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  • Female  (7)
  • Nature Publishing Group (NPG)  (7)
  • American Geophysical Union (AGU)
  • American Institute of Physics
  • National Academy of Sciences
  • 2005-2009  (7)
  • 1955-1959
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  • 1
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    An internal thermal sensor controlling temperature preference in Drosophila (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-06-13
    Description: Animals from flies to humans are able to distinguish subtle gradations in temperature and show strong temperature preferences. Animals move to environments of optimal temperature and some manipulate the temperature of their surroundings, as humans do using clothing and shelter. Despite the ubiquitous influence of environmental temperature on animal behaviour, the neural circuits and strategies through which animals select a preferred temperature remain largely unknown. Here we identify a small set of warmth-activated anterior cell (AC) neurons located in the Drosophila brain, the function of which is critical for preferred temperature selection. AC neuron activation occurs just above the fly's preferred temperature and depends on dTrpA1, an ion channel that functions as a molecular sensor of warmth. Flies that selectively express dTrpA1 in the AC neurons select normal temperatures, whereas flies in which dTrpA1 function is reduced or eliminated choose warmer temperatures. This internal warmth-sensing pathway promotes avoidance of slightly elevated temperatures and acts together with a distinct pathway for cold avoidance to set the fly's preferred temperature. Thus, flies select a preferred temperature by using a thermal sensing pathway tuned to trigger avoidance of temperatures that deviate even slightly from the preferred temperature. This provides a potentially general strategy for robustly selecting a narrow temperature range optimal for survival.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2730888/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2730888/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hamada, Fumika N -- Rosenzweig, Mark -- Kang, Kyeongjin -- Pulver, Stefan R -- Ghezzi, Alfredo -- Jegla, Timothy J -- Garrity, Paul A -- P01 NS044232/NS/NINDS NIH HHS/ -- P01 NS044232-060002/NS/NINDS NIH HHS/ -- P01 NS044232-070002/NS/NINDS NIH HHS/ -- P30 NS045713/NS/NINDS NIH HHS/ -- P30 NS045713-069006/NS/NINDS NIH HHS/ -- P30 NS045713S10/NS/NINDS NIH HHS/ -- R01 EY013874/EY/NEI NIH HHS/ -- R01 EY013874-06/EY/NEI NIH HHS/ -- R01 EY13874/EY/NEI NIH HHS/ -- R01 MH067284/MH/NIMH NIH HHS/ -- R01 MH067284-05/MH/NIMH NIH HHS/ -- RR16780/RR/NCRR NIH HHS/ -- England -- Nature. 2008 Jul 10;454(7201):217-20. doi: 10.1038/nature07001. Epub 2008 Jun 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Center for Behavioral Genomics, Volen Center for Complex Systems, Biology Department, Brandeis University MS-008, 415 South Street, Waltham, Massachusetts 02454, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18548007" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Avoidance Learning ; Body Temperature ; Choice Behavior/*physiology ; Drosophila Proteins/genetics/*metabolism ; Drosophila melanogaster/growth & development/*physiology ; Female ; Larva ; Molecular Sequence Data ; Neurons/metabolism ; Oocytes/metabolism ; TRPC Cation Channels/genetics/*metabolism ; *Temperature ; Xenopus laevis
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
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    HDAC2 negatively regulates memory formation and synaptic plasticity (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-05-09
    Description: Chromatin modifications, especially histone-tail acetylation, have been implicated in memory formation. Increased histone-tail acetylation induced by inhibitors of histone deacetylases (HDACis) facilitates learning and memory in wild-type mice as well as in mouse models of neurodegeneration. Harnessing the therapeutic potential of HDACis requires knowledge of the specific HDAC family member(s) linked to cognitive enhancement. Here we show that neuron-specific overexpression of HDAC2, but not that of HDAC1, decreased dendritic spine density, synapse number, synaptic plasticity and memory formation. Conversely, Hdac2 deficiency resulted in increased synapse number and memory facilitation, similar to chronic treatment with HDACis in mice. Notably, reduced synapse number and learning impairment of HDAC2-overexpressing mice were ameliorated by chronic treatment with HDACis. Correspondingly, treatment with HDACis failed to further facilitate memory formation in Hdac2-deficient mice. Furthermore, analysis of promoter occupancy revealed an association of HDAC2 with the promoters of genes implicated in synaptic plasticity and memory formation. Taken together, our results suggest that HDAC2 functions in modulating synaptic plasticity and long-lasting changes of neural circuits, which in turn negatively regulates learning and memory. These observations encourage the development and testing of HDAC2-selective inhibitors for human diseases associated with memory impairment.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3498958/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3498958/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Guan, Ji-Song -- Haggarty, Stephen J -- Giacometti, Emanuela -- Dannenberg, Jan-Hermen -- Joseph, Nadine -- Gao, Jun -- Nieland, Thomas J F -- Zhou, Ying -- Wang, Xinyu -- Mazitschek, Ralph -- Bradner, James E -- DePinho, Ronald A -- Jaenisch, Rudolf -- Tsai, Li-Huei -- R01 DA028301/DA/NIDA NIH HHS/ -- R01 DA028301-02/DA/NIDA NIH HHS/ -- R01 NS051874/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2009 May 7;459(7243):55-60. doi: 10.1038/nature07925.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Picower Institute for Learning and Memory, Department of Brain and Cognitive Sciences.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19424149" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Butyrates/pharmacology ; Dendritic Spines/physiology ; Electrical Synapses/*physiology ; Female ; Gene Expression Regulation ; Hippocampus/metabolism ; Histone Deacetylase 1 ; Histone Deacetylase 2 ; Histone Deacetylase Inhibitors ; Histone Deacetylases/deficiency/genetics/*metabolism ; Hydroxamic Acids/pharmacology ; Learning/drug effects ; Male ; Memory/drug effects/*physiology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Neurons/metabolism ; Promoter Regions, Genetic/genetics ; Repressor Proteins/antagonists & inhibitors/genetics/*metabolism ; Sodium/pharmacology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
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    The avian Z-linked gene DMRT1 is required for male sex determination in the chicken (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-08-28
    Description: Sex in birds is chromosomally based, as in mammals, but the sex chromosomes are different and the mechanism of avian sex determination has been a long-standing mystery. In the chicken and all other birds, the homogametic sex is male (ZZ) and the heterogametic sex is female (ZW). Two hypotheses have been proposed for the mechanism of avian sex determination. The W (female) chromosome may carry a dominant-acting ovary determinant. Alternatively, the dosage of a Z-linked gene may mediate sex determination, two doses being required for male development (ZZ). A strong candidate avian sex-determinant under the dosage hypothesis is the conserved Z-linked gene, DMRT1 (doublesex and mab-3-related transcription factor 1). Here we used RNA interference (RNAi) to knock down DMRT1 in early chicken embryos. Reduction of DMRT1 protein expression in ovo leads to feminization of the embryonic gonads in genetically male (ZZ) embryos. Affected males show partial sex reversal, characterized by feminization of the gonads. The feminized left gonad shows female-like histology, disorganized testis cords and a decline in the testicular marker, SOX9. The ovarian marker, aromatase, is ectopically activated. The feminized right gonad shows a more variable loss of DMRT1 and ectopic aromatase activation, suggesting differential sensitivity to DMRT1 between left and right gonads. Germ cells also show a female pattern of distribution in the feminized male gonads. These results indicate that DMRT1 is required for testis determination in the chicken. Our data support the Z dosage hypothesis for avian sex determination.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smith, Craig A -- Roeszler, Kelly N -- Ohnesorg, Thomas -- Cummins, David M -- Farlie, Peter G -- Doran, Timothy J -- Sinclair, Andrew H -- England -- Nature. 2009 Sep 10;461(7261):267-71. doi: 10.1038/nature08298. Epub 2009 Aug 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Murdoch Children's Research Institute and Department of Paediatrics, The University of Melbourne, Royal Children's Hospital, Melbourne, Victoria 3052, Australia. craig.smith@mcri.edu.au〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19710650" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomarkers/analysis ; Cell Line ; Chick Embryo ; Chickens/*genetics/*physiology ; Disorders of Sex Development ; Down-Regulation ; Female ; Gene Dosage/genetics ; Male ; MicroRNAs/genetics/metabolism ; Models, Genetic ; Ovary/embryology/metabolism ; RNA Interference ; SOX9 Transcription Factor/genetics/metabolism ; *Sex Characteristics ; Sex Chromosomes/*genetics ; *Sex Determination Processes ; Testis/embryology/metabolism ; Transcription Factors/deficiency/*genetics/*metabolism
    Print ISSN: 0028-0836
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
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    A variant associated with nicotine dependence, lung cancer and peripheral arterial disease (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-04-04
    Description: Smoking is a leading cause of preventable death, causing about 5 million premature deaths worldwide each year. Evidence for genetic influence on smoking behaviour and nicotine dependence (ND) has prompted a search for susceptibility genes. Furthermore, assessing the impact of sequence variants on smoking-related diseases is important to public health. Smoking is the major risk factor for lung cancer (LC) and is one of the main risk factors for peripheral arterial disease (PAD). Here we identify a common variant in the nicotinic acetylcholine receptor gene cluster on chromosome 15q24 with an effect on smoking quantity, ND and the risk of two smoking-related diseases in populations of European descent. The variant has an effect on the number of cigarettes smoked per day in our sample of smokers. The same variant was associated with ND in a previous genome-wide association study that used low-quantity smokers as controls, and with a similar approach we observe a highly significant association with ND. A comparison of cases of LC and PAD with population controls each showed that the variant confers risk of LC and PAD. The findings provide a case study of a gene-environment interaction, highlighting the role of nicotine addiction in the pathology of other serious diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4539558/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4539558/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thorgeirsson, Thorgeir E -- Geller, Frank -- Sulem, Patrick -- Rafnar, Thorunn -- Wiste, Anna -- Magnusson, Kristinn P -- Manolescu, Andrei -- Thorleifsson, Gudmar -- Stefansson, Hreinn -- Ingason, Andres -- Stacey, Simon N -- Bergthorsson, Jon T -- Thorlacius, Steinunn -- Gudmundsson, Julius -- Jonsson, Thorlakur -- Jakobsdottir, Margret -- Saemundsdottir, Jona -- Olafsdottir, Olof -- Gudmundsson, Larus J -- Bjornsdottir, Gyda -- Kristjansson, Kristleifur -- Skuladottir, Halla -- Isaksson, Helgi J -- Gudbjartsson, Tomas -- Jones, Gregory T -- Mueller, Thomas -- Gottsater, Anders -- Flex, Andrea -- Aben, Katja K H -- de Vegt, Femmie -- Mulders, Peter F A -- Isla, Dolores -- Vidal, Maria J -- Asin, Laura -- Saez, Berta -- Murillo, Laura -- Blondal, Thorsteinn -- Kolbeinsson, Halldor -- Stefansson, Jon G -- Hansdottir, Ingunn -- Runarsdottir, Valgerdur -- Pola, Roberto -- Lindblad, Bengt -- van Rij, Andre M -- Dieplinger, Benjamin -- Haltmayer, Meinhard -- Mayordomo, Jose I -- Kiemeney, Lambertus A -- Matthiasson, Stefan E -- Oskarsson, Hogni -- Tyrfingsson, Thorarinn -- Gudbjartsson, Daniel F -- Gulcher, Jeffrey R -- Jonsson, Steinn -- Thorsteinsdottir, Unnur -- Kong, Augustine -- Stefansson, Kari -- R01 DA017932/DA/NIDA NIH HHS/ -- England -- Nature. 2008 Apr 3;452(7187):638-42. doi: 10.1038/nature06846.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉deCODE Genetics, 101 Reykjavik, Iceland. thorgeir@decode.is〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18385739" target="_blank"〉PubMed〈/a〉
    Keywords: Chromosomes, Human, Pair 15/*genetics ; Europe ; Female ; Genetic Predisposition to Disease/*genetics ; Genotype ; Humans ; Lung Neoplasms/*genetics ; Male ; Multigene Family/genetics ; New Zealand ; Odds Ratio ; Peripheral Vascular Diseases/*genetics ; Polymorphism, Single Nucleotide/*genetics ; Receptors, Nicotinic/*genetics ; Smoking/adverse effects/genetics ; Tobacco Use Disorder/*genetics
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  • 5
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    The pluripotency factor Oct4 interacts with Ctcf and also controls X-chromosome pairing and counting (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-06-19
    Description: Pluripotency of embryonic stem (ES) cells is controlled by defined transcription factors. During differentiation, mouse ES cells undergo global epigenetic reprogramming, as exemplified by X-chromosome inactivation (XCI) in which one female X chromosome is silenced to achieve gene dosage parity between the sexes. Somatic XCI is regulated by homologous X-chromosome pairing and counting, and by the random choice of future active and inactive X chromosomes. XCI and cell differentiation are tightly coupled, as blocking one process compromises the other and dedifferentiation of somatic cells to induced pluripotent stem cells is accompanied by X chromosome reactivation. Recent evidence suggests coupling of Xist expression to pluripotency factors occurs, but how the two are interconnected remains unknown. Here we show that Oct4 (also known as Pou5f1) lies at the top of the XCI hierarchy, and regulates XCI by triggering X-chromosome pairing and counting. Oct4 directly binds Tsix and Xite, two regulatory noncoding RNA genes of the X-inactivation centre, and also complexes with XCI trans-factors, Ctcf and Yy1 (ref. 17), through protein-protein interactions. Depletion of Oct4 blocks homologous X-chromosome pairing and results in the inactivation of both X chromosomes in female cells. Thus, we have identified the first trans-factor that regulates counting, and ascribed new functions to Oct4 during X-chromosome reprogramming.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3057664/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3057664/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Donohoe, Mary E -- Silva, Susana S -- Pinter, Stefan F -- Xu, Na -- Lee, Jeannie T -- GM58839/GM/NIGMS NIH HHS/ -- R01 GM058839/GM/NIGMS NIH HHS/ -- R01 GM058839-10/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2009 Jul 2;460(7251):128-32. doi: 10.1038/nature08098. Epub 2009 Jun 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19536159" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; *Chromosome Pairing ; Female ; Humans ; Male ; Mice ; Octamer Transcription Factor-3/deficiency/genetics/*metabolism ; Protein Binding ; RNA, Long Noncoding ; RNA, Untranslated/genetics ; Repressor Proteins/*metabolism ; SOXB1 Transcription Factors ; Transcriptional Activation ; X Chromosome/*genetics/*metabolism ; X Chromosome Inactivation/*genetics ; YY1 Transcription Factor/metabolism
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  • 6
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    An anatomical signature for literacy (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-10-16
    Description: Language is a uniquely human ability that evolved at some point in the roughly 6,000,000 years since human and chimpanzee lines diverged. Even in the most linguistically impoverished environments, children naturally develop sophisticated language systems. In contrast, reading is a learnt skill that does not develop without intensive tuition and practice. Learning to read is likely to involve ontogenic structural brain changes, but these are nearly impossible to isolate in children owing to concurrent biological, environmental and social maturational changes. In Colombia, guerrillas are re-integrating into mainstream society and learning to read for the first time as adults. This presents a unique opportunity to investigate how literacy changes the brain, without the maturational complications present in children. Here we compare structural brain scans from those who learnt to read as adults (late-literates) with those from a carefully matched set of illiterates. Late-literates had more white matter in the splenium of the corpus callosum and more grey matter in bilateral angular, dorsal occipital, middle temporal, left supramarginal and superior temporal gyri. The importance of these brain regions for skilled reading was investigated in early literates, who learnt to read as children. We found anatomical connections linking the left and right angular and dorsal occipital gyri through the area of the corpus callosum where white matter was higher in late-literates than in illiterates; that reading, relative to object naming, increased the interhemispheric functional connectivity between the left and right angular gyri; and that activation in the left angular gyrus exerts top-down modulation on information flow from the left dorsal occipital gyrus to the left supramarginal gyrus. These findings demonstrate how the regions identified in late-literates interact during reading, relative to object naming, in early literates.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carreiras, Manuel -- Seghier, Mohamed L -- Baquero, Silvia -- Estevez, Adelina -- Lozano, Alfonso -- Devlin, Joseph T -- Price, Cathy J -- 082420/Wellcome Trust/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2009 Oct 15;461(7266):983-6. doi: 10.1038/nature08461.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Basque Center on Cognition Brain and Language, Donostia-San Sebastian 20009, Spain [2] IKERBASQUE, Basque Foundation for Science, Bilbao 48011, Spain. m.carreiras@bcbl.eu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19829380" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Aged ; Brain/*anatomy & histology/*physiology ; Child ; Colombia ; Corpus Callosum/anatomy & histology/physiology ; Educational Status ; Female ; Humans ; Language ; Magnetic Resonance Imaging ; Male ; Middle Aged ; Models, Neurological ; Neural Pathways/physiology ; *Reading ; Speech/physiology ; Young Adult
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  • 7
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    Complex landscapes of somatic rearrangement in human breast cancer genomes (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-12-25
    Description: Multiple somatic rearrangements are often found in cancer genomes; however, the underlying processes of rearrangement and their contribution to cancer development are poorly characterized. Here we use a paired-end sequencing strategy to identify somatic rearrangements in breast cancer genomes. There are more rearrangements in some breast cancers than previously appreciated. Rearrangements are more frequent over gene footprints and most are intrachromosomal. Multiple rearrangement architectures are present, but tandem duplications are particularly common in some cancers, perhaps reflecting a specific defect in DNA maintenance. Short overlapping sequences at most rearrangement junctions indicate that these have been mediated by non-homologous end-joining DNA repair, although varying sequence patterns indicate that multiple processes of this type are operative. Several expressed in-frame fusion genes were identified but none was recurrent. The study provides a new perspective on cancer genomes, highlighting the diversity of somatic rearrangements and their potential contribution to cancer development.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3398135/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3398135/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stephens, Philip J -- McBride, David J -- Lin, Meng-Lay -- Varela, Ignacio -- Pleasance, Erin D -- Simpson, Jared T -- Stebbings, Lucy A -- Leroy, Catherine -- Edkins, Sarah -- Mudie, Laura J -- Greenman, Chris D -- Jia, Mingming -- Latimer, Calli -- Teague, Jon W -- Lau, King Wai -- Burton, John -- Quail, Michael A -- Swerdlow, Harold -- Churcher, Carol -- Natrajan, Rachael -- Sieuwerts, Anieta M -- Martens, John W M -- Silver, Daniel P -- Langerod, Anita -- Russnes, Hege E G -- Foekens, John A -- Reis-Filho, Jorge S -- van 't Veer, Laura -- Richardson, Andrea L -- Borresen-Dale, Anne-Lise -- Campbell, Peter J -- Futreal, P Andrew -- Stratton, Michael R -- 077012/Z/05/Z/Wellcome Trust/United Kingdom -- 088340/Wellcome Trust/United Kingdom -- CA089393/CA/NCI NIH HHS/ -- England -- Nature. 2009 Dec 24;462(7276):1005-10. doi: 10.1038/nature08645.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20033038" target="_blank"〉PubMed〈/a〉
    Keywords: Breast Neoplasms/*genetics ; Cell Line, Tumor ; Cells, Cultured ; *Chromosome Aberrations ; DNA Breaks ; Female ; Gene Rearrangement/*genetics ; Genome, Human/*genetics ; Genomic Library ; Humans ; Sequence Analysis, DNA
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