Visualizar Tese - Instituto de Biociências - Unesp
Visualizar Tese - Instituto de Biociências - Unesp Visualizar Tese - Instituto de Biociências - Unesp
[19] Green MR, Aya-Bonilla C, Gandhi MK et al. (2011) Integrative Genomic ProfilingReveals Conserved Genetic Mechanisms for Tumorigenesis in Common Entities of Non-Hodgkin’s Lymphoma. Genes Chrom Cancer 50: 313–326.[20] Jönsson G, Staaf J, Vallon-Christersson J et al. (2010) Genomic subtypes of breastcancer identified by array-comparative genomic hybridization display distinct molecular andclinical characteristics. Breast Cancer Research 12: R42.[21] Noyes RW, Hertig AT, Rock J (1950) Dating the endometrial biopsy. Fertil Steril 1: 3-25.[22] Sanchez-Garcia F, Akavia UD, Mozes E et al. (2010) Identification of SignificantTargets in Cancer. BMC Bioinfo 11: 189-198.[23] Gomes LI, Esteves GH, Carvalho AF, et al. (2005) Expression profile of malignant andnonmalignant lesions of esophagus and stomach: differential activity of functional modulesrelated to inflammation and lipid metabolism. Cancer Res 65: 7127-7136.[24] Tusher VG, Tibshirani R and Chu G (2001) Significance analysis of microarrays appliedto the ionizing radiation response. PNAS 98: 5116–5121.[25] Benjamini Y and Hochberg Y (1995) Controlling the false discovery rate — a practicaland powerful approach to multiple testing. J R Stat Soc Ser B Stat Methodol 57: 289–300.[26] Storey JD and Tibshirani R (2003) Statistical significance for genome-wide studies. ProcNatl Acad Sci U S A 100: 9440–9445.[27] Segal E, Shapira M, Regev A et al. (2003) Module networks: identifying regulatorymodules and their condition-specific regulators from gene expression data. Nat Genetics 34:166-176.[28] Subramanian A, Tamayo P, Mootha VK et al. (2005) Gene set enrichment analysis: Aknowledge-based approach for interpreting genome-wide expression profiles. PNAS 102:15545-15550.[29] Reich M, Liefeld T, Gould J et al. (2006) GenePattern 2.0. Nature Genetics 38: 500-501.[30] Packenham JP, Du Manoir S, Schrock E et al. (1997) Analysis of genetic alterations inuterine leiomyomas and leiomyosarcomas by comparative genomic hybridization. MolCarcinog 19: 273-279.[31] Levy B, Mukherjee T, Hirschhorn K (2000) Molecular cytogenetic analysis of uterineleiomyomata and leiomyosarcoma by comparative genomic hybridization. Cancer GenetCytogenet 121: 1-8.[32] Vanharanta S, Wortham NC, Langford C et al. (2007) Definition of a minimal region ofdeletion of chromosome 7 in uterine leiomyomas by tiling-path microCGH array andmutation analysis of known genes in this region. Genes Chrom Cancer 46: 451–458.[33] Ryan BM, Robles AI and Harris CC (2010) Genetic variation in microRNA networks:the implications for cancer research. Nat Rev Cancer 10: 389-402.[34] Zavadil J, Ye H, Liu Z et al. (2010) Profiling and Functional Analyses of MicroRNAsand Their Target Gene Products in Human Uterine Leiomyomas. PLoS ONE 5: e12362.[35] Hoeijmakers JHJ (2001) Genome maintenance mechanisms for preventing cancer.Nature 411: 366-374.[36] Holthausen JT, Wyman C, Kanaar R (2010) Source. Regulation of DNA strand exchangein homologous recombination. DNA Repair (Amst) 9: 1264-1272.17
[37] Luo X, Ding L, Xu J et al. (2005) Gene expression profiling of leiomyoma andmyometrial smooth muscle cells in response to transforming growth factor-beta. Endocrinol146: 1097–1118.[38] Dimitrova IK, Richer JK, Rudolph MC et al. (2009) Gene expression profiling ofmultiple leiomyomata uteri and matched normal tissue from a single patient. Fertil Steril 91:2650-2663.[39] Crabtree JS, Jelinsky SA, Harris HA et al. (2009) Comparison of human and rat uterineleiomyomata: identification of a dysregulated mammalian target of rapamycin pathway.Cancer Res 69: 6171-6178.[40] Shah AA, Grainger DA (1996) Contemporary Concepts in Managing Menorrhagia.Medscape Womens Health 12: 8.[41] Behera MA, Feng L, Yonish B et al. (2007) Thrombospondin-1 and Thrombospondin-2mRNA and TSP-1 and TSP-2 protein expression in uterine fibroids and correlation to thegenes COL1A1 and COL3A1 and to the collagen cross-link ydroxyproline. Reprod Sci 14:63-76.[42] Desai SS, Hentz VR (2011) The treatment of dupuytren disease. J Hand Surg Am 36:936-942.[43] Shih B, Bayat A (2010) Scientific understanding and clinical management of Dupuytrendisease. Nat Rev Rheumatol 6: 715-726.[44] Yu L, Saile K, Swartz CD et al. (2008) Differential expression of receptor tyrosinekinases (RTKs) and IGF-I pathway activation in human uterine leiomyomas. Mol Med14:264-275.[45] Anania CA, Stewart EA, Quade BJ et al. (1997) Expression of the fibroblast growthfactor receptor in women with leiomyomas and abnormal uterine bleeding. Mol Hum Reprod3: 685-691.[46] Shiang CY, Qi Y, Wang B et al. (2010) Amplification of fibroblast growth factorreceptor-1 in breast cancer and the effects of brivanib alaninate. Breast Cancer Res Treat 123:747-755.[47] Keisner SV, Shah SR (2011) Pazopanib: the newest tyrosine kinase inhibitor for thetreatment of advanced or metastatic renal cell carcinoma. Drugs 71:443-454.[48] Villard E, Perret C, Gary F et al. (2011) A genome-wide association study identifies twoloci associated with heart failure due to dilated cardiomyopathy. Eur Heart J 32:1065-1076.[49] Hou XJ, Zhang YZ, Liu X et al. (2009) Expressions of IGFBP-5, cFLIP in cervicalintraepithelial neoplasia, cervical carcinoma and their clinical significances: a molecularpathology. J Exp Clin Cancer Res 28: 1-16.[50] Taylor KJ, Sims AH, Liang L et al. (2010) Dynamic changes in gene expression in vivopredict prognosis of tamoxifen-treated patients with breast cancer. Breast Cancer Res 12:R39.[51] Galiègue-Zouitina S, Delestré L, Dupont C et al. (2008) Underexpression of RhoH inHairy Cell Leukemia. Cancer Res, 68:4531-4540.[52] Chegini N, Kornberg L (2003) Gonadotropin releasing hormone analogue therapy alterssignal transduction pathways involving mitogen-activated protein and focal adhesion kinasesin leiomyoma. J Soc Gynecol Investig 10:21-26.18
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- Page 261 and 262: 317T_B317T_C13 614T 44 LU prolifera
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- Page 267 and 268: MRPS31, SLC25A15, SUGT1L1 320d-1630
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- Page 271 and 272: Anexo 5. Genes identificados na an
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- Page 275 and 276: ABSTRACTBackground: Uterine leiomyo
- Page 277 and 278: Thus, these findings prompt us to i
- Page 279 and 280: Technologies, Santa Clara, CA). Sta
- Page 281 and 282: mapped at 1p36.13, 1q41, 2q32.1, 2q
- Page 283 and 284: genetic disorder showed the higher
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- Page 293 and 294: AArray CGHExpression arrayBtumoral
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[19] Green MR, Aya-Bonilla C, Gandhi MK et al. (2011) Integrative Genomic ProfilingReveals Conserved Genetic Mechanisms for Tumorigenesis in Common Entities of Non-Hodgkin’s Lymphoma. Genes Chrom Cancer 50: 313–326.[20] Jönsson G, Staaf J, Vallon-Christersson J et al. (2010) Genomic subtypes of breastcancer i<strong>de</strong>ntified by array-comparative genomic hybridization display distinct molecular andclinical characteristics. Breast Cancer Research 12: R42.[21] Noyes RW, Hertig AT, Rock J (1950) Dating the endometrial biopsy. Fertil Steril 1: 3-25.[22] Sanchez-Garcia F, Akavia UD, Mozes E et al. (2010) I<strong>de</strong>ntification of SignificantTargets in Cancer. BMC Bioinfo 11: 189-198.[23] Gomes LI, Esteves GH, Carvalho AF, et al. (2005) Expression profile of malignant andnonmalignant lesions of esophagus and stomach: differential activity of functional modulesrelated to inflammation and lipid metabolism. Cancer Res 65: 7127-7136.[24] Tusher VG, Tibshirani R and Chu G (2001) Significance analysis of microarrays appliedto the ionizing radiation response. PNAS 98: 5116–5121.[25] Benjamini Y and Hochberg Y (1995) Controlling the false discovery rate — a practicaland powerful approach to multiple testing. J R Stat Soc Ser B Stat Methodol 57: 289–300.[26] Storey JD and Tibshirani R (2003) Statistical significance for genome-wi<strong>de</strong> studies. ProcNatl Acad Sci U S A 100: 9440–9445.[27] Segal E, Shapira M, Regev A et al. (2003) Module networks: i<strong>de</strong>ntifying regulatorymodules and their condition-specific regulators from gene expression data. Nat Genetics 34:166-176.[28] Subramanian A, Tamayo P, Mootha VK et al. (2005) Gene set enrichment analysis: Aknowledge-based approach for interpreting genome-wi<strong>de</strong> expression profiles. PNAS 102:15545-15550.[29] Reich M, Liefeld T, Gould J et al. (2006) GenePattern 2.0. Nature Genetics 38: 500-501.[30] Packenham JP, Du Manoir S, Schrock E et al. (1997) Analysis of genetic alterations inuterine leiomyomas and leiomyosarcomas by comparative genomic hybridization. MolCarcinog 19: 273-279.[31] Levy B, Mukherjee T, Hirschhorn K (2000) Molecular cytogenetic analysis of uterineleiomyomata and leiomyosarcoma by comparative genomic hybridization. Cancer GenetCytogenet 121: 1-8.[32] Vanharanta S, Wortham NC, Langford C et al. (2007) Definition of a minimal region of<strong>de</strong>letion of chromosome 7 in uterine leiomyomas by tiling-path microCGH array andmutation analysis of known genes in this region. Genes Chrom Cancer 46: 451–458.[33] Ryan BM, Robles AI and Harris CC (2010) Genetic variation in microRNA networks:the implications for cancer research. Nat Rev Cancer 10: 389-402.[34] Zavadil J, Ye H, Liu Z et al. (2010) Profiling and Functional Analyses of MicroRNAsand Their Target Gene Products in Human Uterine Leiomyomas. PLoS ONE 5: e12362.[35] Hoeijmakers JHJ (2001) Genome maintenance mechanisms for preventing cancer.Nature 411: 366-374.[36] Holthausen JT, Wyman C, Kanaar R (2010) Source. Regulation of DNA strand exchangein homologous recombination. DNA Repair (Amst) 9: 1264-1272.17
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