Cross-species comparison of aCGH data from mouse and human BRCA1- and BRCA2-mutated breast cancers
Background Genomic gains and losses are a result of genomic instability in many types of cancers. BRCA1 - and BRCA2 -mutated breast cancers are associated with increased amounts of chromosomal aberrations, presumably due their functions in genome repair. Some of these genomic aberrations may harbor...
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| Published in: | BMC cancer Vol. 10; no. 1; p. 455 |
|---|---|
| Main Authors: | , , , , , , , , , , , |
| Format: | Journal Article |
| Language: | English |
| Published: |
London
BioMed Central
24.08.2010
BioMed Central Ltd Springer Nature B.V BMC |
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| ISSN: | 1471-2407, 1471-2407 |
| Online Access: | Get full text |
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| Abstract | Background
Genomic gains and losses are a result of genomic instability in many types of cancers.
BRCA1
- and
BRCA2
-mutated breast cancers are associated with increased amounts of chromosomal aberrations, presumably due their functions in genome repair. Some of these genomic aberrations may harbor genes whose absence or overexpression may give rise to cellular growth advantage. So far, it has not been easy to identify the driver genes underlying gains and losses. A powerful approach to identify these driver genes could be a cross-species comparison of array comparative genomic hybridization (aCGH) data from cognate mouse and human tumors. Orthologous regions of mouse and human tumors that are commonly gained or lost might represent essential genomic regions selected for gain or loss during tumor development.
Methods
To identify genomic regions that are associated with
BRCA1
- and
BRCA2
-mutated breast cancers we compared aCGH data from 130 mouse
Brca1
Δ/Δ
;p53
Δ/Δ
,
Brca2
Δ/Δ
;p53
Δ/Δ
and
p53
Δ/Δ
mammary tumor groups with 103 human
BRCA1-
mutated,
BRCA2-
mutated and non-hereditary breast cancers.
Results
Our genome-wide cross-species analysis yielded a complete collection of loci and genes that are commonly gained or lost in mouse and human breast cancer. Principal common CNAs were the well known
MYC
-associated gain and
RB1/INTS6
-associated loss that occurred in all mouse and human tumor groups, and the
AURKA
-associated gain occurred in BRCA2-related tumors from both species. However, there were also important differences between tumor profiles of both species, such as the prominent gain on chromosome 10 in mouse
Brca2
Δ/Δ
;p53
Δ/Δ
tumors and the PIK3CA associated 3q gain in human
BRCA1-
mutated tumors, which occurred in tumors from one species but not in tumors from the other species. This disparity in recurrent aberrations in mouse and human tumors might be due to differences in tumor cell type or genomic organization between both species.
Conclusions
The selection of the oncogenome during mouse and human breast tumor development is markedly different, apart from the MYC gain and RB1-associated loss. These differences should be kept in mind when using mouse models for preclinical studies. |
|---|---|
| AbstractList | Genomic gains and losses are a result of genomic instability in many types of cancers. BRCA1- and BRCA2-mutated breast cancers are associated with increased amounts of chromosomal aberrations, presumably due their functions in genome repair. Some of these genomic aberrations may harbor genes whose absence or overexpression may give rise to cellular growth advantage. So far, it has not been easy to identify the driver genes underlying gains and losses. A powerful approach to identify these driver genes could be a cross-species comparison of array comparative genomic hybridization (aCGH) data from cognate mouse and human tumors. Orthologous regions of mouse and human tumors that are commonly gained or lost might represent essential genomic regions selected for gain or loss during tumor development. To identify genomic regions that are associated with BRCA1- and BRCA2-mutated breast cancers we compared aCGH data from 130 mouse Brca1.sup.[DELTA]/[DELTA].sup.;p53.sup.[DELTA]/[DELTA].sup., Brca2.sup.[DELTA]/[DELTA].sup.;p53.sup.[DELTA]/[DELTA] .sup.and p53.sup.[DELTA]/[DELTA] .sup.mammary tumor groups with 103 human BRCA1-mutated, BRCA2-mutated and non-hereditary breast cancers. Our genome-wide cross-species analysis yielded a complete collection of loci and genes that are commonly gained or lost in mouse and human breast cancer. Principal common CNAs were the well known MYC-associated gain and RB1/INTS6-associated loss that occurred in all mouse and human tumor groups, and the AURKA-associated gain occurred in BRCA2-related tumors from both species. However, there were also important differences between tumor profiles of both species, such as the prominent gain on chromosome 10 in mouse Brca2.sup.[DELTA]/[DELTA].sup.;p53.sup.[DELTA]/[DELTA] .sup.tumors and the PIK3CA associated 3q gain in human BRCA1-mutated tumors, which occurred in tumors from one species but not in tumors from the other species. This disparity in recurrent aberrations in mouse and human tumors might be due to differences in tumor cell type or genomic organization between both species. The selection of the oncogenome during mouse and human breast tumor development is markedly different, apart from the MYC gain and RB1-associated loss. These differences should be kept in mind when using mouse models for preclinical studies. Abstract Background: Genomic gains and losses are a result of genomic instability in many types of cancers. BRCA1 - and BRCA2 -mutated breast cancers are associated with increased amounts of chromosomal aberrations, presumably due their functions in genome repair. Some of these genomic aberrations may harbor genes whose absence or overexpression may give rise to cellular growth advantage. So far, it has not been easy to identify the driver genes underlying gains and losses. A powerful approach to identify these driver genes could be a cross-species comparison of array comparative genomic hybridization (aCGH) data from cognate mouse and human tumors. Orthologous regions of mouse and human tumors that are commonly gained or lost might represent essential genomic regions selected for gain or loss during tumor development. Methods: To identify genomic regions that are associated with BRCA1 - and BRCA2 -mutated breast cancers we compared aCGH data from 130 mouse Brca1Δ/Δ;p53Δ/Δ , Brca2Δ/Δ;p53Δ/Δ and p53Δ/Δ mammary tumor groups with 103 human BRCA1- mutated, BRCA2- mutated and non-hereditary breast cancers. Results: Our genome-wide cross-species analysis yielded a complete collection of loci and genes that are commonly gained or lost in mouse and human breast cancer. Principal common CNAs were the well known MYC -associated gain and RB1/INTS6 -associated loss that occurred in all mouse and human tumor groups, and the AURKA -associated gain occurred in BRCA2-related tumors from both species. However, there were also important differences between tumor profiles of both species, such as the prominent gain on chromosome 10 in mouse Brca2Δ/Δ;p53Δ/Δ tumors and the PIK3CA associated 3q gain in human BRCA1- mutated tumors, which occurred in tumors from one species but not in tumors from the other species. This disparity in recurrent aberrations in mouse and human tumors might be due to differences in tumor cell type or genomic organization between both species. Conclusions: The selection of the oncogenome during mouse and human breast tumor development is markedly different, apart from the MYC gain and RB1-associated loss. These differences should be kept in mind when using mouse models for preclinical studies. Genomic gains and losses are a result of genomic instability in many types of cancers. BRCA1- and BRCA2-mutated breast cancers are associated with increased amounts of chromosomal aberrations, presumably due their functions in genome repair. Some of these genomic aberrations may harbor genes whose absence or overexpression may give rise to cellular growth advantage. So far, it has not been easy to identify the driver genes underlying gains and losses. A powerful approach to identify these driver genes could be a cross-species comparison of array comparative genomic hybridization (aCGH) data from cognate mouse and human tumors. Orthologous regions of mouse and human tumors that are commonly gained or lost might represent essential genomic regions selected for gain or loss during tumor development. To identify genomic regions that are associated with BRCA1- and BRCA2-mutated breast cancers we compared aCGH data from 130 mouse Brca1Δ/Δ;p53Δ/Δ, Brca2Δ/Δ;p53Δ/Δ and p53Δ/Δ mammary tumor groups with 103 human BRCA1-mutated, BRCA2-mutated and non-hereditary breast cancers. Our genome-wide cross-species analysis yielded a complete collection of loci and genes that are commonly gained or lost in mouse and human breast cancer. Principal common CNAs were the well known MYC-associated gain and RB1/INTS6-associated loss that occurred in all mouse and human tumor groups, and the AURKA-associated gain occurred in BRCA2-related tumors from both species. However, there were also important differences between tumor profiles of both species, such as the prominent gain on chromosome 10 in mouse Brca2Δ/Δ;p53Δ/Δ tumors and the PIK3CA associated 3q gain in human BRCA1-mutated tumors, which occurred in tumors from one species but not in tumors from the other species. This disparity in recurrent aberrations in mouse and human tumors might be due to differences in tumor cell type or genomic organization between both species. The selection of the oncogenome during mouse and human breast tumor development is markedly different, apart from the MYC gain and RB1-associated loss. These differences should be kept in mind when using mouse models for preclinical studies. Background Genomic gains and losses are a result of genomic instability in many types of cancers. BRCA1- and BRCA2-mutated breast cancers are associated with increased amounts of chromosomal aberrations, presumably due their functions in genome repair. Some of these genomic aberrations may harbor genes whose absence or overexpression may give rise to cellular growth advantage. So far, it has not been easy to identify the driver genes underlying gains and losses. A powerful approach to identify these driver genes could be a cross-species comparison of array comparative genomic hybridization (aCGH) data from cognate mouse and human tumors. Orthologous regions of mouse and human tumors that are commonly gained or lost might represent essential genomic regions selected for gain or loss during tumor development. Methods To identify genomic regions that are associated with BRCA1- and BRCA2-mutated breast cancers we compared aCGH data from 130 mouse Brca1.sup.[DELTA]/[DELTA].sup.;p53.sup.[DELTA]/[DELTA].sup., Brca2.sup.[DELTA]/[DELTA].sup.;p53.sup.[DELTA]/[DELTA] .sup.and p53.sup.[DELTA]/[DELTA] .sup.mammary tumor groups with 103 human BRCA1-mutated, BRCA2-mutated and non-hereditary breast cancers. Results Our genome-wide cross-species analysis yielded a complete collection of loci and genes that are commonly gained or lost in mouse and human breast cancer. Principal common CNAs were the well known MYC-associated gain and RB1/INTS6-associated loss that occurred in all mouse and human tumor groups, and the AURKA-associated gain occurred in BRCA2-related tumors from both species. However, there were also important differences between tumor profiles of both species, such as the prominent gain on chromosome 10 in mouse Brca2.sup.[DELTA]/[DELTA].sup.;p53.sup.[DELTA]/[DELTA] .sup.tumors and the PIK3CA associated 3q gain in human BRCA1-mutated tumors, which occurred in tumors from one species but not in tumors from the other species. This disparity in recurrent aberrations in mouse and human tumors might be due to differences in tumor cell type or genomic organization between both species. Conclusions The selection of the oncogenome during mouse and human breast tumor development is markedly different, apart from the MYC gain and RB1-associated loss. These differences should be kept in mind when using mouse models for preclinical studies. Genomic gains and losses are a result of genomic instability in many types of cancers. BRCA1- and BRCA2-mutated breast cancers are associated with increased amounts of chromosomal aberrations, presumably due their functions in genome repair. Some of these genomic aberrations may harbor genes whose absence or overexpression may give rise to cellular growth advantage. So far, it has not been easy to identify the driver genes underlying gains and losses. A powerful approach to identify these driver genes could be a cross-species comparison of array comparative genomic hybridization (aCGH) data from cognate mouse and human tumors. Orthologous regions of mouse and human tumors that are commonly gained or lost might represent essential genomic regions selected for gain or loss during tumor development.BACKGROUNDGenomic gains and losses are a result of genomic instability in many types of cancers. BRCA1- and BRCA2-mutated breast cancers are associated with increased amounts of chromosomal aberrations, presumably due their functions in genome repair. Some of these genomic aberrations may harbor genes whose absence or overexpression may give rise to cellular growth advantage. So far, it has not been easy to identify the driver genes underlying gains and losses. A powerful approach to identify these driver genes could be a cross-species comparison of array comparative genomic hybridization (aCGH) data from cognate mouse and human tumors. Orthologous regions of mouse and human tumors that are commonly gained or lost might represent essential genomic regions selected for gain or loss during tumor development.To identify genomic regions that are associated with BRCA1- and BRCA2-mutated breast cancers we compared aCGH data from 130 mouse Brca1Δ/Δ;p53Δ/Δ, Brca2Δ/Δ;p53Δ/Δ and p53Δ/Δ mammary tumor groups with 103 human BRCA1-mutated, BRCA2-mutated and non-hereditary breast cancers.METHODSTo identify genomic regions that are associated with BRCA1- and BRCA2-mutated breast cancers we compared aCGH data from 130 mouse Brca1Δ/Δ;p53Δ/Δ, Brca2Δ/Δ;p53Δ/Δ and p53Δ/Δ mammary tumor groups with 103 human BRCA1-mutated, BRCA2-mutated and non-hereditary breast cancers.Our genome-wide cross-species analysis yielded a complete collection of loci and genes that are commonly gained or lost in mouse and human breast cancer. Principal common CNAs were the well known MYC-associated gain and RB1/INTS6-associated loss that occurred in all mouse and human tumor groups, and the AURKA-associated gain occurred in BRCA2-related tumors from both species. However, there were also important differences between tumor profiles of both species, such as the prominent gain on chromosome 10 in mouse Brca2Δ/Δ;p53Δ/Δ tumors and the PIK3CA associated 3q gain in human BRCA1-mutated tumors, which occurred in tumors from one species but not in tumors from the other species. This disparity in recurrent aberrations in mouse and human tumors might be due to differences in tumor cell type or genomic organization between both species.RESULTSOur genome-wide cross-species analysis yielded a complete collection of loci and genes that are commonly gained or lost in mouse and human breast cancer. Principal common CNAs were the well known MYC-associated gain and RB1/INTS6-associated loss that occurred in all mouse and human tumor groups, and the AURKA-associated gain occurred in BRCA2-related tumors from both species. However, there were also important differences between tumor profiles of both species, such as the prominent gain on chromosome 10 in mouse Brca2Δ/Δ;p53Δ/Δ tumors and the PIK3CA associated 3q gain in human BRCA1-mutated tumors, which occurred in tumors from one species but not in tumors from the other species. This disparity in recurrent aberrations in mouse and human tumors might be due to differences in tumor cell type or genomic organization between both species.The selection of the oncogenome during mouse and human breast tumor development is markedly different, apart from the MYC gain and RB1-associated loss. These differences should be kept in mind when using mouse models for preclinical studies.CONCLUSIONSThe selection of the oncogenome during mouse and human breast tumor development is markedly different, apart from the MYC gain and RB1-associated loss. These differences should be kept in mind when using mouse models for preclinical studies. Background Genomic gains and losses are a result of genomic instability in many types of cancers. BRCA1 - and BRCA2 -mutated breast cancers are associated with increased amounts of chromosomal aberrations, presumably due their functions in genome repair. Some of these genomic aberrations may harbor genes whose absence or overexpression may give rise to cellular growth advantage. So far, it has not been easy to identify the driver genes underlying gains and losses. A powerful approach to identify these driver genes could be a cross-species comparison of array comparative genomic hybridization (aCGH) data from cognate mouse and human tumors. Orthologous regions of mouse and human tumors that are commonly gained or lost might represent essential genomic regions selected for gain or loss during tumor development. Methods To identify genomic regions that are associated with BRCA1 - and BRCA2 -mutated breast cancers we compared aCGH data from 130 mouse Brca1 Δ/Δ ;p53 Δ/Δ , Brca2 Δ/Δ ;p53 Δ/Δ and p53 Δ/Δ mammary tumor groups with 103 human BRCA1- mutated, BRCA2- mutated and non-hereditary breast cancers. Results Our genome-wide cross-species analysis yielded a complete collection of loci and genes that are commonly gained or lost in mouse and human breast cancer. Principal common CNAs were the well known MYC -associated gain and RB1/INTS6 -associated loss that occurred in all mouse and human tumor groups, and the AURKA -associated gain occurred in BRCA2-related tumors from both species. However, there were also important differences between tumor profiles of both species, such as the prominent gain on chromosome 10 in mouse Brca2 Δ/Δ ;p53 Δ/Δ tumors and the PIK3CA associated 3q gain in human BRCA1- mutated tumors, which occurred in tumors from one species but not in tumors from the other species. This disparity in recurrent aberrations in mouse and human tumors might be due to differences in tumor cell type or genomic organization between both species. Conclusions The selection of the oncogenome during mouse and human breast tumor development is markedly different, apart from the MYC gain and RB1-associated loss. These differences should be kept in mind when using mouse models for preclinical studies. |
| ArticleNumber | 455 |
| Audience | Academic |
| Author | van Beers, Erik Liu, Xiaoling Joosse, Simon A Klarenbeek, Sjoerd Schut, Eva Velds, Arno Jonkers, Jos Holstege, Henne Nederlof, Petra M Klijn, Christiaan N Kerkhoven, Ron Wessels, Lodewyk FA |
| AuthorAffiliation | 1 Division of Molecular Biology, Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands 8 Faculty of Electrical Engineering, Mathematics and Computer Science, Delft University of Technology, Delft, The Netherlands 5 Central Microarray Facility, Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands 4 Skyline-Diagnostics B.V., Dr. Molewaterplein 50, 3015 GE Rotterdam, The Netherlands 6 Biomedical Analysis Center, Tsinghua University, Beijing, 100084, China 2 Division of Clinical Genetics, VU Medical Center, de Boelelaan 1118, 1081 HV Amsterdam, The Netherlands 3 Division of Experimental Therapy, Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands 7 Institute of Tumor Biology, University Medical Center Hamburg Eppendorf, Martinistrasse 52, 20246 Hamburg, Germany |
| AuthorAffiliation_xml | – name: 7 Institute of Tumor Biology, University Medical Center Hamburg Eppendorf, Martinistrasse 52, 20246 Hamburg, Germany – name: 2 Division of Clinical Genetics, VU Medical Center, de Boelelaan 1118, 1081 HV Amsterdam, The Netherlands – name: 5 Central Microarray Facility, Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands – name: 4 Skyline-Diagnostics B.V., Dr. Molewaterplein 50, 3015 GE Rotterdam, The Netherlands – name: 6 Biomedical Analysis Center, Tsinghua University, Beijing, 100084, China – name: 8 Faculty of Electrical Engineering, Mathematics and Computer Science, Delft University of Technology, Delft, The Netherlands – name: 1 Division of Molecular Biology, Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands – name: 3 Division of Experimental Therapy, Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands |
| Author_xml | – sequence: 1 givenname: Henne surname: Holstege fullname: Holstege, Henne organization: Division of Molecular Biology, Netherlands Cancer Institute, Division of Clinical Genetics, VU Medical Center – sequence: 2 givenname: Erik surname: van Beers fullname: van Beers, Erik organization: Division of Experimental Therapy, Netherlands Cancer Institute, Skyline-Diagnostics B.V., Dr – sequence: 3 givenname: Arno surname: Velds fullname: Velds, Arno organization: Central Microarray Facility, Netherlands Cancer Institute – sequence: 4 givenname: Xiaoling surname: Liu fullname: Liu, Xiaoling organization: Division of Molecular Biology, Netherlands Cancer Institute, Biomedical Analysis Center, Tsinghua University – sequence: 5 givenname: Simon A surname: Joosse fullname: Joosse, Simon A organization: Division of Experimental Therapy, Netherlands Cancer Institute, Institute of Tumor Biology, University Medical Center Hamburg Eppendorf – sequence: 6 givenname: Sjoerd surname: Klarenbeek fullname: Klarenbeek, Sjoerd organization: Division of Molecular Biology, Netherlands Cancer Institute – sequence: 7 givenname: Eva surname: Schut fullname: Schut, Eva organization: Division of Molecular Biology, Netherlands Cancer Institute – sequence: 8 givenname: Ron surname: Kerkhoven fullname: Kerkhoven, Ron organization: Central Microarray Facility, Netherlands Cancer Institute – sequence: 9 givenname: Christiaan N surname: Klijn fullname: Klijn, Christiaan N organization: Division of Molecular Biology, Netherlands Cancer Institute – sequence: 10 givenname: Lodewyk FA surname: Wessels fullname: Wessels, Lodewyk FA organization: Division of Molecular Biology, Netherlands Cancer Institute, Faculty of Electrical Engineering, Mathematics and Computer Science, Delft University of Technology – sequence: 11 givenname: Petra M surname: Nederlof fullname: Nederlof, Petra M organization: Division of Experimental Therapy, Netherlands Cancer Institute – sequence: 12 givenname: Jos surname: Jonkers fullname: Jonkers, Jos email: j.jonkers@nki.nl organization: Division of Molecular Biology, Netherlands Cancer Institute |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/20735817$$D View this record in MEDLINE/PubMed |
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| ContentType | Journal Article |
| Copyright | Holstege et al; licensee BioMed Central Ltd. 2010 This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. COPYRIGHT 2010 BioMed Central Ltd. 2010 Holstege et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Copyright ©2010 Holstege et al; licensee BioMed Central Ltd. 2010 Holstege et al; licensee BioMed Central Ltd. |
| Copyright_xml | – notice: Holstege et al; licensee BioMed Central Ltd. 2010 This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. – notice: COPYRIGHT 2010 BioMed Central Ltd. – notice: 2010 Holstege et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. – notice: Copyright ©2010 Holstege et al; licensee BioMed Central Ltd. 2010 Holstege et al; licensee BioMed Central Ltd. |
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| DOI | 10.1186/1471-2407-10-455 |
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Genomic gains and losses are a result of genomic instability in many types of cancers.
BRCA1
- and
BRCA2
-mutated breast cancers are associated with... Genomic gains and losses are a result of genomic instability in many types of cancers. BRCA1- and BRCA2-mutated breast cancers are associated with increased... Background Genomic gains and losses are a result of genomic instability in many types of cancers. BRCA1- and BRCA2-mutated breast cancers are associated with... Abstract Background: Genomic gains and losses are a result of genomic instability in many types of cancers. BRCA1 - and BRCA2 -mutated breast cancers are... Abstract Background Genomic gains and losses are a result of genomic instability in many types of cancers. BRCA1- and BRCA2-mutated breast cancers are... |
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| SubjectTerms | Animals Artificial chromosomes Biology Biomarkers, Tumor - genetics Biomarkers, Tumor - metabolism Biomedical and Life Sciences Biomedicine BRCA mutations BRCA1 Protein - genetics BRCA2 Protein - genetics Breast cancer Breast Neoplasms - classification Breast Neoplasms - genetics Breast Neoplasms - pathology Cancer Research Chromosome Aberrations Comparative Genomic Hybridization Computer science Deoxyribonucleic acid DNA Female Females Gene Expression Profiling Genetic aspects Genetic testing Genetics Genomes Genomic Instability genomics and epigenetics Health aspects Health Promotion and Disease Prevention Humans Hybridization Medicine/Public Health Mice Mutation - genetics Oligonucleotide Array Sequence Analysis Oncology Research Article Reverse Transcriptase Polymerase Chain Reaction Risk factors RNA, Messenger - genetics Species Specificity Statistical analysis Statistical methods Surgical Oncology Tumors |
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| Title | Cross-species comparison of aCGH data from mouse and human BRCA1- and BRCA2-mutated breast cancers |
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