Hereditary non-polyposis colorectal cancer - morphologies, genes and mutations
Mutations in human homologue of the yeast DNA mismatch repair gene MSH2 (equivalent to bacterial MutS) cause the condition heredity non-polyposis colorectal cancer (HNPCC). Cancers in HNPCC originate within bengin neoplastic polyps termed adenomas. Adenomas are clonal and each may serve as a marker...
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E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
1994 |
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| Reproduktion: |
Elsevier Journal Backfiles on ScienceDirect 1907 - 2002 |
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| Übergeordnetes Werk: |
in: Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis - Amsterdam : Elsevier, 310(1994), 1, Seite 125-133 |
| Übergeordnetes Werk: |
volume:310 ; year:1994 ; number:1 ; pages:125-133 |
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| 520 | |a Mutations in human homologue of the yeast DNA mismatch repair gene MSH2 (equivalent to bacterial MutS) cause the condition heredity non-polyposis colorectal cancer (HNPCC). Cancers in HNPCC originate within bengin neoplastic polyps termed adenomas. Adenomas are clonal and each may serve as a marker of a single initiating mutation. The progression of adenomas is marked by increasing size, dysplasia and villosity. These characteristics can be taken as the morphological counterparts of the stepwise accumulations implicating ioncogenes and tumour suppressor genes. The aim of this study was to link the morphogenesis of heredity colorectal cancer with recent insights into the role of DNA mismatch repair genes. The frequency and anatomical distribution of adenomas in at-risk members of HNPCC families was the same as in an autopsy population. This suggests that the HNPCC gene does not initiate the process of neoplastic transformation. On the other hand, adenomas in at-risk members of HNPCC families were more likely to show villosity (p<0.001), high grade dysplasia (p=0.002) and probably increased size (p=0.15). These findings are consistent with the observation that the HNPCC gene causes DNA replication errors to develop and accumulate within neoplastic but not normal tissue. The effect of the HNPCC gene is to accelerate the progression of adenoma to carcinoma, but not to initiate adenoma development. | ||
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(DE-627)NLEJ186504144 (DE-599)GBVNLZ186504144 DE-627 ger DE-627 rakwb eng Hereditary non-polyposis colorectal cancer - morphologies, genes and mutations 1994 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Mutations in human homologue of the yeast DNA mismatch repair gene MSH2 (equivalent to bacterial MutS) cause the condition heredity non-polyposis colorectal cancer (HNPCC). Cancers in HNPCC originate within bengin neoplastic polyps termed adenomas. Adenomas are clonal and each may serve as a marker of a single initiating mutation. The progression of adenomas is marked by increasing size, dysplasia and villosity. These characteristics can be taken as the morphological counterparts of the stepwise accumulations implicating ioncogenes and tumour suppressor genes. The aim of this study was to link the morphogenesis of heredity colorectal cancer with recent insights into the role of DNA mismatch repair genes. The frequency and anatomical distribution of adenomas in at-risk members of HNPCC families was the same as in an autopsy population. This suggests that the HNPCC gene does not initiate the process of neoplastic transformation. On the other hand, adenomas in at-risk members of HNPCC families were more likely to show villosity (p<0.001), high grade dysplasia (p=0.002) and probably increased size (p=0.15). These findings are consistent with the observation that the HNPCC gene causes DNA replication errors to develop and accumulate within neoplastic but not normal tissue. The effect of the HNPCC gene is to accelerate the progression of adenoma to carcinoma, but not to initiate adenoma development. Elsevier Journal Backfiles on ScienceDirect 1907 - 2002 Jass, J.R. oth Stewart, S.M. oth Stewart, J. oth Lane, M.R. oth in Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis Amsterdam : Elsevier 310(1994), 1, Seite 125-133 (DE-627)NLEJ177212004 (DE-600)1491099-8 0027-5107 nnns volume:310 year:1994 number:1 pages:125-133 http://linkinghub.elsevier.com/retrieve/pii/0027-5107(94)90016-7 GBV_USEFLAG_H ZDB-1-SDJ GBV_NL_ARTICLE AR 310 1994 1 125-133 |
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(DE-627)NLEJ186504144 (DE-599)GBVNLZ186504144 DE-627 ger DE-627 rakwb eng Hereditary non-polyposis colorectal cancer - morphologies, genes and mutations 1994 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Mutations in human homologue of the yeast DNA mismatch repair gene MSH2 (equivalent to bacterial MutS) cause the condition heredity non-polyposis colorectal cancer (HNPCC). Cancers in HNPCC originate within bengin neoplastic polyps termed adenomas. Adenomas are clonal and each may serve as a marker of a single initiating mutation. The progression of adenomas is marked by increasing size, dysplasia and villosity. These characteristics can be taken as the morphological counterparts of the stepwise accumulations implicating ioncogenes and tumour suppressor genes. The aim of this study was to link the morphogenesis of heredity colorectal cancer with recent insights into the role of DNA mismatch repair genes. The frequency and anatomical distribution of adenomas in at-risk members of HNPCC families was the same as in an autopsy population. This suggests that the HNPCC gene does not initiate the process of neoplastic transformation. On the other hand, adenomas in at-risk members of HNPCC families were more likely to show villosity (p<0.001), high grade dysplasia (p=0.002) and probably increased size (p=0.15). These findings are consistent with the observation that the HNPCC gene causes DNA replication errors to develop and accumulate within neoplastic but not normal tissue. The effect of the HNPCC gene is to accelerate the progression of adenoma to carcinoma, but not to initiate adenoma development. Elsevier Journal Backfiles on ScienceDirect 1907 - 2002 Jass, J.R. oth Stewart, S.M. oth Stewart, J. oth Lane, M.R. oth in Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis Amsterdam : Elsevier 310(1994), 1, Seite 125-133 (DE-627)NLEJ177212004 (DE-600)1491099-8 0027-5107 nnns volume:310 year:1994 number:1 pages:125-133 http://linkinghub.elsevier.com/retrieve/pii/0027-5107(94)90016-7 GBV_USEFLAG_H ZDB-1-SDJ GBV_NL_ARTICLE AR 310 1994 1 125-133 |
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(DE-627)NLEJ186504144 (DE-599)GBVNLZ186504144 DE-627 ger DE-627 rakwb eng Hereditary non-polyposis colorectal cancer - morphologies, genes and mutations 1994 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Mutations in human homologue of the yeast DNA mismatch repair gene MSH2 (equivalent to bacterial MutS) cause the condition heredity non-polyposis colorectal cancer (HNPCC). Cancers in HNPCC originate within bengin neoplastic polyps termed adenomas. Adenomas are clonal and each may serve as a marker of a single initiating mutation. The progression of adenomas is marked by increasing size, dysplasia and villosity. These characteristics can be taken as the morphological counterparts of the stepwise accumulations implicating ioncogenes and tumour suppressor genes. The aim of this study was to link the morphogenesis of heredity colorectal cancer with recent insights into the role of DNA mismatch repair genes. The frequency and anatomical distribution of adenomas in at-risk members of HNPCC families was the same as in an autopsy population. This suggests that the HNPCC gene does not initiate the process of neoplastic transformation. On the other hand, adenomas in at-risk members of HNPCC families were more likely to show villosity (p<0.001), high grade dysplasia (p=0.002) and probably increased size (p=0.15). These findings are consistent with the observation that the HNPCC gene causes DNA replication errors to develop and accumulate within neoplastic but not normal tissue. The effect of the HNPCC gene is to accelerate the progression of adenoma to carcinoma, but not to initiate adenoma development. Elsevier Journal Backfiles on ScienceDirect 1907 - 2002 Jass, J.R. oth Stewart, S.M. oth Stewart, J. oth Lane, M.R. oth in Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis Amsterdam : Elsevier 310(1994), 1, Seite 125-133 (DE-627)NLEJ177212004 (DE-600)1491099-8 0027-5107 nnns volume:310 year:1994 number:1 pages:125-133 http://linkinghub.elsevier.com/retrieve/pii/0027-5107(94)90016-7 GBV_USEFLAG_H ZDB-1-SDJ GBV_NL_ARTICLE AR 310 1994 1 125-133 |
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(DE-627)NLEJ186504144 (DE-599)GBVNLZ186504144 DE-627 ger DE-627 rakwb eng Hereditary non-polyposis colorectal cancer - morphologies, genes and mutations 1994 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Mutations in human homologue of the yeast DNA mismatch repair gene MSH2 (equivalent to bacterial MutS) cause the condition heredity non-polyposis colorectal cancer (HNPCC). Cancers in HNPCC originate within bengin neoplastic polyps termed adenomas. Adenomas are clonal and each may serve as a marker of a single initiating mutation. The progression of adenomas is marked by increasing size, dysplasia and villosity. These characteristics can be taken as the morphological counterparts of the stepwise accumulations implicating ioncogenes and tumour suppressor genes. The aim of this study was to link the morphogenesis of heredity colorectal cancer with recent insights into the role of DNA mismatch repair genes. The frequency and anatomical distribution of adenomas in at-risk members of HNPCC families was the same as in an autopsy population. This suggests that the HNPCC gene does not initiate the process of neoplastic transformation. On the other hand, adenomas in at-risk members of HNPCC families were more likely to show villosity (p<0.001), high grade dysplasia (p=0.002) and probably increased size (p=0.15). These findings are consistent with the observation that the HNPCC gene causes DNA replication errors to develop and accumulate within neoplastic but not normal tissue. The effect of the HNPCC gene is to accelerate the progression of adenoma to carcinoma, but not to initiate adenoma development. Elsevier Journal Backfiles on ScienceDirect 1907 - 2002 Jass, J.R. oth Stewart, S.M. oth Stewart, J. oth Lane, M.R. oth in Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis Amsterdam : Elsevier 310(1994), 1, Seite 125-133 (DE-627)NLEJ177212004 (DE-600)1491099-8 0027-5107 nnns volume:310 year:1994 number:1 pages:125-133 http://linkinghub.elsevier.com/retrieve/pii/0027-5107(94)90016-7 GBV_USEFLAG_H ZDB-1-SDJ GBV_NL_ARTICLE AR 310 1994 1 125-133 |
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(DE-627)NLEJ186504144 (DE-599)GBVNLZ186504144 DE-627 ger DE-627 rakwb eng Hereditary non-polyposis colorectal cancer - morphologies, genes and mutations 1994 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Mutations in human homologue of the yeast DNA mismatch repair gene MSH2 (equivalent to bacterial MutS) cause the condition heredity non-polyposis colorectal cancer (HNPCC). Cancers in HNPCC originate within bengin neoplastic polyps termed adenomas. Adenomas are clonal and each may serve as a marker of a single initiating mutation. The progression of adenomas is marked by increasing size, dysplasia and villosity. These characteristics can be taken as the morphological counterparts of the stepwise accumulations implicating ioncogenes and tumour suppressor genes. The aim of this study was to link the morphogenesis of heredity colorectal cancer with recent insights into the role of DNA mismatch repair genes. The frequency and anatomical distribution of adenomas in at-risk members of HNPCC families was the same as in an autopsy population. This suggests that the HNPCC gene does not initiate the process of neoplastic transformation. On the other hand, adenomas in at-risk members of HNPCC families were more likely to show villosity (p<0.001), high grade dysplasia (p=0.002) and probably increased size (p=0.15). These findings are consistent with the observation that the HNPCC gene causes DNA replication errors to develop and accumulate within neoplastic but not normal tissue. The effect of the HNPCC gene is to accelerate the progression of adenoma to carcinoma, but not to initiate adenoma development. Elsevier Journal Backfiles on ScienceDirect 1907 - 2002 Jass, J.R. oth Stewart, S.M. oth Stewart, J. oth Lane, M.R. oth in Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis Amsterdam : Elsevier 310(1994), 1, Seite 125-133 (DE-627)NLEJ177212004 (DE-600)1491099-8 0027-5107 nnns volume:310 year:1994 number:1 pages:125-133 http://linkinghub.elsevier.com/retrieve/pii/0027-5107(94)90016-7 GBV_USEFLAG_H ZDB-1-SDJ GBV_NL_ARTICLE AR 310 1994 1 125-133 |
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Hereditary non-polyposis colorectal cancer - morphologies, genes and mutations |
| abstract |
Mutations in human homologue of the yeast DNA mismatch repair gene MSH2 (equivalent to bacterial MutS) cause the condition heredity non-polyposis colorectal cancer (HNPCC). Cancers in HNPCC originate within bengin neoplastic polyps termed adenomas. Adenomas are clonal and each may serve as a marker of a single initiating mutation. The progression of adenomas is marked by increasing size, dysplasia and villosity. These characteristics can be taken as the morphological counterparts of the stepwise accumulations implicating ioncogenes and tumour suppressor genes. The aim of this study was to link the morphogenesis of heredity colorectal cancer with recent insights into the role of DNA mismatch repair genes. The frequency and anatomical distribution of adenomas in at-risk members of HNPCC families was the same as in an autopsy population. This suggests that the HNPCC gene does not initiate the process of neoplastic transformation. On the other hand, adenomas in at-risk members of HNPCC families were more likely to show villosity (p<0.001), high grade dysplasia (p=0.002) and probably increased size (p=0.15). These findings are consistent with the observation that the HNPCC gene causes DNA replication errors to develop and accumulate within neoplastic but not normal tissue. The effect of the HNPCC gene is to accelerate the progression of adenoma to carcinoma, but not to initiate adenoma development. |
| abstractGer |
Mutations in human homologue of the yeast DNA mismatch repair gene MSH2 (equivalent to bacterial MutS) cause the condition heredity non-polyposis colorectal cancer (HNPCC). Cancers in HNPCC originate within bengin neoplastic polyps termed adenomas. Adenomas are clonal and each may serve as a marker of a single initiating mutation. The progression of adenomas is marked by increasing size, dysplasia and villosity. These characteristics can be taken as the morphological counterparts of the stepwise accumulations implicating ioncogenes and tumour suppressor genes. The aim of this study was to link the morphogenesis of heredity colorectal cancer with recent insights into the role of DNA mismatch repair genes. The frequency and anatomical distribution of adenomas in at-risk members of HNPCC families was the same as in an autopsy population. This suggests that the HNPCC gene does not initiate the process of neoplastic transformation. On the other hand, adenomas in at-risk members of HNPCC families were more likely to show villosity (p<0.001), high grade dysplasia (p=0.002) and probably increased size (p=0.15). These findings are consistent with the observation that the HNPCC gene causes DNA replication errors to develop and accumulate within neoplastic but not normal tissue. The effect of the HNPCC gene is to accelerate the progression of adenoma to carcinoma, but not to initiate adenoma development. |
| abstract_unstemmed |
Mutations in human homologue of the yeast DNA mismatch repair gene MSH2 (equivalent to bacterial MutS) cause the condition heredity non-polyposis colorectal cancer (HNPCC). Cancers in HNPCC originate within bengin neoplastic polyps termed adenomas. Adenomas are clonal and each may serve as a marker of a single initiating mutation. The progression of adenomas is marked by increasing size, dysplasia and villosity. These characteristics can be taken as the morphological counterparts of the stepwise accumulations implicating ioncogenes and tumour suppressor genes. The aim of this study was to link the morphogenesis of heredity colorectal cancer with recent insights into the role of DNA mismatch repair genes. The frequency and anatomical distribution of adenomas in at-risk members of HNPCC families was the same as in an autopsy population. This suggests that the HNPCC gene does not initiate the process of neoplastic transformation. On the other hand, adenomas in at-risk members of HNPCC families were more likely to show villosity (p<0.001), high grade dysplasia (p=0.002) and probably increased size (p=0.15). These findings are consistent with the observation that the HNPCC gene causes DNA replication errors to develop and accumulate within neoplastic but not normal tissue. The effect of the HNPCC gene is to accelerate the progression of adenoma to carcinoma, but not to initiate adenoma development. |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">NLEJ186504144</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20210707050255.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">070506s1994 xx |||||o 00| ||eng c</controlfield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)NLEJ186504144</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)GBVNLZ186504144</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Hereditary non-polyposis colorectal cancer - morphologies, genes and mutations</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">1994</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Mutations in human homologue of the yeast DNA mismatch repair gene MSH2 (equivalent to bacterial MutS) cause the condition heredity non-polyposis colorectal cancer (HNPCC). Cancers in HNPCC originate within bengin neoplastic polyps termed adenomas. Adenomas are clonal and each may serve as a marker of a single initiating mutation. The progression of adenomas is marked by increasing size, dysplasia and villosity. These characteristics can be taken as the morphological counterparts of the stepwise accumulations implicating ioncogenes and tumour suppressor genes. The aim of this study was to link the morphogenesis of heredity colorectal cancer with recent insights into the role of DNA mismatch repair genes. The frequency and anatomical distribution of adenomas in at-risk members of HNPCC families was the same as in an autopsy population. This suggests that the HNPCC gene does not initiate the process of neoplastic transformation. On the other hand, adenomas in at-risk members of HNPCC families were more likely to show villosity (p<0.001), high grade dysplasia (p=0.002) and probably increased size (p=0.15). These findings are consistent with the observation that the HNPCC gene causes DNA replication errors to develop and accumulate within neoplastic but not normal tissue. The effect of the HNPCC gene is to accelerate the progression of adenoma to carcinoma, but not to initiate adenoma development.</subfield></datafield><datafield tag="533" ind1=" " ind2=" "><subfield code="f">Elsevier Journal Backfiles on ScienceDirect 1907 - 2002</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Jass, J.R.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Stewart, S.M.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Stewart, J.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Lane, M.R.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">in</subfield><subfield code="t">Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis</subfield><subfield code="d">Amsterdam : Elsevier</subfield><subfield code="g">310(1994), 1, Seite 125-133</subfield><subfield code="w">(DE-627)NLEJ177212004</subfield><subfield code="w">(DE-600)1491099-8</subfield><subfield code="x">0027-5107</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:310</subfield><subfield code="g">year:1994</subfield><subfield code="g">number:1</subfield><subfield code="g">pages:125-133</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">http://linkinghub.elsevier.com/retrieve/pii/0027-5107(94)90016-7</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_H</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">ZDB-1-SDJ</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_NL_ARTICLE</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">310</subfield><subfield code="j">1994</subfield><subfield code="e">1</subfield><subfield code="h">125-133</subfield></datafield></record></collection>
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