Simultaneous CXCL12 and ESR1 CpG island hypermethylation correlates with poor prognosis in sporadic breast cancer

Background CXCL12 is a chemokine that is constitutively expressed in many organs and tissues. CXCL12 promoter hypermethylation has been detected in primary breast tumours and contributes to their metastatic potential. It has been shown that the oestrogen receptor α ( ESR1 ) gene can also be silenced...

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Vydáno v:	BMC cancer Ročník 10; číslo 1; s. 23
Hlavní autoři:	Ramos, Edneia AS, Camargo, Anamaria A, Braun, Karin, Slowik, Renata, Cavalli, Iglenir J, Ribeiro, Enilze MSF, Pedrosa, Fábio de O, de Souza, Emanuel M, Costa, Fabrício F, Klassen, Giseli
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	London BioMed Central 28.01.2010 BioMed Central Ltd BMC
Témata:	Adult Aged Aged, 80 and over Biomedical and Life Sciences Biomedicine Breast cancer Breast Neoplasms - genetics Breast Neoplasms - metabolism Breast Neoplasms - pathology Cancer Research Cell Line, Tumor Chemokine CXCL12 - biosynthesis Chemokine CXCL12 - genetics Chemokines CpG Islands Development and progression DNA Methylation DNA Mutational Analysis Estrogen Estrogen Receptor alpha - biosynthesis Estrogen Receptor alpha - genetics Female Gene Silencing Genetic aspects Genetic Predisposition to Disease Health Promotion and Disease Prevention Humans Immunohistochemistry Medicine/Public Health Methylation Middle Aged Oncology Physiological aspects Prognosis Promoter Regions, Genetic Receptors Research Article Reverse Transcriptase Polymerase Chain Reaction Risk factors Surgical Oncology United States CXCL12 Expression Breast Tumour Cell Line ESR1 Gene Primary Breast Tumour Normal Cell Line
ISSN:	1471-2407, 1471-2407
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Abstract	Background CXCL12 is a chemokine that is constitutively expressed in many organs and tissues. CXCL12 promoter hypermethylation has been detected in primary breast tumours and contributes to their metastatic potential. It has been shown that the oestrogen receptor α ( ESR1 ) gene can also be silenced by DNA methylation. In this study, we used methylation-specific PCR (MSP) to analyse the methylation status in two regions of the CXCL12 promoter and ESR1 in tumour cell lines and in primary breast tumour samples, and correlated our results with clinicopathological data. Methods First, we analysed CXCL12 expression in breast tumour cell lines by RT-PCR. We also used 5-aza-2'-deoxycytidine (5-aza-CdR) treatment and DNA bisulphite sequencing to study the promoter methylation for a specific region of CXCL12 in breast tumour cell lines. We evaluated CXCL12 and ESR1 methylation in primary tumour samples by methylation-specific PCR (MSP). Finally, promoter hypermethylation of these genes was analysed using Fisher's exact test and correlated with clinicopathological data using the Chi square test, Kaplan-Meier survival analysis and Cox regression analysis. Results CXCL12 promoter hypermethylation in the first region (island 2) and second region (island 4) was correlated with lack of expression of the gene in tumour cell lines. In the primary tumours, island 2 was hypermethylated in 14.5% of the samples and island 4 was hypermethylated in 54% of the samples. The ESR1 promoter was hypermethylated in 41% of breast tumour samples. In addition, the levels of ERα protein expression diminished with increased frequency of ESR1 methylation (p < 0.0001). This study also demonstrated that CXCL12 island 4 and ESR1 methylation occur simultaneously at a high frequency (p = 0.0220). Conclusions This is the first study showing a simultaneous involvement of epigenetic regulation for both CXCL12 and ESR1 genes in Brazilian women. The methylation status of both genes was significantly correlated with histologically advanced disease, the presence of metastases and death. Therefore, the methylation pattern of these genes could be used as a molecular marker for the prediction of breast cancer outcome.
AbstractList	Abstract Background CXCL12 is a chemokine that is constitutively expressed in many organs and tissues. CXCL12 promoter hypermethylation has been detected in primary breast tumours and contributes to their metastatic potential. It has been shown that the oestrogen receptor α (ESR1) gene can also be silenced by DNA methylation. In this study, we used methylation-specific PCR (MSP) to analyse the methylation status in two regions of the CXCL12 promoter and ESR1 in tumour cell lines and in primary breast tumour samples, and correlated our results with clinicopathological data. Methods First, we analysed CXCL12 expression in breast tumour cell lines by RT-PCR. We also used 5-aza-2'-deoxycytidine (5-aza-CdR) treatment and DNA bisulphite sequencing to study the promoter methylation for a specific region of CXCL12 in breast tumour cell lines. We evaluated CXCL12 and ESR1 methylation in primary tumour samples by methylation-specific PCR (MSP). Finally, promoter hypermethylation of these genes was analysed using Fisher's exact test and correlated with clinicopathological data using the Chi square test, Kaplan-Meier survival analysis and Cox regression analysis. Results CXCL12 promoter hypermethylation in the first region (island 2) and second region (island 4) was correlated with lack of expression of the gene in tumour cell lines. In the primary tumours, island 2 was hypermethylated in 14.5% of the samples and island 4 was hypermethylated in 54% of the samples. The ESR1 promoter was hypermethylated in 41% of breast tumour samples. In addition, the levels of ERα protein expression diminished with increased frequency of ESR1 methylation (p < 0.0001). This study also demonstrated that CXCL12 island 4 and ESR1 methylation occur simultaneously at a high frequency (p = 0.0220). Conclusions This is the first study showing a simultaneous involvement of epigenetic regulation for both CXCL12 and ESR1 genes in Brazilian women. The methylation status of both genes was significantly correlated with histologically advanced disease, the presence of metastases and death. Therefore, the methylation pattern of these genes could be used as a molecular marker for the prediction of breast cancer outcome. CXCL12 is a chemokine that is constitutively expressed in many organs and tissues. CXCL12 promoter hypermethylation has been detected in primary breast tumours and contributes to their metastatic potential. It has been shown that the oestrogen receptor alpha (ESR1) gene can also be silenced by DNA methylation. In this study, we used methylation-specific PCR (MSP) to analyse the methylation status in two regions of the CXCL12 promoter and ESR1 in tumour cell lines and in primary breast tumour samples, and correlated our results with clinicopathological data.BACKGROUNDCXCL12 is a chemokine that is constitutively expressed in many organs and tissues. CXCL12 promoter hypermethylation has been detected in primary breast tumours and contributes to their metastatic potential. It has been shown that the oestrogen receptor alpha (ESR1) gene can also be silenced by DNA methylation. In this study, we used methylation-specific PCR (MSP) to analyse the methylation status in two regions of the CXCL12 promoter and ESR1 in tumour cell lines and in primary breast tumour samples, and correlated our results with clinicopathological data.First, we analysed CXCL12 expression in breast tumour cell lines by RT-PCR. We also used 5-aza-2'-deoxycytidine (5-aza-CdR) treatment and DNA bisulphite sequencing to study the promoter methylation for a specific region of CXCL12 in breast tumour cell lines. We evaluated CXCL12 and ESR1 methylation in primary tumour samples by methylation-specific PCR (MSP). Finally, promoter hypermethylation of these genes was analysed using Fisher's exact test and correlated with clinicopathological data using the Chi square test, Kaplan-Meier survival analysis and Cox regression analysis.METHODSFirst, we analysed CXCL12 expression in breast tumour cell lines by RT-PCR. We also used 5-aza-2'-deoxycytidine (5-aza-CdR) treatment and DNA bisulphite sequencing to study the promoter methylation for a specific region of CXCL12 in breast tumour cell lines. We evaluated CXCL12 and ESR1 methylation in primary tumour samples by methylation-specific PCR (MSP). Finally, promoter hypermethylation of these genes was analysed using Fisher's exact test and correlated with clinicopathological data using the Chi square test, Kaplan-Meier survival analysis and Cox regression analysis.CXCL12 promoter hypermethylation in the first region (island 2) and second region (island 4) was correlated with lack of expression of the gene in tumour cell lines. In the primary tumours, island 2 was hypermethylated in 14.5% of the samples and island 4 was hypermethylated in 54% of the samples. The ESR1 promoter was hypermethylated in 41% of breast tumour samples. In addition, the levels of ER alpha protein expression diminished with increased frequency of ESR1 methylation (p < 0.0001). This study also demonstrated that CXCL12 island 4 and ESR1 methylation occur simultaneously at a high frequency (p = 0.0220).RESULTSCXCL12 promoter hypermethylation in the first region (island 2) and second region (island 4) was correlated with lack of expression of the gene in tumour cell lines. In the primary tumours, island 2 was hypermethylated in 14.5% of the samples and island 4 was hypermethylated in 54% of the samples. The ESR1 promoter was hypermethylated in 41% of breast tumour samples. In addition, the levels of ER alpha protein expression diminished with increased frequency of ESR1 methylation (p < 0.0001). This study also demonstrated that CXCL12 island 4 and ESR1 methylation occur simultaneously at a high frequency (p = 0.0220).This is the first study showing a simultaneous involvement of epigenetic regulation for both CXCL12 and ESR1 genes in Brazilian women. The methylation status of both genes was significantly correlated with histologically advanced disease, the presence of metastases and death. Therefore, the methylation pattern of these genes could be used as a molecular marker for the prediction of breast cancer outcome.CONCLUSIONSThis is the first study showing a simultaneous involvement of epigenetic regulation for both CXCL12 and ESR1 genes in Brazilian women. The methylation status of both genes was significantly correlated with histologically advanced disease, the presence of metastases and death. Therefore, the methylation pattern of these genes could be used as a molecular marker for the prediction of breast cancer outcome. Background CXCL12 is a chemokine that is constitutively expressed in many organs and tissues. CXCL12 promoter hypermethylation has been detected in primary breast tumours and contributes to their metastatic potential. It has been shown that the oestrogen receptor [alpha] (ESR1) gene can also be silenced by DNA methylation. In this study, we used methylation-specific PCR (MSP) to analyse the methylation status in two regions of the CXCL12 promoter and ESR1 in tumour cell lines and in primary breast tumour samples, and correlated our results with clinicopathological data. Methods First, we analysed CXCL12 expression in breast tumour cell lines by RT-PCR. We also used 5-aza-2'-deoxycytidine (5-aza-CdR) treatment and DNA bisulphite sequencing to study the promoter methylation for a specific region of CXCL12 in breast tumour cell lines. We evaluated CXCL12 and ESR1 methylation in primary tumour samples by methylation-specific PCR (MSP). Finally, promoter hypermethylation of these genes was analysed using Fisher's exact test and correlated with clinicopathological data using the Chi square test, Kaplan-Meier survival analysis and Cox regression analysis. Results CXCL12 promoter hypermethylation in the first region (island 2) and second region (island 4) was correlated with lack of expression of the gene in tumour cell lines. In the primary tumours, island 2 was hypermethylated in 14.5% of the samples and island 4 was hypermethylated in 54% of the samples. The ESR1 promoter was hypermethylated in 41% of breast tumour samples. In addition, the levels of ER[alpha] protein expression diminished with increased frequency of ESR1 methylation (p [less than] 0.0001). This study also demonstrated that CXCL12 island 4 and ESR1 methylation occur simultaneously at a high frequency (p = 0.0220). Conclusions This is the first study showing a simultaneous involvement of epigenetic regulation for both CXCL12 and ESR1 genes in Brazilian women. The methylation status of both genes was significantly correlated with histologically advanced disease, the presence of metastases and death. Therefore, the methylation pattern of these genes could be used as a molecular marker for the prediction of breast cancer outcome. CXCL12 is a chemokine that is constitutively expressed in many organs and tissues. CXCL12 promoter hypermethylation has been detected in primary breast tumours and contributes to their metastatic potential. It has been shown that the oestrogen receptor [alpha] (ESR1) gene can also be silenced by DNA methylation. In this study, we used methylation-specific PCR (MSP) to analyse the methylation status in two regions of the CXCL12 promoter and ESR1 in tumour cell lines and in primary breast tumour samples, and correlated our results with clinicopathological data. First, we analysed CXCL12 expression in breast tumour cell lines by RT-PCR. We also used 5-aza-2'-deoxycytidine (5-aza-CdR) treatment and DNA bisulphite sequencing to study the promoter methylation for a specific region of CXCL12 in breast tumour cell lines. We evaluated CXCL12 and ESR1 methylation in primary tumour samples by methylation-specific PCR (MSP). Finally, promoter hypermethylation of these genes was analysed using Fisher's exact test and correlated with clinicopathological data using the Chi square test, Kaplan-Meier survival analysis and Cox regression analysis. CXCL12 promoter hypermethylation in the first region (island 2) and second region (island 4) was correlated with lack of expression of the gene in tumour cell lines. In the primary tumours, island 2 was hypermethylated in 14.5% of the samples and island 4 was hypermethylated in 54% of the samples. The ESR1 promoter was hypermethylated in 41% of breast tumour samples. In addition, the levels of ER[alpha] protein expression diminished with increased frequency of ESR1 methylation (p [less than] 0.0001). This study also demonstrated that CXCL12 island 4 and ESR1 methylation occur simultaneously at a high frequency (p = 0.0220). This is the first study showing a simultaneous involvement of epigenetic regulation for both CXCL12 and ESR1 genes in Brazilian women. The methylation status of both genes was significantly correlated with histologically advanced disease, the presence of metastases and death. Therefore, the methylation pattern of these genes could be used as a molecular marker for the prediction of breast cancer outcome. CXCL12 is a chemokine that is constitutively expressed in many organs and tissues. CXCL12 promoter hypermethylation has been detected in primary breast tumours and contributes to their metastatic potential. It has been shown that the oestrogen receptor alpha (ESR1) gene can also be silenced by DNA methylation. In this study, we used methylation-specific PCR (MSP) to analyse the methylation status in two regions of the CXCL12 promoter and ESR1 in tumour cell lines and in primary breast tumour samples, and correlated our results with clinicopathological data. First, we analysed CXCL12 expression in breast tumour cell lines by RT-PCR. We also used 5-aza-2'-deoxycytidine (5-aza-CdR) treatment and DNA bisulphite sequencing to study the promoter methylation for a specific region of CXCL12 in breast tumour cell lines. We evaluated CXCL12 and ESR1 methylation in primary tumour samples by methylation-specific PCR (MSP). Finally, promoter hypermethylation of these genes was analysed using Fisher's exact test and correlated with clinicopathological data using the Chi square test, Kaplan-Meier survival analysis and Cox regression analysis. CXCL12 promoter hypermethylation in the first region (island 2) and second region (island 4) was correlated with lack of expression of the gene in tumour cell lines. In the primary tumours, island 2 was hypermethylated in 14.5% of the samples and island 4 was hypermethylated in 54% of the samples. The ESR1 promoter was hypermethylated in 41% of breast tumour samples. In addition, the levels of ER alpha protein expression diminished with increased frequency of ESR1 methylation (p < 0.0001). This study also demonstrated that CXCL12 island 4 and ESR1 methylation occur simultaneously at a high frequency (p = 0.0220). This is the first study showing a simultaneous involvement of epigenetic regulation for both CXCL12 and ESR1 genes in Brazilian women. The methylation status of both genes was significantly correlated with histologically advanced disease, the presence of metastases and death. Therefore, the methylation pattern of these genes could be used as a molecular marker for the prediction of breast cancer outcome. Background CXCL12 is a chemokine that is constitutively expressed in many organs and tissues. CXCL12 promoter hypermethylation has been detected in primary breast tumours and contributes to their metastatic potential. It has been shown that the oestrogen receptor α ( ESR1 ) gene can also be silenced by DNA methylation. In this study, we used methylation-specific PCR (MSP) to analyse the methylation status in two regions of the CXCL12 promoter and ESR1 in tumour cell lines and in primary breast tumour samples, and correlated our results with clinicopathological data. Methods First, we analysed CXCL12 expression in breast tumour cell lines by RT-PCR. We also used 5-aza-2'-deoxycytidine (5-aza-CdR) treatment and DNA bisulphite sequencing to study the promoter methylation for a specific region of CXCL12 in breast tumour cell lines. We evaluated CXCL12 and ESR1 methylation in primary tumour samples by methylation-specific PCR (MSP). Finally, promoter hypermethylation of these genes was analysed using Fisher's exact test and correlated with clinicopathological data using the Chi square test, Kaplan-Meier survival analysis and Cox regression analysis. Results CXCL12 promoter hypermethylation in the first region (island 2) and second region (island 4) was correlated with lack of expression of the gene in tumour cell lines. In the primary tumours, island 2 was hypermethylated in 14.5% of the samples and island 4 was hypermethylated in 54% of the samples. The ESR1 promoter was hypermethylated in 41% of breast tumour samples. In addition, the levels of ERα protein expression diminished with increased frequency of ESR1 methylation (p < 0.0001). This study also demonstrated that CXCL12 island 4 and ESR1 methylation occur simultaneously at a high frequency (p = 0.0220). Conclusions This is the first study showing a simultaneous involvement of epigenetic regulation for both CXCL12 and ESR1 genes in Brazilian women. The methylation status of both genes was significantly correlated with histologically advanced disease, the presence of metastases and death. Therefore, the methylation pattern of these genes could be used as a molecular marker for the prediction of breast cancer outcome.
ArticleNumber	23
Audience	Academic
Author	Slowik, Renata Costa, Fabrício F Camargo, Anamaria A Klassen, Giseli Cavalli, Iglenir J Ramos, Edneia AS de Souza, Emanuel M Ribeiro, Enilze MSF Pedrosa, Fábio de O Braun, Karin
AuthorAffiliation	1 Department of Basic Pathology, Federal University of Parana, Curitiba, Brazil 2 Laboratory of Molecular Biology and Genomics, Ludwig Institute for Cancer Research, SP, Brazil 4 Department of Biochemistry and Molecular Biology, Federal University of Parana, Curitiba, Brazil 5 Cancer Biology and Epigenomics Program, Children's Memorial Research Center and Northwestern University's Feinberg School of Medicine, Chicago, USA 3 Department of Genetics, Federal University of Parana, Curitiba, Brazil
AuthorAffiliation_xml	– name: 4 Department of Biochemistry and Molecular Biology, Federal University of Parana, Curitiba, Brazil – name: 3 Department of Genetics, Federal University of Parana, Curitiba, Brazil – name: 5 Cancer Biology and Epigenomics Program, Children's Memorial Research Center and Northwestern University's Feinberg School of Medicine, Chicago, USA – name: 2 Laboratory of Molecular Biology and Genomics, Ludwig Institute for Cancer Research, SP, Brazil – name: 1 Department of Basic Pathology, Federal University of Parana, Curitiba, Brazil
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Cites_doi	10.1093/bioinformatics/bti473 10.1186/1471-2407-9-80 10.1371/journal.pgen.0030087 10.1128/MCB.22.9.3157-3173.2002 10.1101/gad.947102 10.1677/erc.0.0080115 10.1073/pnas.93.18.9821 10.1111/j.1742-4658.2006.05343.x 10.1007/s00432-008-0435-x 10.1038/35065016 10.1634/theoncologist.11-1-1 10.1016/j.cancergencyto.2005.07.023 10.1038/nrc1388 10.1210/me.2002-0438 10.1016/j.breast.2005.11.011 10.1016/S0960-9822(99)80418-7 10.1007/s10555-006-9003-5 10.1016/j.tem.2004.01.008 10.1002/(SICI)1097-0215(19990129)80:3<477::AID-IJC23>3.0.CO;2-W 10.1006/geno.1995.1180 10.1016/j.lfs.2007.05.012 10.1158/0008-5472.CAN-04-2045 10.1016/j.jmb.2005.02.016 10.1002/ijc.2910570616 10.1093/carcin/bgi137 10.1016/j.canlet.2005.06.011 10.1038/sj.onc.1210751 10.1038/sj.onc.1209505 10.1038/nrg816
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Keywords	CXCL12 Expression Breast Tumour Cell Line ESR1 Gene Primary Breast Tumour Normal Cell Line
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References	Li, Rong, Iacopetta (CR20) 2006; 237 Mirza, Sharma, Prasad, Parshad, Srivastava, Gupta, Ralhan (CR10) 2007; 81 Shirozu, Nakano, Inazawa, Tashiro, Tada, Shinohara, Honjo (CR17) 1995; 28 Lapidus, Ferguson, Ottaviano, Parl, Smith, Weitzman, Baylin, Issa, Davidson (CR33) 1996; 2 Kishimoto, Wang, Bhat-Nakshatri, Chang, Clarke, Nakshatri (CR30) 2005; 26 Leu, Yan, Fan, Jin, Liu, Curran, Welshons, Wei, Davuluri, Plass (CR34) 2004; 64 Lin, Vega, Thomsen, Zhang, Kong, Xie, Chiu, Lipovich, Barnett, Stossi (CR29) 2007; 3 Balkwill (CR2) 2004; 4 Antequera, Bird (CR28) 1999; 9 Costa, Paixao, Cavalher, Ribeiro, Cunha, Rinck, O'Hare, Mackay, Soares, Brentani (CR21) 2006; 165 Harris, Eichholtz, Hiles, Page, O'Hare (CR13) 1999; 80 Ben-Baruch (CR1) 2006; 25 Jenuwein (CR25) 2006; 273 Yang, Yan, Davidson (CR26) 2001; 8 Giacinti, Claudio, Lopez, Giordano (CR8) 2006; 11 Hall, Korach (CR14) 2003; 17 Wendt, Cooper, Dwinell (CR6) 2007; 27 Sambrook, Russel (CR16) 2001 Curradi, Izzo, Badaracco, Landsberger (CR32) 2002; 22 Yang, Phillips, Ferguson, Nelson, Herman, Davidson (CR9) 2001; 61 Stamps, Davies, Burman, O'Hare (CR12) 1994; 57 Cartharius, Frech, Grote, Klocke, Haltmeier, Klingenhoff, Frisch, Bayerlein, Werner (CR18) 2005; 21 Jones, Baylin (CR24) 2002; 3 Zhao, Wang, Jin, Ma, Ren, Wen, He, Sun, Tang, Wei (CR11) 2008 Wendt, Johanesen, Kang-Decker, Binion, Shah, Dwinell (CR7) 2006; 25 Lapidus, Nass, Butash, Parl, Weitzman, Graff, Herman, Davidson (CR31) 1998; 58 Veronesi, Viale, Rotmensz, Goldhirsch (CR15) 2006; 15 Herman, Graff, Myohanen, Nelkin, Baylin (CR19) 1996; 93 Garcia-Moruja, Alonso-Lobo, Rueda, Torres, Gonzalez, Bermejo, Luque, Arenzana-Seisdedos, Alcami, Caruz (CR22) 2005; 348 Gruber, Gruber, Gruber, Wieser, Huber (CR23) 2004; 15 Seniski, Camargo, Ierardi, Ramos, Grochoski, Ribeiro, Cavalli, Pedrosa, de Souza, Zanata (CR5) 2009; 9 Muller, Homey, Soto, Ge, Catron, Buchanan, McClanahan, Murphy, Yuan, Wagner (CR3) 2001; 410 Bird (CR4) 2002; 16 Zhou, Jiang, Liu, Xu, Wen, Liu, Zhong, Song, Chang, Zhang (CR27) 2008; 135 MK Wendt (1822_CR7) 2006; 25 H Kishimoto (1822_CR30) 2005; 26 M Curradi (1822_CR32) 2002; 22 JM Hall (1822_CR14) 2003; 17 T Jenuwein (1822_CR25) 2006; 273 AC Stamps (1822_CR12) 1994; 57 F Balkwill (1822_CR2) 2004; 4 PA Jones (1822_CR24) 2002; 3 W Zhou (1822_CR27) 2008; 135 FF Costa (1822_CR21) 2006; 165 F Antequera (1822_CR28) 1999; 9 J Sambrook (1822_CR16) 2001 A Bird (1822_CR4) 2002; 16 RG Lapidus (1822_CR33) 1996; 2 CY Lin (1822_CR29) 2007; 3 A Ben-Baruch (1822_CR1) 2006; 25 L Giacinti (1822_CR8) 2006; 11 K Cartharius (1822_CR18) 2005; 21 S Mirza (1822_CR10) 2007; 81 M Shirozu (1822_CR17) 1995; 28 X Yang (1822_CR9) 2001; 61 RA Harris (1822_CR13) 1999; 80 YW Leu (1822_CR34) 2004; 64 C Garcia-Moruja (1822_CR22) 2005; 348 RG Lapidus (1822_CR31) 1998; 58 L Zhao (1822_CR11) 2008 GG Seniski (1822_CR5) 2009; 9 MK Wendt (1822_CR6) 2007; 27 X Yang (1822_CR26) 2001; 8 U Veronesi (1822_CR15) 2006; 15 S Li (1822_CR20) 2006; 237 JG Herman (1822_CR19) 1996; 93 CJ Gruber (1822_CR23) 2004; 15 A Muller (1822_CR3) 2001; 410 12042769 - Nat Rev Genet. 2002 Jun;3(6):415-28 16401708 - Oncologist. 2006 Jan;11(1):1-8 17542648 - PLoS Genet. 2007 Jun;3(6):e87 11585728 - Cancer Res. 2001 Oct 1;61(19):7025-9 9935193 - Int J Cancer. 1999 Jan 29;80(3):477-84 19267929 - BMC Cancer. 2009;9:80 11940673 - Mol Cell Biol. 2002 May;22(9):3157-73 16568088 - Oncogene. 2006 Aug 17;25(36):4986-97 12586845 - Mol Endocrinol. 2003 May;17(5):792-803 10508580 - Curr Biol. 1999 Sep 9;9(17):R661-7 16527607 - Cancer Genet Cytogenet. 2006 Mar;165(2):135-43 15860560 - Bioinformatics. 2005 Jul 1;21(13):2933-42 18670789 - J Cancer Res Clin Oncol. 2009 Jan;135(1):91-102 11782440 - Genes Dev. 2002 Jan 1;16(1):6-21 8206680 - Int J Cancer. 1994 Jun 15;57(6):865-74 9816234 - Clin Cancer Res. 1996 May;2(5):805-10 7490086 - Genomics. 1995 Aug 10;28(3):495-500 18814026 - Breast Cancer Res Treat. 2009 Sep;117(2):253-9 17724466 - Oncogene. 2008 Feb 28;27(10):1461-71 15917309 - Carcinogenesis. 2005 Oct;26(10):1706-15 15808852 - J Mol Biol. 2005 Apr 22;348(1):43-62 17599361 - Life Sci. 2007 Jul 4;81(4):280-7 15229479 - Nat Rev Cancer. 2004 Jul;4(7):540-50 9635570 - Cancer Res. 1998 Jun 15;58(12):2515-9 16857008 - FEBS J. 2006 Jul;273(14):3121-35 11446343 - Endocr Relat Cancer. 2001 Jun;8(2):115-27 17016763 - Cancer Metastasis Rev. 2006 Sep;25(3):357-71 15036253 - Trends Endocrinol Metab. 2004 Mar;15(2):73-8 11242036 - Nature. 2001 Mar 1;410(6824):50-6 8790415 - Proc Natl Acad Sci U S A. 1996 Sep 3;93(18):9821-6 16473737 - Breast. 2006 Feb;15(1):3-8 15548683 - Cancer Res. 2004 Nov 15;64(22):8184-92 16029926 - Cancer Lett. 2006 Jun 18;237(2):272-80
References_xml	– volume: 21 start-page: 2933 issue: 13 year: 2005 end-page: 2942 ident: CR18 article-title: MatInspector and beyond: promoter analysis based on transcription factor binding sites publication-title: Bioinformatics doi: 10.1093/bioinformatics/bti473 – volume: 9 start-page: 80 year: 2009 ident: CR5 article-title: ADAM33 gene silencing by promoter hypermethylation as a molecular marker in breast invasive lobular carcinoma publication-title: BMC Cancer doi: 10.1186/1471-2407-9-80 – volume: 3 start-page: e87 issue: 6 year: 2007 ident: CR29 article-title: Whole-genome cartography of estrogen receptor alpha binding sites publication-title: PLoS Genet doi: 10.1371/journal.pgen.0030087 – volume: 22 start-page: 3157 issue: 9 year: 2002 end-page: 3173 ident: CR32 article-title: Molecular mechanisms of gene silencing mediated by DNA methylation publication-title: Mol Cell Biol doi: 10.1128/MCB.22.9.3157-3173.2002 – volume: 16 start-page: 6 issue: 1 year: 2002 end-page: 21 ident: CR4 article-title: DNA methylation patterns and epigenetic memory publication-title: Genes Dev doi: 10.1101/gad.947102 – volume: 8 start-page: 115 issue: 2 year: 2001 end-page: 127 ident: CR26 article-title: DNA methylation in breast cancer publication-title: Endocr Relat Cancer doi: 10.1677/erc.0.0080115 – volume: 93 start-page: 9821 issue: 18 year: 1996 end-page: 9826 ident: CR19 article-title: Methylation-specific PCR: a novel PCR assay for methylation status of CpG islands publication-title: Proc Natl Acad Sci USA doi: 10.1073/pnas.93.18.9821 – volume: 273 start-page: 3121 issue: 14 year: 2006 end-page: 3135 ident: CR25 article-title: The epigenetic magic of histone lysine methylation publication-title: FEBS J doi: 10.1111/j.1742-4658.2006.05343.x – volume: 2 start-page: 805 issue: 5 year: 1996 end-page: 810 ident: CR33 article-title: Methylation of estrogen and progesterone receptor gene 5' CpG islands correlates with lack of estrogen and progesterone receptor gene expression in breast tumors publication-title: Clin Cancer Res – volume: 135 start-page: 91 issue: 1 year: 2008 end-page: 102 ident: CR27 article-title: Down-regulation of CXCL12 mRNA expression by promoter hypermethylation and its association with metastatic progression in human breast carcinomas publication-title: J Cancer Res Clin Oncol doi: 10.1007/s00432-008-0435-x – volume: 410 start-page: 50 issue: 6824 year: 2001 end-page: 56 ident: CR3 article-title: Involvement of chemokine receptors in breast cancer metastasis publication-title: Nature doi: 10.1038/35065016 – volume: 11 start-page: 1 issue: 1 year: 2006 end-page: 8 ident: CR8 article-title: Epigenetic information and estrogen receptor alpha expression in breast cancer publication-title: Oncologist doi: 10.1634/theoncologist.11-1-1 – volume: 165 start-page: 135 issue: 2 year: 2006 end-page: 143 ident: CR21 article-title: SATR-1 hypomethylation is a common and early event in breast cancer publication-title: Cancer Genet Cytogenet doi: 10.1016/j.cancergencyto.2005.07.023 – volume: 4 start-page: 540 issue: 7 year: 2004 end-page: 550 ident: CR2 article-title: Cancer and the chemokine network publication-title: Nat Rev Cancer doi: 10.1038/nrc1388 – volume: 17 start-page: 792 issue: 5 year: 2003 end-page: 803 ident: CR14 article-title: Stromal cell-derived factor 1, a novel target of estrogen receptor action, mediates the mitogenic effects of estradiol in ovarian and breast cancer cells publication-title: Mol Endocrinol doi: 10.1210/me.2002-0438 – volume: 15 start-page: 3 issue: 1 year: 2006 end-page: 8 ident: CR15 article-title: Rethinking TNM: breast cancer TNM classification for treatment decision-making and research publication-title: Breast doi: 10.1016/j.breast.2005.11.011 – volume: 9 start-page: R661 issue: 17 year: 1999 end-page: 667 ident: CR28 article-title: CpG islands as genomic footprints of promoters that are associated with replication origins publication-title: Curr Biol doi: 10.1016/S0960-9822(99)80418-7 – volume: 25 start-page: 357 issue: 3 year: 2006 end-page: 371 ident: CR1 article-title: The multifaceted roles of chemokines in malignancy publication-title: Cancer Metastasis Rev doi: 10.1007/s10555-006-9003-5 – volume: 15 start-page: 73 issue: 2 year: 2004 end-page: 78 ident: CR23 article-title: Anatomy of the estrogen response element publication-title: Trends Endocrinol Metab doi: 10.1016/j.tem.2004.01.008 – volume: 80 start-page: 477 issue: 3 year: 1999 end-page: 484 ident: CR13 article-title: New model of ErbB-2 over-expression in human mammary luminal epithelial cells publication-title: Int J Cancer doi: 10.1002/(SICI)1097-0215(19990129)80:3<477::AID-IJC23>3.0.CO;2-W – volume: 28 start-page: 495 issue: 3 year: 1995 end-page: 500 ident: CR17 article-title: Structure and chromosomal localization of the human stromal cell-derived factor 1 (SDF1) gene publication-title: Genomics doi: 10.1006/geno.1995.1180 – volume: 81 start-page: 280 issue: 4 year: 2007 end-page: 287 ident: CR10 article-title: Promoter hypermethylation of TMS1, BRCA1, ERalpha and PRB in serum and tumor DNA of invasive ductal breast carcinoma patients publication-title: Life Sci doi: 10.1016/j.lfs.2007.05.012 – volume: 64 start-page: 8184 issue: 22 year: 2004 end-page: 8192 ident: CR34 article-title: Loss of estrogen receptor signaling triggers epigenetic silencing of downstream targets in breast cancer publication-title: Cancer Res doi: 10.1158/0008-5472.CAN-04-2045 – volume: 58 start-page: 2515 issue: 12 year: 1998 end-page: 2519 ident: CR31 article-title: Mapping of ER gene CpG island methylation-specific polymerase chain reaction publication-title: Cancer Res – volume: 61 start-page: 7025 issue: 19 year: 2001 end-page: 7029 ident: CR9 article-title: Synergistic activation of functional estrogen receptor (ER)-alpha by DNA methyltransferase and histone deacetylase inhibition in human ER-alpha-negative breast cancer cells publication-title: Cancer Res – year: 2001 ident: CR16 publication-title: Molecular cloning: A laboratory manual – volume: 348 start-page: 43 issue: 1 year: 2005 end-page: 62 ident: CR22 article-title: Functional characterization of SDF-1 proximal promoter publication-title: J Mol Biol doi: 10.1016/j.jmb.2005.02.016 – volume: 57 start-page: 865 issue: 6 year: 1994 end-page: 874 ident: CR12 article-title: Analysis of proviral integration in human mammary epithelial cell lines immortalized by retroviral infection with a temperature-sensitive SV40 T-antigen construct publication-title: Int J Cancer doi: 10.1002/ijc.2910570616 – volume: 26 start-page: 1706 issue: 10 year: 2005 end-page: 1715 ident: CR30 article-title: The p160 family coactivators regulate breast cancer cell proliferation and invasion through autocrine/paracrine activity of SDF-1alpha/CXCL12 publication-title: Carcinogenesis doi: 10.1093/carcin/bgi137 – volume: 3 start-page: 415 issue: 6 year: 2002 end-page: 428 ident: CR24 article-title: The fundamental role of epigenetic events in cancer publication-title: Nat Rev Genet – volume: 237 start-page: 272 issue: 2 year: 2006 end-page: 280 ident: CR20 article-title: DNA hypermethylation in breast cancer and its association with clinicopathological features publication-title: Cancer Lett doi: 10.1016/j.canlet.2005.06.011 – year: 2008 ident: CR11 article-title: Silencing of estrogen receptor alpha (ERalpha) gene by promoter hypermethylation is a frequent event in Chinese women with sporadic breast cancer publication-title: Breast Cancer Res Treat – volume: 27 start-page: 1461 issue: 10 year: 2007 end-page: 1471 ident: CR6 article-title: Epigenetic silencing of CXCL12 increases the metastatic potential of mammary carcinoma cells publication-title: Oncogene doi: 10.1038/sj.onc.1210751 – volume: 25 start-page: 4986 issue: 36 year: 2006 end-page: 4997 ident: CR7 article-title: Silencing of epithelial CXCL12 expression by DNA hypermethylation promotes colonic carcinoma metastasis publication-title: Oncogene doi: 10.1038/sj.onc.1209505 – volume: 135 start-page: 91 issue: 1 year: 2008 ident: 1822_CR27 publication-title: J Cancer Res Clin Oncol doi: 10.1007/s00432-008-0435-x – volume: 15 start-page: 73 issue: 2 year: 2004 ident: 1822_CR23 publication-title: Trends Endocrinol Metab doi: 10.1016/j.tem.2004.01.008 – volume: 58 start-page: 2515 issue: 12 year: 1998 ident: 1822_CR31 publication-title: Cancer Res – volume: 22 start-page: 3157 issue: 9 year: 2002 ident: 1822_CR32 publication-title: Mol Cell Biol doi: 10.1128/MCB.22.9.3157-3173.2002 – volume: 57 start-page: 865 issue: 6 year: 1994 ident: 1822_CR12 publication-title: Int J Cancer doi: 10.1002/ijc.2910570616 – volume: 348 start-page: 43 issue: 1 year: 2005 ident: 1822_CR22 publication-title: J Mol Biol doi: 10.1016/j.jmb.2005.02.016 – volume: 9 start-page: R661 issue: 17 year: 1999 ident: 1822_CR28 publication-title: Curr Biol doi: 10.1016/S0960-9822(99)80418-7 – volume: 25 start-page: 357 issue: 3 year: 2006 ident: 1822_CR1 publication-title: Cancer Metastasis Rev doi: 10.1007/s10555-006-9003-5 – volume: 3 start-page: e87 issue: 6 year: 2007 ident: 1822_CR29 publication-title: PLoS Genet doi: 10.1371/journal.pgen.0030087 – volume: 28 start-page: 495 issue: 3 year: 1995 ident: 1822_CR17 publication-title: Genomics doi: 10.1006/geno.1995.1180 – volume: 81 start-page: 280 issue: 4 year: 2007 ident: 1822_CR10 publication-title: Life Sci doi: 10.1016/j.lfs.2007.05.012 – volume: 410 start-page: 50 issue: 6824 year: 2001 ident: 1822_CR3 publication-title: Nature doi: 10.1038/35065016 – volume: 11 start-page: 1 issue: 1 year: 2006 ident: 1822_CR8 publication-title: Oncologist doi: 10.1634/theoncologist.11-1-1 – volume: 64 start-page: 8184 issue: 22 year: 2004 ident: 1822_CR34 publication-title: Cancer Res doi: 10.1158/0008-5472.CAN-04-2045 – volume: 4 start-page: 540 issue: 7 year: 2004 ident: 1822_CR2 publication-title: Nat Rev Cancer doi: 10.1038/nrc1388 – volume: 80 start-page: 477 issue: 3 year: 1999 ident: 1822_CR13 publication-title: Int J Cancer doi: 10.1002/(SICI)1097-0215(19990129)80:3<477::AID-IJC23>3.0.CO;2-W – volume: 165 start-page: 135 issue: 2 year: 2006 ident: 1822_CR21 publication-title: Cancer Genet Cytogenet doi: 10.1016/j.cancergencyto.2005.07.023 – volume: 273 start-page: 3121 issue: 14 year: 2006 ident: 1822_CR25 publication-title: FEBS J doi: 10.1111/j.1742-4658.2006.05343.x – volume: 2 start-page: 805 issue: 5 year: 1996 ident: 1822_CR33 publication-title: Clin Cancer Res – volume: 9 start-page: 80 year: 2009 ident: 1822_CR5 publication-title: BMC Cancer doi: 10.1186/1471-2407-9-80 – volume: 237 start-page: 272 issue: 2 year: 2006 ident: 1822_CR20 publication-title: Cancer Lett doi: 10.1016/j.canlet.2005.06.011 – volume: 26 start-page: 1706 issue: 10 year: 2005 ident: 1822_CR30 publication-title: Carcinogenesis doi: 10.1093/carcin/bgi137 – volume: 21 start-page: 2933 issue: 13 year: 2005 ident: 1822_CR18 publication-title: Bioinformatics doi: 10.1093/bioinformatics/bti473 – volume-title: Breast Cancer Res Treat year: 2008 ident: 1822_CR11 – volume: 17 start-page: 792 issue: 5 year: 2003 ident: 1822_CR14 publication-title: Mol Endocrinol doi: 10.1210/me.2002-0438 – volume: 25 start-page: 4986 issue: 36 year: 2006 ident: 1822_CR7 publication-title: Oncogene doi: 10.1038/sj.onc.1209505 – volume: 8 start-page: 115 issue: 2 year: 2001 ident: 1822_CR26 publication-title: Endocr Relat Cancer doi: 10.1677/erc.0.0080115 – volume: 61 start-page: 7025 issue: 19 year: 2001 ident: 1822_CR9 publication-title: Cancer Res – volume: 15 start-page: 3 issue: 1 year: 2006 ident: 1822_CR15 publication-title: Breast doi: 10.1016/j.breast.2005.11.011 – volume: 27 start-page: 1461 issue: 10 year: 2007 ident: 1822_CR6 publication-title: Oncogene doi: 10.1038/sj.onc.1210751 – volume: 16 start-page: 6 issue: 1 year: 2002 ident: 1822_CR4 publication-title: Genes Dev doi: 10.1101/gad.947102 – volume-title: Molecular cloning: A laboratory manual year: 2001 ident: 1822_CR16 – volume: 93 start-page: 9821 issue: 18 year: 1996 ident: 1822_CR19 publication-title: Proc Natl Acad Sci USA doi: 10.1073/pnas.93.18.9821 – volume: 3 start-page: 415 issue: 6 year: 2002 ident: 1822_CR24 publication-title: Nat Rev Genet doi: 10.1038/nrg816 – reference: 15808852 - J Mol Biol. 2005 Apr 22;348(1):43-62 – reference: 12042769 - Nat Rev Genet. 2002 Jun;3(6):415-28 – reference: 11446343 - Endocr Relat Cancer. 2001 Jun;8(2):115-27 – reference: 16473737 - Breast. 2006 Feb;15(1):3-8 – reference: 19267929 - BMC Cancer. 2009;9:80 – reference: 11585728 - Cancer Res. 2001 Oct 1;61(19):7025-9 – reference: 11782440 - Genes Dev. 2002 Jan 1;16(1):6-21 – reference: 15036253 - Trends Endocrinol Metab. 2004 Mar;15(2):73-8 – reference: 7490086 - Genomics. 1995 Aug 10;28(3):495-500 – reference: 15860560 - Bioinformatics. 2005 Jul 1;21(13):2933-42 – reference: 16029926 - Cancer Lett. 2006 Jun 18;237(2):272-80 – reference: 11940673 - Mol Cell Biol. 2002 May;22(9):3157-73 – reference: 16527607 - Cancer Genet Cytogenet. 2006 Mar;165(2):135-43 – reference: 18670789 - J Cancer Res Clin Oncol. 2009 Jan;135(1):91-102 – reference: 17016763 - Cancer Metastasis Rev. 2006 Sep;25(3):357-71 – reference: 17599361 - Life Sci. 2007 Jul 4;81(4):280-7 – reference: 15917309 - Carcinogenesis. 2005 Oct;26(10):1706-15 – reference: 15548683 - Cancer Res. 2004 Nov 15;64(22):8184-92 – reference: 16401708 - Oncologist. 2006 Jan;11(1):1-8 – reference: 8790415 - Proc Natl Acad Sci U S A. 1996 Sep 3;93(18):9821-6 – reference: 10508580 - Curr Biol. 1999 Sep 9;9(17):R661-7 – reference: 9935193 - Int J Cancer. 1999 Jan 29;80(3):477-84 – reference: 17542648 - PLoS Genet. 2007 Jun;3(6):e87 – reference: 18814026 - Breast Cancer Res Treat. 2009 Sep;117(2):253-9 – reference: 15229479 - Nat Rev Cancer. 2004 Jul;4(7):540-50 – reference: 16568088 - Oncogene. 2006 Aug 17;25(36):4986-97 – reference: 9635570 - Cancer Res. 1998 Jun 15;58(12):2515-9 – reference: 11242036 - Nature. 2001 Mar 1;410(6824):50-6 – reference: 8206680 - Int J Cancer. 1994 Jun 15;57(6):865-74 – reference: 16857008 - FEBS J. 2006 Jul;273(14):3121-35 – reference: 12586845 - Mol Endocrinol. 2003 May;17(5):792-803 – reference: 9816234 - Clin Cancer Res. 1996 May;2(5):805-10 – reference: 17724466 - Oncogene. 2008 Feb 28;27(10):1461-71
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Snippet	Background CXCL12 is a chemokine that is constitutively expressed in many organs and tissues. CXCL12 promoter hypermethylation has been detected in primary... CXCL12 is a chemokine that is constitutively expressed in many organs and tissues. CXCL12 promoter hypermethylation has been detected in primary breast tumours... Background CXCL12 is a chemokine that is constitutively expressed in many organs and tissues. CXCL12 promoter hypermethylation has been detected in primary... Abstract Background CXCL12 is a chemokine that is constitutively expressed in many organs and tissues. CXCL12 promoter hypermethylation has been detected in...
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SubjectTerms	Adult Aged Aged, 80 and over Biomedical and Life Sciences Biomedicine Breast cancer Breast Neoplasms - genetics Breast Neoplasms - metabolism Breast Neoplasms - pathology Cancer Research Cell Line, Tumor Chemokine CXCL12 - biosynthesis Chemokine CXCL12 - genetics Chemokines CpG Islands Development and progression DNA Methylation DNA Mutational Analysis Estrogen Estrogen Receptor alpha - biosynthesis Estrogen Receptor alpha - genetics Female Gene Silencing Genetic aspects Genetic Predisposition to Disease Health Promotion and Disease Prevention Humans Immunohistochemistry Medicine/Public Health Methylation Middle Aged Oncology Physiological aspects Prognosis Promoter Regions, Genetic Receptors Research Article Reverse Transcriptase Polymerase Chain Reaction Risk factors Surgical Oncology
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Title	Simultaneous CXCL12 and ESR1 CpG island hypermethylation correlates with poor prognosis in sporadic breast cancer
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