Breast cancer online : BCO最新文献

{"title":"Bisphosphonates and prevention of metastases: the AZURE study","authors":"R. Burkinshaw, H. Thorpe, R. Coleman","doi":"10.1017/S1470903107005147","DOIUrl":"https://doi.org/10.1017/S1470903107005147","url":null,"abstract":"Most patients present with disease that appears to be confined to the breast. However, a significant proportion of women will go on to develop metastatic breast cancer with bone being the most frequent site of distant relapse. The bone microenvironment provides a fertile soil for circulating metastatic cells as resorbing bone releases growth factors that are thought to attract circulating cancer cells to the bone surface and facilitate their growth and proliferation. These infiltrating tumour cells in turn produce bone cell-activating factors, which lead to increased bone resorption and further release of growth factors in a ‘vicious cycle’. The third-generation bisphosphonate zoledronic acid is a potent inhibitor of osteoclast-mediated bone resorption. It also has effects on numerous processes in the metastatic cascade, with in vitro and animal studies showing synergistic antitumour effects with a range of cytotoxic and endocrine treatments. The addition of zoledronic acid to adjuvant therapy could therefore be a therapeutic strategy of potential importance. To investigate this, the AZURE trial was designed to determine whether adjuvant zoledronic acid improves the disease-free and bone metastasis-free survival of women with stage II/III breast cancer. Recruitment of 3300 subjects was completed in January 2006. First efficacy data are expected in 2008. There is a potential for synergistic action with chemotherapy to manifest as enhanced toxicity. Reassuringly, initial safety data show that zoledronic acid is well tolerated and can be safely combined with adjuvant chemotherapy without any increase in myelotoxicity or effect on dose intensity.","PeriodicalId":89901,"journal":{"name":"Breast cancer online : BCO","volume":"815 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2007-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1017/S1470903107005147","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"56920627","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Breast cancer and pregnancy.","authors":"Alistair Ring","doi":"10.1017/S1470903107006505","DOIUrl":"https://doi.org/10.1017/S1470903107006505","url":null,"abstract":"The frequency with which breast cancer is diagnosed in pregnant women is low (in the region of 1 in 1000 pregnancies), but the management of these women presents a considerable challenge to those involved in their care. Women frequently present with tumours displaying adverse pathological prognostic features. Initial investigation may be carried out as for non-pregnant women, but with particular attention paid to the risks of exposure to the foetus of ionizing radiation. Surgery can be carried out with seemingly little increased risk to the mother or foetus, but radiotherapy is usually avoided. In terms of short-term complications chemotherapy may be given relatively safely when administered outside of the first trimester and not around the time of delivery. However, the principle concern with all of these interventions is what the long-term implications for the newborn might be.","PeriodicalId":89901,"journal":{"name":"Breast cancer online : BCO","volume":"16 Suppl 2 1","pages":"S155-8"},"PeriodicalIF":0.0,"publicationDate":"2007-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1017/S1470903107006505","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"56921348","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tamoxifen: using pharmacogenetics to rediscover an old drug","authors":"A. Kamal, M. Goetz","doi":"10.1017/S1470903107005858","DOIUrl":"https://doi.org/10.1017/S1470903107005858","url":null,"abstract":"Tamoxifen can be considered a classic ‘pro-drug’, requiring metabolic activation to elicit pharmacological activity. Our findings suggest that both genetic and drug-induced factors that alter CYP2D6 enzyme activity influence the clinical response to tamoxifen. Given the small differences in disease-free survival comparing tamoxifen to third-generation aromatase inhibitors, knowledge of the genetic and environmental factors that influence CYP2D6 enzyme activity may provide a robust tool to individualize the hormonal therapy to breast cancer.","PeriodicalId":89901,"journal":{"name":"Breast cancer online : BCO","volume":"10 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2007-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1017/S1470903107005858","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"56921097","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integration of post-mastectomy radiation and breast reconstruction","authors":"J. Wright, P. Cordeiro, B. McCormick","doi":"10.1017/S147090310700644X","DOIUrl":"https://doi.org/10.1017/S147090310700644X","url":null,"abstract":"The following is a brief description of the reconstructive options available to patients undergoing mastectomy, and a review of the data available to guide clinicians who seek to safely integrate postmastectomy radiotherapy and breast reconstruction.","PeriodicalId":89901,"journal":{"name":"Breast cancer online : BCO","volume":"10 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2007-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1017/S147090310700644X","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"56921303","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Basic science: (JULY 2007)","authors":"R. Sutherland","doi":"10.1017/S1470903107006621","DOIUrl":"https://doi.org/10.1017/S1470903107006621","url":null,"abstract":"1. Barrett A, Santangelo S, Tan K, Catchpole S, Roberts K, Spencer-Dene B, Hall D, Scibetta A, Burchell J, Verdin E, Freemont P, TaylorPapadimitriou J. Breast cancer associated transcriptional repressor PLU-1/JARID1B interacts directly with histone deacetylases. Int J Cancer 2007; 121: 265–275. 2. Bergman I, Griffin JA, Gao YH, WhitakerDowling P. Treatment of implanted mammary tumors with recombinant vesicular stomatitis virus targeted to Her2/neu. Int J Cancer 2007; 121: 425–430. 3. Bocca C, Bozzo F, Francica S, Colombatto S, Miglietta A. Involvement of PPAR U and Ecadherin/b-catenin pathway in the antiproliferative effect of conjugated linoleic acid in MCF-7 cells. Int J Cancer 2007; 121: 248–256. 4. Budhram-Mahadeo VS, Irshad S, Bowen S, Lee SA, Samady L, Tonini GP, Latchman DS. Proliferation-associated Brn-3b transcription factor can activate cyclin D1 expression in neuroblastoma and breast cancer cells. Oncogene: 10.1038/sj.onc.1210621. 5. Bultman SJ, Herschkowitz JI, Godfrey V, Gebuhr TC, Yaniv M, Perou CM, Magnuson T. Characterization of mammary tumors from Brg1 heterozygous mice. Oncogene: 10.1038/sj.onc. 1210664. 6. Cascio S, Bartella V, Auriemma A, Johannes GJ, Russo A, Giordano A, Surmacz E. Mechanism of leptin expression in breast cancer cells: role of hypoxia-inducible factor-1a. Oncogene: 10.1038/sj.onc.1210660. 7. Chang TW, Chen CC, Chen KY, Su JH, Chang JH, Chang MC. Ribosomal phosphoprotein P0 interacts with GCIP and overexpression of P0 is associated with cellular proliferation in breast and liver carcinoma cells. Oncogene: 10.1038/ sj.onc.1210651. 8. Chen CS, Zhou ZM, Ross JS, Zhou W, Dong JT. The amplified WWP1 gene is a potential molecular target in breast cancer. Int J Cancer 2007; 121: 80–87. 9. Elsheikh S, Green A, Aleskandarany M, Grainge M, Paish C, Lambros M, Reis-Filho J, Ellis I. CCND1 amplification and cyclin D1 expression in breast cancer and their relation with proteomic subgroups and patient outcome. Breast Cancer Res Treat: 10.1007/s10549-007-9659-8. 10. Feng YM, Sun BC, Li XQ, Zhang L, Niu Y, Xiao CH, Ning LS, Fang Z, Wang YL, Zhang LN, Cheng J, Zhang W, Hao XS. Differentially expressed genes between primary cancer and paired lymph node metastases predict clinical outcome of node-positive breast cancer patients. Breast Cancer Res Treat 2007; 103: 319–329. 11. Hao L, ElShamy WM. BRCA1-IRIS activates cyclin D1 expression in breast cancer cells by downregulating the JNK phosphatase DUSP3/ VHR. Int J Cancer 2007; 121: 39–46. 12. Hatsell S, Frost A. Hedgehog Signaling in Mammary Gland Development and Breast Cancer. J Mammary Gland Biol Neoplasia 2007; 12: 163–173. 13. John EM, Phipps AI, Knight JA, Milne RL, Dite GS, Hopper JL, Andrulis IL, Southey M, Giles GG, West DW, Whittemore AS. Medical radiation exposure and breast cancer risk: findings from the Breast Cancer Family Registry. Int J Cancer 2007; 121: 386–394. 14. Katz M, Amit I, Citri A, Shay T, Carvalho S, Lavi S, Milanezi F, Lyass L, Amariglio N, JacobHirsch ","PeriodicalId":89901,"journal":{"name":"Breast cancer online : BCO","volume":"10 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2007-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1017/S1470903107006621","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"56921003","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Review of: Metalloproteinase axes increase β-catenin signaling in primary mouse mammary epithelial cells lacking TIMP3","authors":"D. Salomon","doi":"10.1017/S1470903107006566","DOIUrl":"https://doi.org/10.1017/S1470903107006566","url":null,"abstract":"of the original article: Multiple cancers exhibit mutations in b-catenin that lead to increased stability, altered localization or amplified activity. b-Catenin is situated at the junction between the cadherin-mediated cell adhesion and Wnt signaling pathways, and TIMP3 functions to alter b-catenin signaling. Here we demonstrate that primary mouse embryonic fibroblasts (MEFs) and mammary epithelial cells (MECs) deficient in Timp3 have increased b-catenin signaling. Functionally, the loss of TIMP3 exerted cell-type-specific effects, with Timp3 MEFs being more sensitive and Timp3 MECs more resistant to EGTA-induced cell detachment than the wild type. Timp3 MECs had higher dephosphorylated b-catenin levels and increased b-catenin transcriptional activity as measured by TCF/LEF-responsive reporter assays. Real-time PCR analysis of b-catenin target genes in MEFs and MECs showed no alteration in Myc, decreased Ccnd1 (cyclin D1) and increased Mmp7 mRNA levels upon loss of TIMP3, with the latter occurring only in epithelial cells. Recombinant TIMP3 and synthetic metalloproteinase inhibitors reverted the increase in dephosphorylated b-catenin, decrease in Ccnd1 gene expression and increase in Mmp7 gene expression. Physiologically, Timp3 mammary glands displayed accelerated mammary ductal elongation during pubertal morphogenesis. Gain-of-function studies using slow-release TIMP-containing pellets revealed distinct effects of individual TIMPs on ductal morphogenesis. Recombinant TIMP1, TIMP3 and TIMP4 inhibited ductal elongation whereas TIMP2 promoted this process.","PeriodicalId":89901,"journal":{"name":"Breast cancer online : BCO","volume":"10 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2007-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1017/S1470903107006566","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"56921397","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Male breast cancer – how to treat?","authors":"E. Rossmann, A. Liljegren, J. Bergh","doi":"10.1017/S1470903107006463","DOIUrl":"https://doi.org/10.1017/S1470903107006463","url":null,"abstract":"Treatment principles of breast cancer in males are derived from studies performed among females, while the low incidence in males has so far precluded such studies. The therapy recommendations for males therefore lack the solid evidence, frequently present for females with breast cancer. The primary breast cancer diagnosis in males is not infrequently in stage III/IV and at higher age, thereby requiring multiprofessional and multimodal management including preoperative therapy and adjuvant therapies based on the tumour’s biological characteristics and the clinical circumstances. The majority of male breast cancer tumours are oestrogen-receptor positive and adjuvant/neoadjuvant tamoxifen is therefore recommended, surgery is frequently radical mastectomy and adjuvant radiotherapy should likely be used on wider indications. Chemotherapy should be considered both in the adjuvant and metastatic setting for receptor-negative cancers and for patients with biologically aggressive disease. Trastuzumab should be offered to patients with Her-2/neu-positive disease, while the use of aromatase inhibitors is more uncertain due to differences in the hormonal environment in males.","PeriodicalId":89901,"journal":{"name":"Breast cancer online : BCO","volume":"10 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2007-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1017/S1470903107006463","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"56921313","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Basic science: (JUNE 2007)","authors":"R. Sutherland","doi":"10.1017/S147090310700661X","DOIUrl":"https://doi.org/10.1017/S147090310700661X","url":null,"abstract":"1. Alarmo EL, Kuukasjarvi T, Karhu R, Kallioniemi A. A comprehensive expression survey of bone morphogenetic proteins in breast cancer highlights the importance of BMP4 and BMP7. Breast Cancer Res Treat 2007; 103: 239–246. 2. Boehm JS, Zhao JJ, Yao J, Kim SY, Firestein R, Dunn IF, Sjostrom SK, Garraway LA, Weremowicz S, Richardson AL, Greulich H, Stewart CJ, Mulvey LA, Shen RR, Ambrogio L, HirozaneKishikawa T, Hill DE, Vidal M, Meyerson M, Grenier JK, Hinkle G, Root DE, Roberts TM, Lander ES, Polyak K, Hahn WC. Integrative genomic approaches identify IKBKE as a breast cancer oncogene. Cell 2007; 129: 1065–1079. 3. Chang Y, Zuka M, Perez-Pinera P, Astudillo A, Mortimer J, Berenson JR, Deuel TF. Secretion of pleiotrophin stimulates breast cancer progression through remodeling of the tumor microenvironment. Proc Natl Acad Sci USA 2007; 104: 10888–10893. 4. Desmedt C, Piette F, Loi S, Wang YX, d’assignies MS, Bergh J, Lidereau R, Ellis P, Harris AL, Klijn JGM, Foekens JA, Cardoso F, Piccart MJ, Buyse M, Sotiriou C. Strong time dependence of the 76-gene prognostic signature for node-negative breast cancer patients in the TRANSBIG multicenter independent validation series. Clin Cancer Res 2007; 13: 3207–3214. 5. Easton DF, Pooley KA, Dunning AM, Pharoah PDP, Thompson D, Ballinger DG, Struewing JP, Morrison J, Field H, Luben R, Wareham N, Ahmed S, Healey CS, Bowman R, Luccarini C, Conroy D, Shah M, Munday H, Jordan C, Perkins B, West J, Redman K, Meyer KB, Haiman CA, Kolonel LK, Henderson BE, Le Marchand L, Brennan P, Sangrajrang S, Gaborieau V, Odefrey F, Shen CY, Wu PE, Wang HC, Eccles D, Evans DG, Peto J, Fletcher O, Johnson N, Seal S, Stratton MR, Rahman N, Chenevix-Trench G, Bojesen SE, Nordestgaard BG, Axelsson CK, Garcia-Closas M, Brinton L, Chanock S, Lissowska J, Peplonska B, Nevanlinna H, Fagerholm R, Eerola H, Kang D, Yoo KY, Noh DY, Ahn SH, Hunter DJ, Hankinson SE, Cox DG, Hall P, Wedren S, Liu J, Low YL, Bogdanova N, Schuermann P, Doerk T, Tollenaar R, Jacobi CE, Devilee P, Klijn JGM, Sigurdson AJ, Doody MM, Alexander BH, Zhang J, Cox A, Brock IW, MacPherson G, Reed MWR, Couch FJ, Goode EL, Olson JE, Meijers-Heijboer H, van den Ouweland A, Uitterlinden A, Rivadeneira F, Milne RL, Ribas G, Gonzalez-Neira A, Benitez J, Hopper JL, McCredie M, Southey M, Giles GG, Schroen C, Justenhoven C, Brauch H, Hamann U, Ko YD, et al. Genome-wide association study identifies novel breast cancer susceptibility loci. Nature 2007; 477: 1087–1093. 6. Esseghir S, Kennedy A, Seedhar P, Nerurkar A, Poulsom R, Reis JS, Isacke CM. Identification of NTN4, TRA1, and STC2 as prognostic markers in breast cancer in a screen for signal sequence encoding proteins. Clin Cancer Res 2007; 13: 3164–3173. 7. Gaedcke J, Traub F, Milde S, Wilkens L, Stan A, Ostertag H, Christgen M, von Wasielewski R, Kreipe HH. Predominance of the basal type and HER-2/neu type in brain metastasis from breast cancer. Mod Pathol 2007; 20: 864–870. Epub 1 June 2007. 8. Gudmundsdottir K, Lord CJ, As","PeriodicalId":89901,"journal":{"name":"Breast cancer online : BCO","volume":"10 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2007-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1017/S147090310700661X","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"56920990","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Review of:Estrogen receptor β expression is associated with tamoxifen response in ERα-negative breast carcinoma","authors":"L. Murphy","doi":"10.1017/S1470903107006578","DOIUrl":"https://doi.org/10.1017/S1470903107006578","url":null,"abstract":"Citation of original article: S. K. Gruvberger-Saal, P.-O. Bendahl, L. H. Saal, M. Laakso, C. Hegardt, P. Edeen, C. Peterson, P. Malmstrom, J. Isola, A. Borg, M. Fernoo. Clinical Cancer Research 2007; 13 : 1987–1994. Abstract of the original article: Purpose Endocrine therapies, such as tamoxifen, are commonly given to most patients with estrogen receptor (ERα)-positive breast carcinoma but are not indicated for persons with ERα-negative cancer. The factors responsible for response to tamoxifen in 5% to 10% of patients with ERα-negative tumors are not clear. The aim of the present study was to elucidate the biology and prognostic role of the second ER, ERβ, in patients treated with adjuvant tamoxifen. Experimental design We investigated ERβ by immunohistochemistry in 353 stage II primary breast tumors from patients treated with 2 years adjuvant tamoxifen, and generated gene expression profiles for a representative subset of 88 tumors. Results ERβ was associated with increased survival (distant disease-free survival, P = 0.01; overall survival, P = 0.22), and in particular within ERα-negative patients ( P = 0.003; P = 0.04), but not in the ERα-positive subgroup ( P = 0.49; P = 0.88). Lack of ERβ conferred early relapse (hazards ratio, 14; 95% confidence interval, 1.8–106; P = 0.01) within the ERα-negative subgroup even after adjustment for other markers. ERα was an independent marker only within the ERβ-negative tumors (hazards ratio, 0.44; 95% confidence interval, 0.21–0.89; P = 0.02). An ERβ gene expression profile was identified and was markedly different from the ERα signature. Conclusion Expression of ERβ is an independent marker for favorable prognosis after adjuvant tamoxifen treatment in ERα-negative breast cancer patients and involves a gene expression program distinct from ERα. These results may be highly clinically significant, because in the United States alone, approximately 10 000 women are diagnosed annually with ERα-negative/ERβ-positive breast carcinoma and may benefit from adjuvant tamoxifen.","PeriodicalId":89901,"journal":{"name":"Breast cancer online : BCO","volume":"10 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2007-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1017/S1470903107006578","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"56921442","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Basic science: (MAY 2007)","authors":"R. Sutherland","doi":"10.1017/S1470903107006608","DOIUrl":"https://doi.org/10.1017/S1470903107006608","url":null,"abstract":"1. Adamovic T, Roshani L, Chen L, Schaffer BS, Helou K, Levan G, Olsson B, Shull JD. Nonrandom pattern of chromosome aberrations in 17 b-estradiol-induced rat mammary tumors: indications of distinct pathways for tumor development. Genes Chromosomes Cancer 2007; 46: 459–469. 2. Adams BD, Furneaux H, White BA. The microribonucleic acid (miRNA) miR-206 targets the human estrogen receptor-a (ERa) and represses ERa messenger RNA and protein expression in breast cancer cell lines. Mol Endocrinol 2007; 21: 1132–1147. 3. Aupperlee MD, Haslam SZ. Differential hormonal regulation and function of progesterone receptor isoforms in normal adult mouse mammary gland. Endocrinology 2007; 148: 2290–2300. 4. Borgquist S, Anagnostaki L, Jirstrom K, Landberg G, Manjer J. Breast tumours following combined hormone replacement therapy express favourable prognostic factors. Int J Cancer 2007; 120: 2202–2207. 5. Holst F, Stahl PR, Ruiz C, Hellwinkel O, Jehan Z, Wendland M, Lebeau A, Terracciano L, AlKuraya K, Janicke F, Sauter G, Simon R. Estrogen receptor a (ESR1) gene amplification is frequent in breast cancer. Nat Genet 2007; 39: 655–660. 6. Hunter DJ, Kraft P, Jacobs KB, Cox DG, Yeager M, Hankinson SE, Wacholder S, Wang Z, Welch R, Hutchinson A, Wang J, Yu K, Chatterjee N, Orr N, Willett WC, Colditz GA, Ziegler RG, Berg CD, Buys SS, McCarty CA, Feigelson HS, Calle EE, Thun MJ, Hayes RB, Tucker M, Gerhard DS, Fraumeni JF, Hoover RN, Thomas G, Chanock SJ. A genome-wide association study identifies alleles in FGFR2 associated with risk of sporadic postmenopausal breast cancer. Nat Genet 2007; 39: 870–874. 7. Kim H, Chen JJ, Yu XH. Ubiquitin-binding protein RAP80 mediates BRCA1-dependent DNA damage response. Science 2007; 316: 1202–1205. 8. Li W, Xiao C, Vonderhaar BK, Deng CX. A role of estrogen/ERa signaling in BRCA1-associated tissue-specific tumor formation. Oncogene 2007 May 14; [Epub ahead of print], doi:10.1038/sj.onc.1210527. 9. Liu BL, Ordonez-Ercan D, Fan ZY, Edgerton SM, Yang XH, Thor AD. Downregulation of erbB3 abrogates erbB2-mediated tamoxifen resistance in breast cancer cells. Int J Cancer 2007; 120: 1874–1882. 10. Maiello MR, D’Alessio A, De Luca A, Carotenuto A, Rachiglio AM, Napolitano M, Cito L, Guzzo A, Normanno N. AZD3409 inhibits the growth of breast cancer cells with intrinsic resistance to the EGFR tyrosine kinase inhibitor gefitinib. Breast Cancer Res Treat 2007; 102: 275–282. 11. McBryan J, Howlin J, Kenny PA, Shioda T, Martin F. ERa-CITED1 co-regulated genes expressed during pubertal mammary gland development: implications for breast cancer prognosis. Oncogene 2007 May 7; [Epub ahead of print], doi:10.1038/sj.onc.1210468. 12. Monaco SE, Angelastro JM, Szabolcs M, Greene LA. The transcription factor ATF5 is widely expressed in carcinomas, and interference with its function selectively kills neoplastic, but not nontransformed, breast cell lines. Int J Cancer 2007; 120: 1883–1890. 13. Paterson AL, Pole JCM, Blood KA, Garcia MJ, Cooke SL, Teschendo","PeriodicalId":89901,"journal":{"name":"Breast cancer online : BCO","volume":"10 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2007-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1017/S1470903107006608","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"56921454","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}