p73 mutations are not detected in sporadic and hereditary breast cancer
Abstract Recently, a novel tumor suppressor gene, p73, was isolated and mapped to chromosome 1p36, a region commonly associated with loss of heterozygosity in neuroblastoma and other human malignancies, including breast cancer. The p73 gene shares considerable homology with the common tumor suppress...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
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| Format: |
E-Artikel |
|---|---|
| Sprache: |
Englisch |
| Erschienen: |
1999 |
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| Umfang: |
5 |
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| Reproduktion: |
Springer Online Journal Archives 1860-2002 |
|---|---|
| Übergeordnetes Werk: |
in: Breast cancer research and treatment - 1981, 58(1999) vom: Jan., Seite 25-29 |
| Übergeordnetes Werk: |
volume:58 ; year:1999 ; month:01 ; pages:25-29 ; extent:5 |
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| 520 | |a Abstract Recently, a novel tumor suppressor gene, p73, was isolated and mapped to chromosome 1p36, a region commonly associated with loss of heterozygosity in neuroblastoma and other human malignancies, including breast cancer. The p73 gene shares considerable homology with the common tumor suppressor gene p53, both in composition and function. This study examines the potential participation of p73 in the pathogenesis of sporadic and hereditary breast cancers. Mutation analysis of 29 hereditary breast cancer cases revealed five independent silent mutations in the hereditary cases that are unlikely to play a role in tumor development. Mutation analysis of 48 sporadic breast tumors did not identify any unique variants. Eleven common polymorphisms scattered throughout the gene were also detected. Thus, mutations in the p73 gene appear to play little if any role in hereditary or sporadic breast cancer. | ||
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| 700 | 1 | |a Schwartz, David I. |4 oth | |
| 700 | 1 | |a Lindor, Noralane M. |4 oth | |
| 700 | 1 | |a Walsh-Vockley, Cate |4 oth | |
| 700 | 1 | |a Roche, Patrick C. |4 oth | |
| 700 | 1 | |a Mai, Ming |4 oth | |
| 700 | 1 | |a Smith, David I. |4 oth | |
| 700 | 1 | |a Liu, Wanguo |4 oth | |
| 700 | 1 | |a Couch, Fergus J. |4 oth | |
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(DE-627)NLEJ196742528 DE-627 ger DE-627 rakwb eng p73 mutations are not detected in sporadic and hereditary breast cancer 1999 5 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Recently, a novel tumor suppressor gene, p73, was isolated and mapped to chromosome 1p36, a region commonly associated with loss of heterozygosity in neuroblastoma and other human malignancies, including breast cancer. The p73 gene shares considerable homology with the common tumor suppressor gene p53, both in composition and function. This study examines the potential participation of p73 in the pathogenesis of sporadic and hereditary breast cancers. Mutation analysis of 29 hereditary breast cancer cases revealed five independent silent mutations in the hereditary cases that are unlikely to play a role in tumor development. Mutation analysis of 48 sporadic breast tumors did not identify any unique variants. Eleven common polymorphisms scattered throughout the gene were also detected. Thus, mutations in the p73 gene appear to play little if any role in hereditary or sporadic breast cancer. Springer Online Journal Archives 1860-2002 Schwartz, David I. oth Lindor, Noralane M. oth Walsh-Vockley, Cate oth Roche, Patrick C. oth Mai, Ming oth Smith, David I. oth Liu, Wanguo oth Couch, Fergus J. oth in Breast cancer research and treatment 1981 58(1999) vom: Jan., Seite 25-29 (DE-627)NLEJ188984240 (DE-600)2004077-5 1573-7217 nnns volume:58 year:1999 month:01 pages:25-29 extent:5 http://dx.doi.org/10.1023/A:1006237031070 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 58 1999 1 25-29 5 |
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(DE-627)NLEJ196742528 DE-627 ger DE-627 rakwb eng p73 mutations are not detected in sporadic and hereditary breast cancer 1999 5 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Recently, a novel tumor suppressor gene, p73, was isolated and mapped to chromosome 1p36, a region commonly associated with loss of heterozygosity in neuroblastoma and other human malignancies, including breast cancer. The p73 gene shares considerable homology with the common tumor suppressor gene p53, both in composition and function. This study examines the potential participation of p73 in the pathogenesis of sporadic and hereditary breast cancers. Mutation analysis of 29 hereditary breast cancer cases revealed five independent silent mutations in the hereditary cases that are unlikely to play a role in tumor development. Mutation analysis of 48 sporadic breast tumors did not identify any unique variants. Eleven common polymorphisms scattered throughout the gene were also detected. Thus, mutations in the p73 gene appear to play little if any role in hereditary or sporadic breast cancer. Springer Online Journal Archives 1860-2002 Schwartz, David I. oth Lindor, Noralane M. oth Walsh-Vockley, Cate oth Roche, Patrick C. oth Mai, Ming oth Smith, David I. oth Liu, Wanguo oth Couch, Fergus J. oth in Breast cancer research and treatment 1981 58(1999) vom: Jan., Seite 25-29 (DE-627)NLEJ188984240 (DE-600)2004077-5 1573-7217 nnns volume:58 year:1999 month:01 pages:25-29 extent:5 http://dx.doi.org/10.1023/A:1006237031070 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 58 1999 1 25-29 5 |
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(DE-627)NLEJ196742528 DE-627 ger DE-627 rakwb eng p73 mutations are not detected in sporadic and hereditary breast cancer 1999 5 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Recently, a novel tumor suppressor gene, p73, was isolated and mapped to chromosome 1p36, a region commonly associated with loss of heterozygosity in neuroblastoma and other human malignancies, including breast cancer. The p73 gene shares considerable homology with the common tumor suppressor gene p53, both in composition and function. This study examines the potential participation of p73 in the pathogenesis of sporadic and hereditary breast cancers. Mutation analysis of 29 hereditary breast cancer cases revealed five independent silent mutations in the hereditary cases that are unlikely to play a role in tumor development. Mutation analysis of 48 sporadic breast tumors did not identify any unique variants. Eleven common polymorphisms scattered throughout the gene were also detected. Thus, mutations in the p73 gene appear to play little if any role in hereditary or sporadic breast cancer. Springer Online Journal Archives 1860-2002 Schwartz, David I. oth Lindor, Noralane M. oth Walsh-Vockley, Cate oth Roche, Patrick C. oth Mai, Ming oth Smith, David I. oth Liu, Wanguo oth Couch, Fergus J. oth in Breast cancer research and treatment 1981 58(1999) vom: Jan., Seite 25-29 (DE-627)NLEJ188984240 (DE-600)2004077-5 1573-7217 nnns volume:58 year:1999 month:01 pages:25-29 extent:5 http://dx.doi.org/10.1023/A:1006237031070 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 58 1999 1 25-29 5 |
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(DE-627)NLEJ196742528 DE-627 ger DE-627 rakwb eng p73 mutations are not detected in sporadic and hereditary breast cancer 1999 5 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Recently, a novel tumor suppressor gene, p73, was isolated and mapped to chromosome 1p36, a region commonly associated with loss of heterozygosity in neuroblastoma and other human malignancies, including breast cancer. The p73 gene shares considerable homology with the common tumor suppressor gene p53, both in composition and function. This study examines the potential participation of p73 in the pathogenesis of sporadic and hereditary breast cancers. Mutation analysis of 29 hereditary breast cancer cases revealed five independent silent mutations in the hereditary cases that are unlikely to play a role in tumor development. Mutation analysis of 48 sporadic breast tumors did not identify any unique variants. Eleven common polymorphisms scattered throughout the gene were also detected. Thus, mutations in the p73 gene appear to play little if any role in hereditary or sporadic breast cancer. Springer Online Journal Archives 1860-2002 Schwartz, David I. oth Lindor, Noralane M. oth Walsh-Vockley, Cate oth Roche, Patrick C. oth Mai, Ming oth Smith, David I. oth Liu, Wanguo oth Couch, Fergus J. oth in Breast cancer research and treatment 1981 58(1999) vom: Jan., Seite 25-29 (DE-627)NLEJ188984240 (DE-600)2004077-5 1573-7217 nnns volume:58 year:1999 month:01 pages:25-29 extent:5 http://dx.doi.org/10.1023/A:1006237031070 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 58 1999 1 25-29 5 |
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(DE-627)NLEJ196742528 DE-627 ger DE-627 rakwb eng p73 mutations are not detected in sporadic and hereditary breast cancer 1999 5 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Recently, a novel tumor suppressor gene, p73, was isolated and mapped to chromosome 1p36, a region commonly associated with loss of heterozygosity in neuroblastoma and other human malignancies, including breast cancer. The p73 gene shares considerable homology with the common tumor suppressor gene p53, both in composition and function. This study examines the potential participation of p73 in the pathogenesis of sporadic and hereditary breast cancers. Mutation analysis of 29 hereditary breast cancer cases revealed five independent silent mutations in the hereditary cases that are unlikely to play a role in tumor development. Mutation analysis of 48 sporadic breast tumors did not identify any unique variants. Eleven common polymorphisms scattered throughout the gene were also detected. Thus, mutations in the p73 gene appear to play little if any role in hereditary or sporadic breast cancer. Springer Online Journal Archives 1860-2002 Schwartz, David I. oth Lindor, Noralane M. oth Walsh-Vockley, Cate oth Roche, Patrick C. oth Mai, Ming oth Smith, David I. oth Liu, Wanguo oth Couch, Fergus J. oth in Breast cancer research and treatment 1981 58(1999) vom: Jan., Seite 25-29 (DE-627)NLEJ188984240 (DE-600)2004077-5 1573-7217 nnns volume:58 year:1999 month:01 pages:25-29 extent:5 http://dx.doi.org/10.1023/A:1006237031070 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 58 1999 1 25-29 5 |
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p73 mutations are not detected in sporadic and hereditary breast cancer |
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p73 mutations are not detected in sporadic and hereditary breast cancer |
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Abstract Recently, a novel tumor suppressor gene, p73, was isolated and mapped to chromosome 1p36, a region commonly associated with loss of heterozygosity in neuroblastoma and other human malignancies, including breast cancer. The p73 gene shares considerable homology with the common tumor suppressor gene p53, both in composition and function. This study examines the potential participation of p73 in the pathogenesis of sporadic and hereditary breast cancers. Mutation analysis of 29 hereditary breast cancer cases revealed five independent silent mutations in the hereditary cases that are unlikely to play a role in tumor development. Mutation analysis of 48 sporadic breast tumors did not identify any unique variants. Eleven common polymorphisms scattered throughout the gene were also detected. Thus, mutations in the p73 gene appear to play little if any role in hereditary or sporadic breast cancer. |
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Abstract Recently, a novel tumor suppressor gene, p73, was isolated and mapped to chromosome 1p36, a region commonly associated with loss of heterozygosity in neuroblastoma and other human malignancies, including breast cancer. The p73 gene shares considerable homology with the common tumor suppressor gene p53, both in composition and function. This study examines the potential participation of p73 in the pathogenesis of sporadic and hereditary breast cancers. Mutation analysis of 29 hereditary breast cancer cases revealed five independent silent mutations in the hereditary cases that are unlikely to play a role in tumor development. Mutation analysis of 48 sporadic breast tumors did not identify any unique variants. Eleven common polymorphisms scattered throughout the gene were also detected. Thus, mutations in the p73 gene appear to play little if any role in hereditary or sporadic breast cancer. |
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Abstract Recently, a novel tumor suppressor gene, p73, was isolated and mapped to chromosome 1p36, a region commonly associated with loss of heterozygosity in neuroblastoma and other human malignancies, including breast cancer. The p73 gene shares considerable homology with the common tumor suppressor gene p53, both in composition and function. This study examines the potential participation of p73 in the pathogenesis of sporadic and hereditary breast cancers. Mutation analysis of 29 hereditary breast cancer cases revealed five independent silent mutations in the hereditary cases that are unlikely to play a role in tumor development. Mutation analysis of 48 sporadic breast tumors did not identify any unique variants. Eleven common polymorphisms scattered throughout the gene were also detected. Thus, mutations in the p73 gene appear to play little if any role in hereditary or sporadic breast cancer. |
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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">NLEJ196742528</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20210705195439.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">070526s1999 xx |||||o 00| ||eng c</controlfield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)NLEJ196742528</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">p73 mutations are not detected in sporadic and hereditary breast cancer</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">1999</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">5</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">Abstract Recently, a novel tumor suppressor gene, p73, was isolated and mapped to chromosome 1p36, a region commonly associated with loss of heterozygosity in neuroblastoma and other human malignancies, including breast cancer. The p73 gene shares considerable homology with the common tumor suppressor gene p53, both in composition and function. This study examines the potential participation of p73 in the pathogenesis of sporadic and hereditary breast cancers. Mutation analysis of 29 hereditary breast cancer cases revealed five independent silent mutations in the hereditary cases that are unlikely to play a role in tumor development. Mutation analysis of 48 sporadic breast tumors did not identify any unique variants. Eleven common polymorphisms scattered throughout the gene were also detected. Thus, mutations in the p73 gene appear to play little if any role in hereditary or sporadic breast cancer.</subfield></datafield><datafield tag="533" ind1=" " ind2=" "><subfield code="f">Springer Online Journal Archives 1860-2002</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Schwartz, David I.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Lindor, Noralane M.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Walsh-Vockley, Cate</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Roche, Patrick C.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Mai, Ming</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Smith, David I.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Liu, Wanguo</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Couch, Fergus J.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">in</subfield><subfield code="t">Breast cancer research and treatment</subfield><subfield code="d">1981</subfield><subfield code="g">58(1999) vom: Jan., Seite 25-29</subfield><subfield code="w">(DE-627)NLEJ188984240</subfield><subfield code="w">(DE-600)2004077-5</subfield><subfield code="x">1573-7217</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:58</subfield><subfield code="g">year:1999</subfield><subfield code="g">month:01</subfield><subfield code="g">pages:25-29</subfield><subfield code="g">extent:5</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">http://dx.doi.org/10.1023/A:1006237031070</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">ZDB-1-SOJ</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">58</subfield><subfield code="j">1999</subfield><subfield code="c">1</subfield><subfield code="h">25-29</subfield><subfield code="g">5</subfield></datafield></record></collection>
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