Knockout and transgenic mice of Trp53: what have we learned about p53 in breast cancer?

Abstract The human p53 tumor suppressor gene TP53 is mutated at a high frequency in sporadic breast cancer, and Li-Fraumeni syndrome patients who carry germline mutations in one TP53 allele have a high incidence of breast cancer. In the 10 years since the first knockout of the mouse p53 tumor suppre...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Blackburn, Anneke C [verfasserIn] Jerry, D Joseph

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2002

Schlagwörter:	breast cancer knockout p53 transgenic

Anmerkung:	© BioMed Central Ltd 2002

Übergeordnetes Werk:	Enthalten in: Breast cancer research - London : BioMed Central, 1999, 4(2002), 3 vom: 01. Juni
Übergeordnetes Werk:	volume:4 ; year:2002 ; number:3 ; day:01 ; month:06

Links:	Volltext

DOI / URN:	10.1186/bcr427

Katalog-ID:	SPR02991714X

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allfields	10.1186/bcr427 doi (DE-627)SPR02991714X (SPR)bcr427-e DE-627 ger DE-627 rakwb eng Blackburn, Anneke C verfasserin aut Knockout and transgenic mice of Trp53: what have we learned about p53 in breast cancer? 2002 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © BioMed Central Ltd 2002 Abstract The human p53 tumor suppressor gene TP53 is mutated at a high frequency in sporadic breast cancer, and Li-Fraumeni syndrome patients who carry germline mutations in one TP53 allele have a high incidence of breast cancer. In the 10 years since the first knockout of the mouse p53 tumor suppressor gene (designated Trp53) was published, much has been learned about the contribution of p53 to biology and tumor suppression in the breast through the use of p53 transgenic and knockout mice. The original mice deficient in p53 showed no mammary gland phenotype. However, studies using BALB/c-Trp53-deficient mice have demonstrated a delayed involution phenotype and a mammary tumor phenotype. Together with other studies of mutant p53 transgenes and p53 bitransgenics, a greater understanding has been gained of the role of p53 in involution, of the regulation of p53 activity by hormones, of the effect of mouse strain and modifier genes on tumor phenotype, and of the cooperation between p53 and other oncogenic pathways, chemical carcinogens and hormonal stimulation in mammary tumorigenesis. Both p53 transgenic and knockout mice are important in vivo tools for understanding breast cancer, and are yet to be exploited for developing therapeutic strategies in breast cancer. breast cancer (dpeaa)DE-He213 knockout (dpeaa)DE-He213 p53 (dpeaa)DE-He213 transgenic (dpeaa)DE-He213 Jerry, D Joseph aut Enthalten in Breast cancer research London : BioMed Central, 1999 4(2002), 3 vom: 01. Juni (DE-627)326645950 (DE-600)2041618-0 1465-542X nnns volume:4 year:2002 number:3 day:01 month:06 https://dx.doi.org/10.1186/bcr427 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 4 2002 3 01 06
spelling	10.1186/bcr427 doi (DE-627)SPR02991714X (SPR)bcr427-e DE-627 ger DE-627 rakwb eng Blackburn, Anneke C verfasserin aut Knockout and transgenic mice of Trp53: what have we learned about p53 in breast cancer? 2002 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © BioMed Central Ltd 2002 Abstract The human p53 tumor suppressor gene TP53 is mutated at a high frequency in sporadic breast cancer, and Li-Fraumeni syndrome patients who carry germline mutations in one TP53 allele have a high incidence of breast cancer. In the 10 years since the first knockout of the mouse p53 tumor suppressor gene (designated Trp53) was published, much has been learned about the contribution of p53 to biology and tumor suppression in the breast through the use of p53 transgenic and knockout mice. The original mice deficient in p53 showed no mammary gland phenotype. However, studies using BALB/c-Trp53-deficient mice have demonstrated a delayed involution phenotype and a mammary tumor phenotype. Together with other studies of mutant p53 transgenes and p53 bitransgenics, a greater understanding has been gained of the role of p53 in involution, of the regulation of p53 activity by hormones, of the effect of mouse strain and modifier genes on tumor phenotype, and of the cooperation between p53 and other oncogenic pathways, chemical carcinogens and hormonal stimulation in mammary tumorigenesis. Both p53 transgenic and knockout mice are important in vivo tools for understanding breast cancer, and are yet to be exploited for developing therapeutic strategies in breast cancer. breast cancer (dpeaa)DE-He213 knockout (dpeaa)DE-He213 p53 (dpeaa)DE-He213 transgenic (dpeaa)DE-He213 Jerry, D Joseph aut Enthalten in Breast cancer research London : BioMed Central, 1999 4(2002), 3 vom: 01. Juni (DE-627)326645950 (DE-600)2041618-0 1465-542X nnns volume:4 year:2002 number:3 day:01 month:06 https://dx.doi.org/10.1186/bcr427 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 4 2002 3 01 06
allfields_unstemmed	10.1186/bcr427 doi (DE-627)SPR02991714X (SPR)bcr427-e DE-627 ger DE-627 rakwb eng Blackburn, Anneke C verfasserin aut Knockout and transgenic mice of Trp53: what have we learned about p53 in breast cancer? 2002 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © BioMed Central Ltd 2002 Abstract The human p53 tumor suppressor gene TP53 is mutated at a high frequency in sporadic breast cancer, and Li-Fraumeni syndrome patients who carry germline mutations in one TP53 allele have a high incidence of breast cancer. In the 10 years since the first knockout of the mouse p53 tumor suppressor gene (designated Trp53) was published, much has been learned about the contribution of p53 to biology and tumor suppression in the breast through the use of p53 transgenic and knockout mice. The original mice deficient in p53 showed no mammary gland phenotype. However, studies using BALB/c-Trp53-deficient mice have demonstrated a delayed involution phenotype and a mammary tumor phenotype. Together with other studies of mutant p53 transgenes and p53 bitransgenics, a greater understanding has been gained of the role of p53 in involution, of the regulation of p53 activity by hormones, of the effect of mouse strain and modifier genes on tumor phenotype, and of the cooperation between p53 and other oncogenic pathways, chemical carcinogens and hormonal stimulation in mammary tumorigenesis. Both p53 transgenic and knockout mice are important in vivo tools for understanding breast cancer, and are yet to be exploited for developing therapeutic strategies in breast cancer. breast cancer (dpeaa)DE-He213 knockout (dpeaa)DE-He213 p53 (dpeaa)DE-He213 transgenic (dpeaa)DE-He213 Jerry, D Joseph aut Enthalten in Breast cancer research London : BioMed Central, 1999 4(2002), 3 vom: 01. Juni (DE-627)326645950 (DE-600)2041618-0 1465-542X nnns volume:4 year:2002 number:3 day:01 month:06 https://dx.doi.org/10.1186/bcr427 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 4 2002 3 01 06
allfieldsGer	10.1186/bcr427 doi (DE-627)SPR02991714X (SPR)bcr427-e DE-627 ger DE-627 rakwb eng Blackburn, Anneke C verfasserin aut Knockout and transgenic mice of Trp53: what have we learned about p53 in breast cancer? 2002 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © BioMed Central Ltd 2002 Abstract The human p53 tumor suppressor gene TP53 is mutated at a high frequency in sporadic breast cancer, and Li-Fraumeni syndrome patients who carry germline mutations in one TP53 allele have a high incidence of breast cancer. In the 10 years since the first knockout of the mouse p53 tumor suppressor gene (designated Trp53) was published, much has been learned about the contribution of p53 to biology and tumor suppression in the breast through the use of p53 transgenic and knockout mice. The original mice deficient in p53 showed no mammary gland phenotype. However, studies using BALB/c-Trp53-deficient mice have demonstrated a delayed involution phenotype and a mammary tumor phenotype. Together with other studies of mutant p53 transgenes and p53 bitransgenics, a greater understanding has been gained of the role of p53 in involution, of the regulation of p53 activity by hormones, of the effect of mouse strain and modifier genes on tumor phenotype, and of the cooperation between p53 and other oncogenic pathways, chemical carcinogens and hormonal stimulation in mammary tumorigenesis. Both p53 transgenic and knockout mice are important in vivo tools for understanding breast cancer, and are yet to be exploited for developing therapeutic strategies in breast cancer. breast cancer (dpeaa)DE-He213 knockout (dpeaa)DE-He213 p53 (dpeaa)DE-He213 transgenic (dpeaa)DE-He213 Jerry, D Joseph aut Enthalten in Breast cancer research London : BioMed Central, 1999 4(2002), 3 vom: 01. Juni (DE-627)326645950 (DE-600)2041618-0 1465-542X nnns volume:4 year:2002 number:3 day:01 month:06 https://dx.doi.org/10.1186/bcr427 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 4 2002 3 01 06
allfieldsSound	10.1186/bcr427 doi (DE-627)SPR02991714X (SPR)bcr427-e DE-627 ger DE-627 rakwb eng Blackburn, Anneke C verfasserin aut Knockout and transgenic mice of Trp53: what have we learned about p53 in breast cancer? 2002 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © BioMed Central Ltd 2002 Abstract The human p53 tumor suppressor gene TP53 is mutated at a high frequency in sporadic breast cancer, and Li-Fraumeni syndrome patients who carry germline mutations in one TP53 allele have a high incidence of breast cancer. In the 10 years since the first knockout of the mouse p53 tumor suppressor gene (designated Trp53) was published, much has been learned about the contribution of p53 to biology and tumor suppression in the breast through the use of p53 transgenic and knockout mice. The original mice deficient in p53 showed no mammary gland phenotype. However, studies using BALB/c-Trp53-deficient mice have demonstrated a delayed involution phenotype and a mammary tumor phenotype. Together with other studies of mutant p53 transgenes and p53 bitransgenics, a greater understanding has been gained of the role of p53 in involution, of the regulation of p53 activity by hormones, of the effect of mouse strain and modifier genes on tumor phenotype, and of the cooperation between p53 and other oncogenic pathways, chemical carcinogens and hormonal stimulation in mammary tumorigenesis. Both p53 transgenic and knockout mice are important in vivo tools for understanding breast cancer, and are yet to be exploited for developing therapeutic strategies in breast cancer. breast cancer (dpeaa)DE-He213 knockout (dpeaa)DE-He213 p53 (dpeaa)DE-He213 transgenic (dpeaa)DE-He213 Jerry, D Joseph aut Enthalten in Breast cancer research London : BioMed Central, 1999 4(2002), 3 vom: 01. Juni (DE-627)326645950 (DE-600)2041618-0 1465-542X nnns volume:4 year:2002 number:3 day:01 month:06 https://dx.doi.org/10.1186/bcr427 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 4 2002 3 01 06
language	English
source	Enthalten in Breast cancer research 4(2002), 3 vom: 01. Juni volume:4 year:2002 number:3 day:01 month:06
sourceStr	Enthalten in Breast cancer research 4(2002), 3 vom: 01. Juni volume:4 year:2002 number:3 day:01 month:06
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institution	findex.gbv.de
topic_facet	breast cancer knockout p53 transgenic
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container_title	Breast cancer research
authorswithroles_txt_mv	Blackburn, Anneke C @@aut@@ Jerry, D Joseph @@aut@@
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author	Blackburn, Anneke C
spellingShingle	Blackburn, Anneke C misc breast cancer misc knockout misc p53 misc transgenic Knockout and transgenic mice of Trp53: what have we learned about p53 in breast cancer?
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topic_title	Knockout and transgenic mice of Trp53: what have we learned about p53 in breast cancer? breast cancer (dpeaa)DE-He213 knockout (dpeaa)DE-He213 p53 (dpeaa)DE-He213 transgenic (dpeaa)DE-He213
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title	Knockout and transgenic mice of Trp53: what have we learned about p53 in breast cancer?
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title_full	Knockout and transgenic mice of Trp53: what have we learned about p53 in breast cancer?
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title_sort	knockout and transgenic mice of trp53: what have we learned about p53 in breast cancer?
title_auth	Knockout and transgenic mice of Trp53: what have we learned about p53 in breast cancer?
abstract	Abstract The human p53 tumor suppressor gene TP53 is mutated at a high frequency in sporadic breast cancer, and Li-Fraumeni syndrome patients who carry germline mutations in one TP53 allele have a high incidence of breast cancer. In the 10 years since the first knockout of the mouse p53 tumor suppressor gene (designated Trp53) was published, much has been learned about the contribution of p53 to biology and tumor suppression in the breast through the use of p53 transgenic and knockout mice. The original mice deficient in p53 showed no mammary gland phenotype. However, studies using BALB/c-Trp53-deficient mice have demonstrated a delayed involution phenotype and a mammary tumor phenotype. Together with other studies of mutant p53 transgenes and p53 bitransgenics, a greater understanding has been gained of the role of p53 in involution, of the regulation of p53 activity by hormones, of the effect of mouse strain and modifier genes on tumor phenotype, and of the cooperation between p53 and other oncogenic pathways, chemical carcinogens and hormonal stimulation in mammary tumorigenesis. Both p53 transgenic and knockout mice are important in vivo tools for understanding breast cancer, and are yet to be exploited for developing therapeutic strategies in breast cancer. © BioMed Central Ltd 2002
abstractGer	Abstract The human p53 tumor suppressor gene TP53 is mutated at a high frequency in sporadic breast cancer, and Li-Fraumeni syndrome patients who carry germline mutations in one TP53 allele have a high incidence of breast cancer. In the 10 years since the first knockout of the mouse p53 tumor suppressor gene (designated Trp53) was published, much has been learned about the contribution of p53 to biology and tumor suppression in the breast through the use of p53 transgenic and knockout mice. The original mice deficient in p53 showed no mammary gland phenotype. However, studies using BALB/c-Trp53-deficient mice have demonstrated a delayed involution phenotype and a mammary tumor phenotype. Together with other studies of mutant p53 transgenes and p53 bitransgenics, a greater understanding has been gained of the role of p53 in involution, of the regulation of p53 activity by hormones, of the effect of mouse strain and modifier genes on tumor phenotype, and of the cooperation between p53 and other oncogenic pathways, chemical carcinogens and hormonal stimulation in mammary tumorigenesis. Both p53 transgenic and knockout mice are important in vivo tools for understanding breast cancer, and are yet to be exploited for developing therapeutic strategies in breast cancer. © BioMed Central Ltd 2002
abstract_unstemmed	Abstract The human p53 tumor suppressor gene TP53 is mutated at a high frequency in sporadic breast cancer, and Li-Fraumeni syndrome patients who carry germline mutations in one TP53 allele have a high incidence of breast cancer. In the 10 years since the first knockout of the mouse p53 tumor suppressor gene (designated Trp53) was published, much has been learned about the contribution of p53 to biology and tumor suppression in the breast through the use of p53 transgenic and knockout mice. The original mice deficient in p53 showed no mammary gland phenotype. However, studies using BALB/c-Trp53-deficient mice have demonstrated a delayed involution phenotype and a mammary tumor phenotype. Together with other studies of mutant p53 transgenes and p53 bitransgenics, a greater understanding has been gained of the role of p53 in involution, of the regulation of p53 activity by hormones, of the effect of mouse strain and modifier genes on tumor phenotype, and of the cooperation between p53 and other oncogenic pathways, chemical carcinogens and hormonal stimulation in mammary tumorigenesis. Both p53 transgenic and knockout mice are important in vivo tools for understanding breast cancer, and are yet to be exploited for developing therapeutic strategies in breast cancer. © BioMed Central Ltd 2002
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title_short	Knockout and transgenic mice of Trp53: what have we learned about p53 in breast cancer?
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up_date	2024-07-04T02:41:39.120Z
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