-2005 |2003|||||||||| colon AJIOKA, Y. verfasserin aut RADOJKOVIC, M. verfasserin aut ALLISON, L.J. oth LANE, M.R. oth In Histopathology Oxford [u.a.] : Wiley-Blackwell, 1977 30(1997), 3, Seite 0 Online-Ressource (DE-627)NLEJ243927045 (DE-600)2006447-0 1365-2559 nnns volume:30 year:1997 number:3 pages:0 http://dx.doi.org/10.1046/j.1365-2559.1997.d01-589.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 30 1997 3 0 |
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10.1046/j.1365-2559.1997.d01-589.x doi (DE-627)NLEJ242777147 DE-627 ger DE-627 rakwb JASS, J.R. verfasserin aut Failure to detect colonic mucosal hyperproliferation in mutation positive members of a family with hereditary non-polyposis colorectal cancer Oxford, U.K. and Cambridge, USA Blackwell Science Ltd 1997 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Mucosal proliferation was studied in biopsies obtained from the ascending colon from four mutation positive members of a hereditary non-polyposis colorectal cancer family (group I) and compared to subjects with some positive family history of colorectal cancer but lacking the clinical and pathological features of hereditary non-polyposis colorectal cancer (group II). Labelling indices were derived through immunohistochemical staining of the cell cycle associated nuclear proteins proliferating cell nuclear antigen (PCNA) and Ki–67. Only perfectly longitudinally sectioned crypts were assessed and good intra- and interobserver reproducibility was demonstrated. The labelling indices and proliferative compartment locations were similar in both groups. The mean Ki-67 derived labelling indices (group I 18.0% and group II 17.5%) were similar to values obtained for normal subjects in other studies. PCNA derived labelling indices (group I 58.5% and group II 57.0%) were high, but probably reflect optimization of staining through methacarn fixation. The negative findings do not fit with most published data but critical appraisal of the literature indicates that they are likely to be correct. 2003 Blackwell Publishing Journal Backfiles 1879-2005 |2003|||||||||| colon AJIOKA, Y. verfasserin aut RADOJKOVIC, M. verfasserin aut ALLISON, L.J. oth LANE, M.R. oth In Histopathology Oxford [u.a.] : Wiley-Blackwell, 1977 30(1997), 3, Seite 0 Online-Ressource (DE-627)NLEJ243927045 (DE-600)2006447-0 1365-2559 nnns volume:30 year:1997 number:3 pages:0 http://dx.doi.org/10.1046/j.1365-2559.1997.d01-589.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 30 1997 3 0 |
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10.1046/j.1365-2559.1997.d01-589.x doi (DE-627)NLEJ242777147 DE-627 ger DE-627 rakwb JASS, J.R. verfasserin aut Failure to detect colonic mucosal hyperproliferation in mutation positive members of a family with hereditary non-polyposis colorectal cancer Oxford, U.K. and Cambridge, USA Blackwell Science Ltd 1997 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Mucosal proliferation was studied in biopsies obtained from the ascending colon from four mutation positive members of a hereditary non-polyposis colorectal cancer family (group I) and compared to subjects with some positive family history of colorectal cancer but lacking the clinical and pathological features of hereditary non-polyposis colorectal cancer (group II). Labelling indices were derived through immunohistochemical staining of the cell cycle associated nuclear proteins proliferating cell nuclear antigen (PCNA) and Ki–67. Only perfectly longitudinally sectioned crypts were assessed and good intra- and interobserver reproducibility was demonstrated. The labelling indices and proliferative compartment locations were similar in both groups. The mean Ki-67 derived labelling indices (group I 18.0% and group II 17.5%) were similar to values obtained for normal subjects in other studies. PCNA derived labelling indices (group I 58.5% and group II 57.0%) were high, but probably reflect optimization of staining through methacarn fixation. The negative findings do not fit with most published data but critical appraisal of the literature indicates that they are likely to be correct. 2003 Blackwell Publishing Journal Backfiles 1879-2005 |2003|||||||||| colon AJIOKA, Y. verfasserin aut RADOJKOVIC, M. verfasserin aut ALLISON, L.J. oth LANE, M.R. oth In Histopathology Oxford [u.a.] : Wiley-Blackwell, 1977 30(1997), 3, Seite 0 Online-Ressource (DE-627)NLEJ243927045 (DE-600)2006447-0 1365-2559 nnns volume:30 year:1997 number:3 pages:0 http://dx.doi.org/10.1046/j.1365-2559.1997.d01-589.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 30 1997 3 0 |
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Failure to detect colonic mucosal hyperproliferation in mutation positive members of a family with hereditary non-polyposis colorectal cancer |
| abstract |
Mucosal proliferation was studied in biopsies obtained from the ascending colon from four mutation positive members of a hereditary non-polyposis colorectal cancer family (group I) and compared to subjects with some positive family history of colorectal cancer but lacking the clinical and pathological features of hereditary non-polyposis colorectal cancer (group II). Labelling indices were derived through immunohistochemical staining of the cell cycle associated nuclear proteins proliferating cell nuclear antigen (PCNA) and Ki–67. Only perfectly longitudinally sectioned crypts were assessed and good intra- and interobserver reproducibility was demonstrated. The labelling indices and proliferative compartment locations were similar in both groups. The mean Ki-67 derived labelling indices (group I 18.0% and group II 17.5%) were similar to values obtained for normal subjects in other studies. PCNA derived labelling indices (group I 58.5% and group II 57.0%) were high, but probably reflect optimization of staining through methacarn fixation. The negative findings do not fit with most published data but critical appraisal of the literature indicates that they are likely to be correct. |
| abstractGer |
Mucosal proliferation was studied in biopsies obtained from the ascending colon from four mutation positive members of a hereditary non-polyposis colorectal cancer family (group I) and compared to subjects with some positive family history of colorectal cancer but lacking the clinical and pathological features of hereditary non-polyposis colorectal cancer (group II). Labelling indices were derived through immunohistochemical staining of the cell cycle associated nuclear proteins proliferating cell nuclear antigen (PCNA) and Ki–67. Only perfectly longitudinally sectioned crypts were assessed and good intra- and interobserver reproducibility was demonstrated. The labelling indices and proliferative compartment locations were similar in both groups. The mean Ki-67 derived labelling indices (group I 18.0% and group II 17.5%) were similar to values obtained for normal subjects in other studies. PCNA derived labelling indices (group I 58.5% and group II 57.0%) were high, but probably reflect optimization of staining through methacarn fixation. The negative findings do not fit with most published data but critical appraisal of the literature indicates that they are likely to be correct. |
| abstract_unstemmed |
Mucosal proliferation was studied in biopsies obtained from the ascending colon from four mutation positive members of a hereditary non-polyposis colorectal cancer family (group I) and compared to subjects with some positive family history of colorectal cancer but lacking the clinical and pathological features of hereditary non-polyposis colorectal cancer (group II). Labelling indices were derived through immunohistochemical staining of the cell cycle associated nuclear proteins proliferating cell nuclear antigen (PCNA) and Ki–67. Only perfectly longitudinally sectioned crypts were assessed and good intra- and interobserver reproducibility was demonstrated. The labelling indices and proliferative compartment locations were similar in both groups. The mean Ki-67 derived labelling indices (group I 18.0% and group II 17.5%) were similar to values obtained for normal subjects in other studies. PCNA derived labelling indices (group I 58.5% and group II 57.0%) were high, but probably reflect optimization of staining through methacarn fixation. The negative findings do not fit with most published data but critical appraisal of the literature indicates that they are likely to be correct. |
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AJIOKA, Y. RADOJKOVIC, M. ALLISON, L.J. LANE, M.R. |
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10.1046/j.1365-2559.1997.d01-589.x |
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