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BRCA1 is associated with the centrosome during mitosis
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16 Hsu LC, White RL: BRCA1 is associated with the centrosome during mitosis. Proc Natl Acad Sci U S A 1998, 95:12983-12988. This was the first study to show an association between BRCA1 and the centrosome.
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Hsu, L.C.1
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p34cdc2 is located in both nucleus and cytoplasm: Part is centrosomally associated at G2/M and enters vesicles at anaphase
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18 Bailly E, Doree M, Nurse P, Bornens M: p34cdc2 is located in both nucleus and cytoplasm: part is centrosomally associated at G2/M and enters vesicles at anaphase. EMBO J 1989, 8:3985-3995.
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Cell cycle independent interaction of CDC2 with the centrosome, which is associated with the nuclear matrix-intermediate filament scaffold
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19 Pockwinse SM, Krockmalnic G, Doxsey SJ, Nickerson J, Lian JB, van Wijnen AJ, et al.: Cell cycle independent interaction of CDC2 with the centrosome, which is associated with the nuclear matrix-intermediate filament scaffold. Proc Natl Acad Sci U S A 1997, 94(7):3022-3027.
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21 Brown CR, Doxsey SJ, White E, Welch WJ: Both viral (adenovirus E1B) and cellular (hsp 70, p53) components interact with centrosomes. J Cell Physiol 1994, 160:47-60.
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23
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Centrosome amplification and a defective G2-M cell cycle checkpoint induce genetic instability in BRCA1 exon 11 isoform-deficient cells
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23 Xu X, Weaver Z, Linke SP, Li C, Gotay J, Wang XW, et al.: Centrosome amplification and a defective G2-M cell cycle checkpoint induce genetic instability in BRCA1 exon 11 isoform-deficient cells. Mol Cell 1999, 3:389-395. This well-controlled study documents a defective G2-M checkpoint, chromosomal abnormalities, multiple centrosomes, and aneuploidy in mouse embryo fibroblasts with a targeted deletion of BRCA1.
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BRCA1 interacts with components of the histone deacetylase complex
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25 Yarden RI, Bordy LC: BRCA1 interacts with components of the histone deacetylase complex. Proc Natl Acad Sci U S A 1999, 96:4983-4988. The interaction of BRCA1 with components of the histone deacetylase complex, retinoblastoma protein, and retinoblastoma protein-binding proteins is documented.
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Proc Natl Acad Sci U S A
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Yarden, R.I.1
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26
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Induction of GADD45 and JNK/SAPK-dependent apoptosis following inducible expression of BRCA1
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26 Harkin DP, Bean JM, Miklos D, Song YH, Truong VB, Englert C, et al.: Induction of GADD45 and JNK/SAPK-dependent apoptosis following inducible expression of BRCA1. Cell 1999, 97:575-586. This elegant study suggests a p53-independent BRCA1-induced apoptotic pathway.
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Harkin, D.P.1
Bean, J.M.2
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27
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BRCA1 required for transcription-coupled repair of oxidative DNA damage
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27 Gowen LC, Avrutskaya AV, Latour AM, Koller BH, Leadon SA: BRCA1 required for transcription-coupled repair of oxidative DNA damage. Science 1998, 281:1009-1012. This study indicates that BRCA1 participates in transcription-coupled repair of DNA damage induced by ionizing radiation or oxidative damage but not by ultraviolet radiation.
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Gowen, L.C.1
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28
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BRCA1 expression restores radiation resistance in BRCA1-defective cancer cells through enhancement transcription-coupled repair
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28 Abbott DW, Thompson ME, Robinson-Benion C, Tomlinson G, Jensen RA, Holt JT: BRCA1 expression restores radiation resistance in BRCA1-defective cancer cells through enhancement transcription-coupled repair. J Biol Chem 1999, 274:18808-18812. This study documents that human cancer cells containing mutated BRCA1 are hypersensitive to ionizing radiation that can be reversed by the expression of nonmutated forms of BRCA1.
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29
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BRCA1 deficiency results in early embryonic lethality characterized by neuroepithelial abnormalities
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29 Gowen LC, Johnson BL, Latour AM, Sulik KK, Koller BH: BRCA1 deficiency results in early embryonic lethality characterized by neuroepithelial abnormalities. Nat Genet 1996 12:191-194.
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30
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The tumor suppressor gene BRCA1 is required for embryonic cellular proliferation in the mouse
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30 Hakem R, de la Pompa JL, Sirard C, Mo R, Woo M, Hakem A, et al.: The tumor suppressor gene BRCA1 is required for embryonic cellular proliferation in the mouse. Cell 1996, 85:1009-1023.
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Hakem, R.1
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31
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Inactivation of the mouse BRCA1 gene leads to failure in the morphogenesis of the egg cylinder in early postimplantation development
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31 Liu C, Flesken-Nikitin A, Li S, Zeng Y, Lee WH: Inactivation of the mouse BRCA1 gene leads to failure in the morphogenesis of the egg cylinder in early postimplantation development. Genes Dev 1996, 10:1835-1843.
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32
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Conditional mutation of BRCA1 in mammary epithelial cells results in blunted ductal morphogenesis and tumour formation
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32 Xu X, Wagner KU, Larson D, Weaver Z, Li C, Ried T, et al: Conditional mutation of BRCA1 in mammary epithelial cells results in blunted ductal morphogenesis and tumour formation. Nat Genet 1999, 22:37-43. This elegant paper describes the first significant model system to study the genetic pathways dysregulated in familial breast cancer.
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Xu, X.1
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33 Shiloh Y: Ataxia-telangiectasia, ATM, and genomic stability: maintaining a delicate balance. Two international workshops on ataxia-telangiectasia, related disorders, and the ATM protein. Biochim Biophys Acta 1998, 1378:R11-R18. This is an excellent review of the ATM gene and the ATM protein.
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35 Hoekstra MF: Responses to DNA damage and regulation of cell cycle checkpoints by the ATM protein kinase family. Curr Opin Genet Dev 1997, 7:170-175.
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39 Vorechovsky I, Luo L, Lindblom A, Negrini M, Webster AD, Croce CM, Hammarstrom L: ATM mutations in cancer families. Cancer Res 1996, 56:4130-4133.
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Heterozygous ATM mutations do not contribute to early onset of breast cancer
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40 FitzGerald MG, Bean JM, Hegde SR, Unsal H, MacDonald DJ, Harkin DP, et al.: Heterozygous ATM mutations do not contribute to early onset of breast cancer. Nat Genet 1997, 15:307-310.
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Absence of linkage to the ataxia telangiectasia locus in familial breast cancer
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Molecular genotyping shows that ataxia-telangiectasia heterozygotes are predisposed to breast cancer
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43 Chen J, Birkholtz GG, Lindblom P, Rubio C, Lindblom A: The role of ataxia-telangiectasia heterozygotes in familial breast cancer. Cancer Res 1998, 58:1376-1379. This study suggests that heterozygous ATM mutations make a minimal contribution to familial breast cancer and indicates that ATM is not likely to act as a tumor suppressor.
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Linkage analysis of DRD2, a marker linked to the ataxia-telangiectasia gene, in 64 families with premenopausal bilateral breast cancer
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