Somatic loss of BRCA1 and p53 in mice induces mammary tumors with features of human BRCA1-mutated basal-like breast cancer
Women carrying germ-line mutations in BRCA1 are strongly predisposed to developing breast cancers with characteristic features also observed in sporadic basal-like breast cancers. They appear as high-grade tumors with high proliferation rates and pushing borders. On the molecular level, they are neg...
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| Veröffentlicht in: | Proceedings of the National Academy of Sciences - PNAS Jg. 104; H. 29; S. 12111 |
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| Format: | Journal Article |
| Sprache: | Englisch |
| Veröffentlicht: |
United States
17.07.2007
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| ISSN: | 0027-8424 |
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| Abstract | Women carrying germ-line mutations in BRCA1 are strongly predisposed to developing breast cancers with characteristic features also observed in sporadic basal-like breast cancers. They appear as high-grade tumors with high proliferation rates and pushing borders. On the molecular level, they are negative for hormone receptors and ERBB2, display frequent TP53 mutations, and express basal epithelial markers. To study the role of BRCA1 and P53 loss of function in breast cancer development, we generated conditional mouse models with tissue-specific mutation of Brca1 and/or p53 in basal epithelial cells. Somatic loss of both BRCA1 and p53 resulted in the rapid and efficient formation of highly proliferative, poorly differentiated, estrogen receptor-negative mammary carcinomas with pushing borders and increased expression of basal epithelial markers, reminiscent of human basal-like breast cancer. BRCA1- and p53-deficient mouse mammary tumors exhibit dramatic genomic instability, and their molecular signatures resemble those of human BRCA1-mutated breast cancers. Thus, these tumors display important hallmarks of hereditary breast cancers in BRCA1-mutation carriers. |
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| AbstractList | Women carrying germ-line mutations in BRCA1 are strongly predisposed to developing breast cancers with characteristic features also observed in sporadic basal-like breast cancers. They appear as high-grade tumors with high proliferation rates and pushing borders. On the molecular level, they are negative for hormone receptors and ERBB2, display frequent TP53 mutations, and express basal epithelial markers. To study the role of BRCA1 and P53 loss of function in breast cancer development, we generated conditional mouse models with tissue-specific mutation of Brca1 and/or p53 in basal epithelial cells. Somatic loss of both BRCA1 and p53 resulted in the rapid and efficient formation of highly proliferative, poorly differentiated, estrogen receptor-negative mammary carcinomas with pushing borders and increased expression of basal epithelial markers, reminiscent of human basal-like breast cancer. BRCA1- and p53-deficient mouse mammary tumors exhibit dramatic genomic instability, and their molecular signatures resemble those of human BRCA1-mutated breast cancers. Thus, these tumors display important hallmarks of hereditary breast cancers in BRCA1-mutation carriers. Women carrying germ-line mutations in BRCA1 are strongly predisposed to developing breast cancers with characteristic features also observed in sporadic basal-like breast cancers. They appear as high-grade tumors with high proliferation rates and pushing borders. On the molecular level, they are negative for hormone receptors and ERBB2, display frequent TP53 mutations, and express basal epithelial markers. To study the role of BRCA1 and P53 loss of function in breast cancer development, we generated conditional mouse models with tissue-specific mutation of Brca1 and/or p53 in basal epithelial cells. Somatic loss of both BRCA1 and p53 resulted in the rapid and efficient formation of highly proliferative, poorly differentiated, estrogen receptor-negative mammary carcinomas with pushing borders and increased expression of basal epithelial markers, reminiscent of human basal-like breast cancer. BRCA1- and p53-deficient mouse mammary tumors exhibit dramatic genomic instability, and their molecular signatures resemble those of human BRCA1-mutated breast cancers. Thus, these tumors display important hallmarks of hereditary breast cancers in BRCA1-mutation carriers.Women carrying germ-line mutations in BRCA1 are strongly predisposed to developing breast cancers with characteristic features also observed in sporadic basal-like breast cancers. They appear as high-grade tumors with high proliferation rates and pushing borders. On the molecular level, they are negative for hormone receptors and ERBB2, display frequent TP53 mutations, and express basal epithelial markers. To study the role of BRCA1 and P53 loss of function in breast cancer development, we generated conditional mouse models with tissue-specific mutation of Brca1 and/or p53 in basal epithelial cells. Somatic loss of both BRCA1 and p53 resulted in the rapid and efficient formation of highly proliferative, poorly differentiated, estrogen receptor-negative mammary carcinomas with pushing borders and increased expression of basal epithelial markers, reminiscent of human basal-like breast cancer. BRCA1- and p53-deficient mouse mammary tumors exhibit dramatic genomic instability, and their molecular signatures resemble those of human BRCA1-mutated breast cancers. Thus, these tumors display important hallmarks of hereditary breast cancers in BRCA1-mutation carriers. |
| Author | Wessels, Lodewyk F A Liu, Xiaoling van der Gulden, Hanneke Berns, Anton Treur-Mulder, Marcelle Peterse, Johannes L Velds, Arno Jonkers, Jos Holstege, Henne Zevenhoven, John van Vliet, Martin H Kerkhoven, Ron M |
| Author_xml | – sequence: 1 givenname: Xiaoling surname: Liu fullname: Liu, Xiaoling organization: Division of Molecular Biology Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX, Amsterdam, The Netherlands – sequence: 2 givenname: Henne surname: Holstege fullname: Holstege, Henne – sequence: 3 givenname: Hanneke surname: van der Gulden fullname: van der Gulden, Hanneke – sequence: 4 givenname: Marcelle surname: Treur-Mulder fullname: Treur-Mulder, Marcelle – sequence: 5 givenname: John surname: Zevenhoven fullname: Zevenhoven, John – sequence: 6 givenname: Arno surname: Velds fullname: Velds, Arno – sequence: 7 givenname: Ron M surname: Kerkhoven fullname: Kerkhoven, Ron M – sequence: 8 givenname: Martin H surname: van Vliet fullname: van Vliet, Martin H – sequence: 9 givenname: Lodewyk F A surname: Wessels fullname: Wessels, Lodewyk F A – sequence: 10 givenname: Johannes L surname: Peterse fullname: Peterse, Johannes L – sequence: 11 givenname: Anton surname: Berns fullname: Berns, Anton – sequence: 12 givenname: Jos surname: Jonkers fullname: Jonkers, Jos |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/17626182$$D View this record in MEDLINE/PubMed |
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| References_xml | – reference: 11358863 - Genes Dev. 2001 May 15;15(10):1188-93 – reference: 12032322 - Proc Natl Acad Sci U S A. 2002 May 28;99(11):7560-5 – reference: 9171368 - Genes Dev. 1997 May 15;11(10):1226-41 – reference: 11431698 - Nat Genet. 2001 Jul;28(3):266-71 – reference: 14519755 - J Natl Cancer Inst. 2003 Oct 1;95(19):1482-5 – reference: 15510162 - Nat Rev Cancer. 2004 Oct;4(10):814-9 – reference: 15967981 - Proc Natl Acad Sci U S A. 2005 Jun 28;102(26):9176-81 – reference: 16397499 - Nature. 2006 Jan 5;439(7072):84-8 – reference: 10319859 - Nat Genet. 1999 May;22(1):37-43 – reference: 17016441 - Oncogene. 2007 Mar 29;26(14):2126-32 – reference: 11077440 - Oncogene. 2000 Nov 2;19(46):5237-43 – reference: 11709723 - Oncogene. 2001 Nov 8;20(51):7514-23 – reference: 15829967 - Nature. 2005 Apr 14;434(7035):917-21 – reference: 8563759 - Nat Genet. 1996 Feb;12(2):191-4 – reference: 10198641 - Mol Cell. 1999 Mar;3(3):389-95 – reference: 16446310 - Hum Mol Genet. 2006 Mar 15;15(6):831-8 – reference: 16998503 - Oncogene. 2006 Sep 25;25(43):5885-97 – reference: 16522673 - Bioinformatics. 2006 May 1;22(9):1111-21 – reference: 12788999 - N Engl J Med. 2003 Jun 5;348(23):2339-47 – reference: 12419249 - Cell. 2002 Nov 1;111(3):393-405 – reference: 11832208 - Cell. 2002 Jan 25;108(2):171-82 – reference: 8290271 - Oncogene. 1994 Feb;9(2):603-9 – reference: 9288052 - Lancet. 1997 Aug 30;350(9078):638-9 – reference: 11309499 - Proc Natl Acad Sci U S A. 2001 Apr 24;98(9):5116-21 – reference: 12957283 - Cancer Cell. 2003 Aug;4(2):89-94 – reference: 11694875 - Nat Genet. 2001 Dec;29(4):418-25 – reference: 12001987 - Nat Rev Cancer. 2002 Apr;2(4):251-65 – reference: 11100717 - Nature. 2000 Nov 23;408(6811):429-32 – reference: 15829966 - Nature. 2005 Apr 14;434(7035):913-7 – reference: 9701363 - J Natl Cancer Inst. 1998 Aug 5;90(15):1138-45 – reference: 12829800 - Proc Natl Acad Sci U S A. 2003 Jul 8;100(14):8418-23 – reference: 12237281 - J Natl Cancer Inst. 2002 Sep 18;94(18):1358-65 – reference: 1552940 - Nature. 1992 Mar 19;356(6366):215-21 – reference: 8674108 - Cell. 1996 Jun 28;85(7):1009-23 – reference: 15343273 - Nat Rev Cancer. 2004 Sep;4(9):665-76 – reference: 16241993 - Histopathology. 2005 Nov;47(5):458-66 – reference: 16395311 - Nature. 2006 Feb 23;439(7079):993-7 – reference: 10963602 - Nature. 2000 Aug 17;406(6797):747-52 – reference: 17626183 - Proc Natl Acad Sci U S A. 2007 Jul 17;104(29):12117-22 – reference: 14707179 - Genome Res. 2004 Jan;14(1):188-96 – reference: 7922305 - Curr Biol. 1994 Jan 1;4(1):1-7 – reference: 16033833 - Clin Cancer Res. 2005 Jul 15;11(14):5175-80 – reference: 16199517 - Proc Natl Acad Sci U S A. 2005 Oct 25;102(43):15545-50 – reference: 8596939 - Science. 1996 Mar 22;271(5256):1744-7 – reference: 17097565 - Cancer Cell. 2006 Nov;10(5):437-49 |
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| Snippet | Women carrying germ-line mutations in BRCA1 are strongly predisposed to developing breast cancers with characteristic features also observed in sporadic... |
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| SubjectTerms | Alleles Animals Biomarkers, Tumor - metabolism BRCA1 Protein - deficiency Breast Neoplasms - pathology Cluster Analysis Epithelial Cells - pathology Female Genomic Instability - genetics Humans Loss of Heterozygosity Mammary Neoplasms, Animal - classification Mammary Neoplasms, Animal - pathology Mice Mutation - genetics Species Specificity Tumor Suppressor Protein p53 - deficiency |
| Title | Somatic loss of BRCA1 and p53 in mice induces mammary tumors with features of human BRCA1-mutated basal-like breast cancer |
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