Inflammatory Processes Triggered by Helicobacter pylori Infection Cause Aberrant DNA Methylation in Gastric Epithelial Cells
Altered patterns of DNA methylation associated with Helicobacter pylori (HP) infection of gastric epithelial cells are thought to contribute to gastric cancer risk. However, it is unclear whether this increased risk reflects an infection-associated inflammatory response or the infection itself. In t...
Saved in:
Published in | Cancer research (Chicago, Ill.) Vol. 70; no. 4; pp. 1430 - 1440 |
---|---|
Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Philadelphia, PA
American Association for Cancer Research
15.02.2010
|
Subjects | |
Online Access | Get full text |
Cover
Loading…
Abstract | Altered patterns of DNA methylation associated with Helicobacter pylori (HP) infection of gastric epithelial cells are thought to contribute to gastric cancer risk. However, it is unclear whether this increased risk reflects an infection-associated inflammatory response or the infection itself. In this study, we sought to clarify mechanisms in a gerbil model of gastric cancer where we showed that HP infection is causally involved in induction of aberrant DNA methylation. By genome-wide screening, CpG islands that were aberrantly methylated in gerbil gastric cancer cell lines were isolated, and 10 islands were shown to be specifically methylated only in gastric mucosae infected with HP. By temporal analysis, methylation levels in gastric epithelial cells started to increase at 5 to 10 weeks after infection and reached high levels by 50 weeks. When HP was eradicated, methylation levels markedly decreased 10 and 20 weeks later, but they remained higher than those in gerbils that were not infected by HP. Expression levels of several inflammation-related genes (CXCL2, IL-1β, NOS2, and TNF-α) paralleled the temporal changes of methylation levels. Significantly suppressing inflammation with the immunosuppressive drug cyclosporin A did not affect colonization by HP but blocked the induction of altered DNA methylation. Our findings argue that DNA methylation alterations that occur in gastric mucosae after HP infection are composed of transient components and permanent components, and that it is the infection-associated inflammatory response, rather than HP itself, which is responsible for inducing the altered DNA methylation. Cancer Res; 70(4); 1430–40 |
---|---|
AbstractList | Altered patterns of DNA methylation associated with Helicobacter pylori (HP) infection of gastric epithelial cells are thought to contribute to gastric cancer risk. However, it is unclear whether this increased risk reflects an infection-associated inflammatory response or the infection itself. In this study, we sought to clarify mechanisms in a gerbil model of gastric cancer where we showed that HP infection is causally involved in induction of aberrant DNA methylation. By genome-wide screening, CpG islands that were aberrantly methylated in gerbil gastric cancer cell lines were isolated, and 10 islands were shown to be specifically methylated only in gastric mucosae infected with HP. By temporal analysis, methylation levels in gastric epithelial cells started to increase at 5 to 10 weeks after infection and reached high levels by 50 weeks. When HP was eradicated, methylation levels markedly decreased 10 and 20 weeks later, but they remained higher than those in gerbils that were not infected by HP. Expression levels of several inflammation-related genes (CXCL2, IL-1beta, NOS2, and TNF-alpha) paralleled the temporal changes of methylation levels. Significantly suppressing inflammation with the immunosuppressive drug cyclosporin A did not affect colonization by HP but blocked the induction of altered DNA methylation. Our findings argue that DNA methylation alterations that occur in gastric mucosae after HP infection are composed of transient components and permanent components, and that it is the infection-associated inflammatory response, rather than HP itself, which is responsible for inducing the altered DNA methylation. Altered patterns of DNA methylation associated with Helicobacter pylori (HP) infection of gastric epithelial cells are thought to contribute to gastric cancer risk. However, it is unclear whether this increased risk reflects an infection-associated inflammatory response or the infection itself. In this study, we sought to clarify mechanisms in a gerbil model of gastric cancer where we showed that HP infection is causally involved in induction of aberrant DNA methylation. By genome-wide screening, CpG islands that were aberrantly methylated in gerbil gastric cancer cell lines were isolated, and 10 islands were shown to be specifically methylated only in gastric mucosae infected with HP. By temporal analysis, methylation levels in gastric epithelial cells started to increase at 5 to 10 weeks after infection and reached high levels by 50 weeks. When HP was eradicated, methylation levels markedly decreased 10 and 20 weeks later, but they remained higher than those in gerbils that were not infected by HP. Expression levels of several inflammation-related genes (CXCL2, IL-1beta, NOS2, and TNF-alpha) paralleled the temporal changes of methylation levels. Significantly suppressing inflammation with the immunosuppressive drug cyclosporin A did not affect colonization by HP but blocked the induction of altered DNA methylation. Our findings argue that DNA methylation alterations that occur in gastric mucosae after HP infection are composed of transient components and permanent components, and that it is the infection-associated inflammatory response, rather than HP itself, which is responsible for inducing the altered DNA methylation.Altered patterns of DNA methylation associated with Helicobacter pylori (HP) infection of gastric epithelial cells are thought to contribute to gastric cancer risk. However, it is unclear whether this increased risk reflects an infection-associated inflammatory response or the infection itself. In this study, we sought to clarify mechanisms in a gerbil model of gastric cancer where we showed that HP infection is causally involved in induction of aberrant DNA methylation. By genome-wide screening, CpG islands that were aberrantly methylated in gerbil gastric cancer cell lines were isolated, and 10 islands were shown to be specifically methylated only in gastric mucosae infected with HP. By temporal analysis, methylation levels in gastric epithelial cells started to increase at 5 to 10 weeks after infection and reached high levels by 50 weeks. When HP was eradicated, methylation levels markedly decreased 10 and 20 weeks later, but they remained higher than those in gerbils that were not infected by HP. Expression levels of several inflammation-related genes (CXCL2, IL-1beta, NOS2, and TNF-alpha) paralleled the temporal changes of methylation levels. Significantly suppressing inflammation with the immunosuppressive drug cyclosporin A did not affect colonization by HP but blocked the induction of altered DNA methylation. Our findings argue that DNA methylation alterations that occur in gastric mucosae after HP infection are composed of transient components and permanent components, and that it is the infection-associated inflammatory response, rather than HP itself, which is responsible for inducing the altered DNA methylation. Altered patterns of DNA methylation associated with Helicobacter pylori (HP) infection of gastric epithelial cells are thought to contribute to gastric cancer risk. However, it is unclear whether this increased risk reflects an infection-associated inflammatory response or the infection itself. In this study, we sought to clarify mechanisms in a gerbil model of gastric cancer where we showed that HP infection is causally involved in induction of aberrant DNA methylation. By genome-wide screening, CpG islands that were aberrantly methylated in gerbil gastric cancer cell lines were isolated, and 10 islands were shown to be specifically methylated only in gastric mucosae infected with HP. By temporal analysis, methylation levels in gastric epithelial cells started to increase at 5 to 10 weeks after infection and reached high levels by 50 weeks. When HP was eradicated, methylation levels markedly decreased 10 and 20 weeks later, but they remained higher than those in gerbils that were not infected by HP. Expression levels of several inflammation-related genes (CXCL2, IL-1β, NOS2, and TNF-α) paralleled the temporal changes of methylation levels. Significantly suppressing inflammation with the immunosuppressive drug cyclosporin A did not affect colonization by HP but blocked the induction of altered DNA methylation. Our findings argue that DNA methylation alterations that occur in gastric mucosae after HP infection are composed of transient components and permanent components, and that it is the infection-associated inflammatory response, rather than HP itself, which is responsible for inducing the altered DNA methylation. Cancer Res; 70(4); 1430–40 |
Author | Tsukamoto, Tetsuya Tanaka, Harunari Niwa, Tohru Tatematsu, Masae Maekita, Takao Ushijima, Toshikazu Mori, Akiko Ichinose, Masao Toyoda, Takeshi |
Author_xml | – sequence: 1 givenname: Tohru surname: Niwa fullname: Niwa, Tohru – sequence: 2 givenname: Tetsuya surname: Tsukamoto fullname: Tsukamoto, Tetsuya – sequence: 3 givenname: Takeshi surname: Toyoda fullname: Toyoda, Takeshi – sequence: 4 givenname: Akiko surname: Mori fullname: Mori, Akiko – sequence: 5 givenname: Harunari surname: Tanaka fullname: Tanaka, Harunari – sequence: 6 givenname: Takao surname: Maekita fullname: Maekita, Takao – sequence: 7 givenname: Masao surname: Ichinose fullname: Ichinose, Masao – sequence: 8 givenname: Masae surname: Tatematsu fullname: Tatematsu, Masae – sequence: 9 givenname: Toshikazu surname: Ushijima fullname: Ushijima, Toshikazu |
BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=22486770$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/20124475$$D View this record in MEDLINE/PubMed |
BookMark | eNp9kc9vFCEUx4mpsdvqn6DhYjxNhWEYZuNpM61tk1o91DPhx6PFMMMK7GES_3jZdquJB0_khc_3PXifE3Q0xxkQekvJGaV8-EgIGRreifZs3Nw2ZN20gvMXaEU5GxrRdfwIrf4wx-gk5x-15JTwV-i4JbTtOsFX6Nf17IKaJlViWvC3FA3kDBnfJX9_Dwks1gu-guBN1MoUSHi7hJg8rjkwxccZj2qXAW80pKTmgs9vN_gLlIclqMdrP-NLlUvyBl9sfXmovVTAI4SQX6OXToUMbw7nKfr--eJuvGpuvl5ej5ubxnRMlEZbwTX0a7am1KnWEm2JcARIrzUB2zmmLKOW257prnXG9YoLEJT2zAKhip2iD099tyn-3EEucvLZ1BeoGeIuS8HYwId-oJV8dyB3egIrt8lPKi3yeWEVeH8AVDYquPpl4_Nfru2GXghSuU9PnEkx5wROGl8eF1KS8kFSIvca5V6R3CuSVaMka7nXWNP8n_TzgP_nfgNNTKH8 |
CODEN | CNREA8 |
CitedBy_id | crossref_primary_10_1016_j_freeradbiomed_2012_02_009 crossref_primary_10_32074_1591_951X_163 crossref_primary_10_1093_carcin_bgt212 crossref_primary_10_1007_s10120_019_00949_5 crossref_primary_10_1007_s12079_016_0327_9 crossref_primary_10_2217_epi_13_17 crossref_primary_10_1093_carcin_bgs006 crossref_primary_10_1159_000516478 crossref_primary_10_3389_fcell_2021_756458 crossref_primary_10_1093_mutage_gev016 crossref_primary_10_1007_s11010_024_05105_x crossref_primary_10_5966_sctm_2014_0090 crossref_primary_10_1177_17588359231220511 crossref_primary_10_23922_jarc_2017_055 crossref_primary_10_3389_fmicb_2014_00115 crossref_primary_10_1186_s40170_018_0182_7 crossref_primary_10_1007_s10555_010_9227_2 crossref_primary_10_1002_ijc_31381 crossref_primary_10_1007_s00432_015_1972_8 crossref_primary_10_3389_fphar_2018_01347 crossref_primary_10_1073_pnas_1717340115 crossref_primary_10_1016_j_forsciint_2022_111445 crossref_primary_10_3390_microorganisms8040479 crossref_primary_10_1016_j_ebiom_2023_104844 crossref_primary_10_4137_CGast_S11917 crossref_primary_10_1016_j_devcel_2010_10_005 crossref_primary_10_1111_cas_13136 crossref_primary_10_3892_etm_2016_3648 crossref_primary_10_3892_ol_2012_708 crossref_primary_10_17816_ecogen17491_102 crossref_primary_10_1016_S1590_8658_11_60593_8 crossref_primary_10_1089_gtmb_2020_0299 crossref_primary_10_2334_josnusd_20_0138 crossref_primary_10_5230_jgc_2013_13_4_232 crossref_primary_10_2174_0109298673284520240112055108 crossref_primary_10_3892_ijo_2019_4877 crossref_primary_10_1186_gm307 crossref_primary_10_1007_s00432_018_2824_0 crossref_primary_10_1371_journal_pone_0059089 crossref_primary_10_1007_s11515_011_1123_9 crossref_primary_10_1007_s00345_018_2422_4 crossref_primary_10_1073_pnas_1620661114 crossref_primary_10_1111_den_14980 crossref_primary_10_3748_wjg_v21_i45_12742 crossref_primary_10_1017_erm_2024_16 crossref_primary_10_3748_wjg_v20_i36_12860 crossref_primary_10_18632_oncotarget_3601 crossref_primary_10_1007_s00535_013_0861_7 crossref_primary_10_3390_cancers12103037 crossref_primary_10_1002_cam4_1474 crossref_primary_10_1158_1940_6207_CAPR_13_0067 crossref_primary_10_3390_pathogens8010023 crossref_primary_10_1016_j_molmet_2023_101755 crossref_primary_10_1242_jeb_089920 crossref_primary_10_1016_j_jcmgh_2019_08_008 crossref_primary_10_2183_pjab_97_023 crossref_primary_10_1038_onc_2011_558 crossref_primary_10_1016_j_lfs_2020_118513 crossref_primary_10_1177_0022034510378683 crossref_primary_10_3390_cancers14020425 crossref_primary_10_1136_gutjnl_2023_329492 crossref_primary_10_3389_fonc_2022_849552 crossref_primary_10_1007_s10120_016_0593_5 crossref_primary_10_1002_cnr2_70063 crossref_primary_10_1080_15592294_2022_2160568 crossref_primary_10_1177_0300060514527910 crossref_primary_10_1038_onc_2012_228 crossref_primary_10_1128_mBio_00649_18 crossref_primary_10_1016_j_canlet_2013_08_016 crossref_primary_10_1111_1751_2980_12105 crossref_primary_10_1038_s41598_019_56883_0 crossref_primary_10_1146_annurev_nutr_121415_112634 crossref_primary_10_1158_1940_6207_CAPR_12_0369 crossref_primary_10_1111_j_1749_6632_2010_05882_x crossref_primary_10_1158_1078_0432_CCR_11_2011 crossref_primary_10_3389_fcell_2022_931493 crossref_primary_10_1093_jb_mvu038 crossref_primary_10_1080_15592294_2023_2254976 crossref_primary_10_1111_prd_12000 crossref_primary_10_1007_s00109_022_02264_6 crossref_primary_10_1016_j_canlet_2013_07_034 crossref_primary_10_1093_carcin_bgs294 crossref_primary_10_2217_epi_2018_0096 crossref_primary_10_1016_j_canlet_2010_07_014 crossref_primary_10_1016_j_cca_2013_05_002 crossref_primary_10_4132_KoreanJPathol_2012_46_1_1 crossref_primary_10_1038_s41698_019_0079_0 crossref_primary_10_1093_gastro_goac035 crossref_primary_10_1002_dev_21801 crossref_primary_10_1111_cas_13731 crossref_primary_10_3389_fimmu_2021_696280 crossref_primary_10_1172_JCI69735 crossref_primary_10_1038_onc_2011_241 crossref_primary_10_1186_s13148_022_01406_4 crossref_primary_10_2217_epi_15_75 crossref_primary_10_1016_j_canlet_2012_11_022 crossref_primary_10_1371_journal_pone_0222295 crossref_primary_10_1016_j_biopha_2018_10_094 crossref_primary_10_1021_acs_jpcb_6b08433 crossref_primary_10_1080_20013078_2019_1669881 crossref_primary_10_1007_s10120_015_0544_6 crossref_primary_10_1007_s00011_017_1124_5 crossref_primary_10_1186_s40064_016_2443_7 crossref_primary_10_1186_s13148_019_0789_8 crossref_primary_10_1053_j_gastro_2015_05_059 crossref_primary_10_1002_jcp_27030 crossref_primary_10_2217_epi_12_5 crossref_primary_10_3389_fimmu_2022_947802 crossref_primary_10_1159_000511243 crossref_primary_10_7704_kjhugr_2021_0042 crossref_primary_10_1093_carcin_bgaa083 crossref_primary_10_3390_cells9061540 crossref_primary_10_1002_ajmg_b_32567 crossref_primary_10_5230_jgc_2021_21_e35 crossref_primary_10_1053_j_gastro_2012_10_002 crossref_primary_10_1158_1940_6207_CAPR_12_0056 crossref_primary_10_1158_0008_5472_CAN_10_1335 crossref_primary_10_1016_j_canlet_2014_11_038 crossref_primary_10_1111_hel_12650 crossref_primary_10_4103_1673_5374_392890 crossref_primary_10_1016_j_febslet_2010_12_001 crossref_primary_10_1016_j_ejca_2013_03_031 crossref_primary_10_1002_ijc_25534 crossref_primary_10_1002_jcb_22964 crossref_primary_10_3390_jcm5100084 crossref_primary_10_1097_MCG_0000000000000164 crossref_primary_10_1172_JCI124070 crossref_primary_10_15430_JCP_2014_19_4_259 crossref_primary_10_1007_s10120_020_01117_w crossref_primary_10_3892_ijo_2014_2490 crossref_primary_10_3390_ijms18102063 crossref_primary_10_1016_j_pmu_2012_05_002 crossref_primary_10_1111_cas_13880 crossref_primary_10_1136_gutjnl_2014_307094 crossref_primary_10_1016_j_tim_2010_07_003 crossref_primary_10_1007_s00018_015_2045_5 crossref_primary_10_1245_s10434_010_1393_5 crossref_primary_10_33483_jfpau_544386 crossref_primary_10_3390_diseases2020168 crossref_primary_10_1038_s41388_019_0792_8 crossref_primary_10_1016_j_bbcan_2022_188846 crossref_primary_10_1016_j_semcdb_2023_01_008 crossref_primary_10_1111_cas_14633 crossref_primary_10_1016_j_jcmgh_2017_02_003 crossref_primary_10_1371_journal_pone_0159090 crossref_primary_10_1186_s13073_016_0267_2 crossref_primary_10_1097_CCO_0000000000001020 crossref_primary_10_1111_j_1600_065X_2010_00987_x crossref_primary_10_1007_s12029_020_00536_3 crossref_primary_10_1093_carcin_bgv125 crossref_primary_10_1016_j_semcdb_2022_11_001 crossref_primary_10_1016_j_prp_2024_155768 crossref_primary_10_1038_s41392_023_01693_0 crossref_primary_10_1128_microbiolspec_BAI_0015_2019 crossref_primary_10_1158_1940_6207_CAPR_19_0035 crossref_primary_10_4166_kjg_2017_70_1_27 crossref_primary_10_1016_j_molmed_2021_12_005 crossref_primary_10_18632_oncotarget_14817 crossref_primary_10_1146_annurev_physiol_021119_034359 crossref_primary_10_1016_j_semcancer_2013_07_004 crossref_primary_10_3892_or_2016_4743 crossref_primary_10_3168_jds_2015_10331 crossref_primary_10_1007_s10120_017_0714_9 crossref_primary_10_1002_mc_20759 crossref_primary_10_1038_s41419_024_06885_2 crossref_primary_10_1111_j_1349_7006_2011_01955_x crossref_primary_10_3748_wjg_v20_i34_11991 crossref_primary_10_1111_ijcp_12295 crossref_primary_10_1186_1753_6561_7_S2_K22 crossref_primary_10_1186_s13148_020_00832_6 crossref_primary_10_5230_jgc_2018_18_e3 crossref_primary_10_18632_oncotarget_7125 crossref_primary_10_1093_carcin_bgq203 crossref_primary_10_1186_1757_4749_4_18 crossref_primary_10_1016_j_tcb_2014_06_002 crossref_primary_10_1002_cncr_27604 crossref_primary_10_1007_s10620_016_4361_5 crossref_primary_10_1007_s00535_017_1329_y crossref_primary_10_3389_fmed_2017_00047 crossref_primary_10_5009_gnl_2014_8_2_131 crossref_primary_10_1007_s10120_018_0803_4 crossref_primary_10_1093_toxsci_kfq370 crossref_primary_10_1016_j_gtc_2015_05_011 crossref_primary_10_4254_wjh_v8_i28_1194 crossref_primary_10_1002_ijc_27514 crossref_primary_10_3748_wjg_v21_i30_9021 crossref_primary_10_3897_pharmacia_72_e144177 crossref_primary_10_1111_den_12032 crossref_primary_10_1016_j_ccell_2017_11_018 crossref_primary_10_1093_carcin_bgq219 crossref_primary_10_1186_s12916_023_02842_6 crossref_primary_10_1007_s00430_013_0301_6 crossref_primary_10_1111_pin_13456 crossref_primary_10_1038_bjc_2014_406 crossref_primary_10_1016_j_micpath_2017_05_003 crossref_primary_10_1053_j_gastro_2012_07_009 crossref_primary_10_2217_fvl_13_97 crossref_primary_10_1007_s10147_021_01968_y crossref_primary_10_1111_vco_12624 crossref_primary_10_1186_s12885_016_2247_8 crossref_primary_10_1186_s13071_019_3684_4 crossref_primary_10_1016_j_pharmthera_2017_10_004 crossref_primary_10_22376_ijpbs_2017_8_1_b603_609 crossref_primary_10_1080_15592294_2019_1634986 crossref_primary_10_1158_1078_0432_CCR_13_2637 crossref_primary_10_1093_ckj_sfaa122 crossref_primary_10_1007_s10120_023_01399_w crossref_primary_10_1158_0008_5472_CAN_23_0269 crossref_primary_10_1016_j_bbadis_2016_11_030 crossref_primary_10_2217_epi_15_4 crossref_primary_10_3389_fonc_2021_614927 crossref_primary_10_3389_fonc_2021_655630 crossref_primary_10_1158_1940_6207_CAPR_13_0320 crossref_primary_10_1038_s12276_018_0179_x crossref_primary_10_4161_epi_20524 crossref_primary_10_3109_10409238_2013_875514 crossref_primary_10_4161_epi_26072 crossref_primary_10_1016_j_mrgentox_2014_04_012 crossref_primary_10_3390_ijms22063192 crossref_primary_10_1016_j_canlet_2012_03_016 crossref_primary_10_1136_gutjnl_2011_301625 crossref_primary_10_1053_j_gastro_2022_01_046 crossref_primary_10_1016_j_gendis_2023_02_038 crossref_primary_10_3390_cancers14246183 crossref_primary_10_3746_jfn_2011_16_4_394 crossref_primary_10_1186_s12920_022_01209_9 crossref_primary_10_1007_s00535_021_01848_2 crossref_primary_10_1097_MD_0000000000040492 crossref_primary_10_1177_1758835918786228 crossref_primary_10_3390_ijms21051782 crossref_primary_10_1053_j_gastro_2013_10_056 crossref_primary_10_1002_ijc_33891 crossref_primary_10_1038_nrgastro_2017_53 crossref_primary_10_1007_s12192_017_0871_0 crossref_primary_10_1158_1940_6207_CAPR_23_0423 crossref_primary_10_4161_gmic_25720 crossref_primary_10_1038_onc_2016_91 crossref_primary_10_1016_j_cca_2015_07_001 crossref_primary_10_1016_j_jtbi_2010_02_040 crossref_primary_10_1016_j_vetimm_2014_04_005 crossref_primary_10_1053_j_gastro_2024_07_001 crossref_primary_10_3892_ol_2016_4296 crossref_primary_10_1016_j_jep_2024_117999 crossref_primary_10_1371_journal_pone_0139902 crossref_primary_10_1007_s10620_019_05771_8 crossref_primary_10_4161_epi_26645 crossref_primary_10_1089_dna_2011_1477 crossref_primary_10_2183_pjab_94_016 crossref_primary_10_1007_s42764_020_00010_1 crossref_primary_10_1016_j_canlet_2011_06_038 crossref_primary_10_1002_advs_202309712 crossref_primary_10_1371_journal_pone_0130409 crossref_primary_10_3748_wjg_v20_i33_11770 crossref_primary_10_1371_journal_pone_0086097 crossref_primary_10_1371_journal_pone_0146521 crossref_primary_10_1038_s41598_021_02761_7 crossref_primary_10_1007_s11033_023_09003_1 crossref_primary_10_1007_s11434_012_5578_0 crossref_primary_10_1002_ijc_31120 crossref_primary_10_1038_s41388_020_1241_4 crossref_primary_10_3390_cancers13174436 crossref_primary_10_1038_srep30861 crossref_primary_10_3389_fmicb_2017_01682 crossref_primary_10_2217_epi_2017_0018 crossref_primary_10_3390_cancers14051221 crossref_primary_10_1158_1055_9965_EPI_15_0388 crossref_primary_10_1038_s41568_021_00412_7 crossref_primary_10_1016_j_mrgentox_2010_07_014 crossref_primary_10_1158_0008_5472_CAN_17_0056 crossref_primary_10_1097_ACI_0b013e32835ad0e7 crossref_primary_10_3390_cancers10080251 crossref_primary_10_3390_cancers13236051 crossref_primary_10_1007_s00535_023_02055_x crossref_primary_10_1186_s13059_021_02375_2 crossref_primary_10_2217_epi_14_49 crossref_primary_10_1111_j_1349_7006_2011_02129_x |
Cites_doi | 10.1038/357695a0 10.1007/BF00220822 10.1002/ijc.24018 10.1136/gut.33.9.1214 10.1016/j.cell.2007.01.029 10.1158/1055-9965.EPI-06-0436 10.1128/MCB.24.11.4781-4790.2004 10.1136/gut.2006.113258 10.1002/(SICI)1096-9896(199701)181:1<87::AID-PATH736>3.0.CO;2-J 10.1101/gr.093310.109 10.1128/JB.183.2.443-450.2001 10.1136/gut.2005.077776 10.1073/pnas.94.6.2284 10.1093/carcin/bgm206 10.1053/jhep.2000.19797 10.1016/S0140-6736(08)61159-9 10.1158/1078-0432.CCR-05-2442 10.1016/S0168-8278(96)80140-1 10.1111/j.1349-7006.2005.00035.x 10.1007/s10120-006-0372-9 10.1158/0008-5472.CAN-07-5282 10.1038/sj.onc.1205153 10.1016/j.canlet.2006.08.014 10.1038/ncponc0081 10.1111/j.1349-7006.2005.00030.x 10.1016/0016-5085(84)90592-4 10.1158/1541-7786.MCR-05-0261 10.1056/NEJMoa001999 10.1111/j.1523-5378.2005.00305.x 10.1007/BF02259494 10.1002/aja.1001720305 10.1158/1078-0432.CCR-05-2096 10.1007/BF03326425 10.1038/nrc1433 10.1093/nar/gki987 10.1038/35006081 10.1084/jem.190.11.1595 10.1111/j.1349-7006.2003.tb01426.x 10.1101/gr.969603 10.1111/j.1349-7006.2005.00068.x 10.1002/hep.510260228 10.1111/j.1523-5378.2008.00572.x 10.1001/jama.291.2.187 10.1111/j.1572-0241.2007.01284.x |
ContentType | Journal Article |
Copyright | 2015 INIST-CNRS |
Copyright_xml | – notice: 2015 INIST-CNRS |
DBID | AAYXX CITATION IQODW CGR CUY CVF ECM EIF NPM 7X8 |
DOI | 10.1158/0008-5472.CAN-09-2755 |
DatabaseName | CrossRef Pascal-Francis Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed MEDLINE - Academic |
DatabaseTitle | CrossRef MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) MEDLINE - Academic |
DatabaseTitleList | MEDLINE MEDLINE - Academic CrossRef |
Database_xml | – sequence: 1 dbid: NPM name: PubMed url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 2 dbid: EIF name: MEDLINE url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search sourceTypes: Index Database |
DeliveryMethod | fulltext_linktorsrc |
Discipline | Medicine |
EISSN | 1538-7445 |
EndPage | 1440 |
ExternalDocumentID | 20124475 22486770 10_1158_0008_5472_CAN_09_2755 |
Genre | Research Support, Non-U.S. Gov't Journal Article Comparative Study |
GroupedDBID | --- -ET 18M 29B 2WC 34G 39C 3O- 53G 5GY 5RE 5VS 6J9 AAFWJ AAJMC AAYXX ABOCM ACGFO ACIWK ACPRK ACSVP ADBBV ADCOW AENEX AETEA AFFNX AFHIN AFOSN AFRAH AFUMD ALMA_UNASSIGNED_HOLDINGS BAWUL BTFSW C1A CITATION CS3 DIK DU5 EBS EJD F5P FRP GX1 H13 IH2 KQ8 L7B LSO OK1 P0W P2P PQQKQ RCR RHI RNS SJN TR2 UDS W2D W8F WH7 WOQ XJT YKV YZZ .55 .GJ 8WZ A6W ADNWM AI. D0S IQODW J5H MVM OHT VH1 WHG X7M ZCG ZGI CGR CUY CVF ECM EIF NPM 7X8 |
ID | FETCH-LOGICAL-c437t-bd75be693911fa2d0bd07f0e06bb0ed4f3ad31d5d63b42fcf6a57e71163de01a3 |
ISSN | 0008-5472 1538-7445 |
IngestDate | Fri Jul 11 05:21:04 EDT 2025 Thu Apr 03 06:59:44 EDT 2025 Mon Jul 21 09:18:41 EDT 2025 Tue Jul 01 03:44:41 EDT 2025 Thu Apr 24 22:53:24 EDT 2025 |
IsPeerReviewed | true |
IsScholarly | true |
Issue | 4 |
Keywords | Infection Stomach Spirillales Helicobacter pylori Digestive system DNA Spirillaceae Bacteriosis Bacteria Epithelial cell Inflammation Methylation |
Language | English |
License | CC BY 4.0 |
LinkModel | OpenURL |
MergedId | FETCHMERGED-LOGICAL-c437t-bd75be693911fa2d0bd07f0e06bb0ed4f3ad31d5d63b42fcf6a57e71163de01a3 |
Notes | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 |
PMID | 20124475 |
PQID | 733858681 |
PQPubID | 23479 |
PageCount | 11 |
ParticipantIDs | proquest_miscellaneous_733858681 pubmed_primary_20124475 pascalfrancis_primary_22486770 crossref_citationtrail_10_1158_0008_5472_CAN_09_2755 crossref_primary_10_1158_0008_5472_CAN_09_2755 |
ProviderPackageCode | CITATION AAYXX |
PublicationCentury | 2000 |
PublicationDate | 2010-02-15 |
PublicationDateYYYYMMDD | 2010-02-15 |
PublicationDate_xml | – month: 02 year: 2010 text: 2010-02-15 day: 15 |
PublicationDecade | 2010 |
PublicationPlace | Philadelphia, PA |
PublicationPlace_xml | – name: Philadelphia, PA – name: United States |
PublicationTitle | Cancer research (Chicago, Ill.) |
PublicationTitleAlternate | Cancer Res |
PublicationYear | 2010 |
Publisher | American Association for Cancer Research |
Publisher_xml | – name: American Association for Cancer Research |
References | Yamashita (2022061702412192400_bib22) 2008; 68 Kaneda (2022061702412192400_bib24) 2002; 62 Chan (2022061702412192400_bib13) 2006; 55 Toyota (2022061702412192400_bib6) 2002; 37 Suppl 14 Niwa (2022061702412192400_bib25) 2005; 96 Kanai (2022061702412192400_bib33) 2007; 28 Ushijima (2022061702412192400_bib7) 2007; 40 Clipstone (2022061702412192400_bib28) 1992; 357 Nakajima (2022061702412192400_bib10) 2006; 15 Lu (2022061702412192400_bib2) 2006; 4 Uemura (2022061702412192400_bib9) 2001; 345 Maekita (2022061702412192400_bib5) 2006; 12 Hattori (2022061702412192400_bib43) 1976; 175 McLaughlan (2022061702412192400_bib38) 1997; 181 Lee (2022061702412192400_bib44) 1985; 172 Perri (2022061702412192400_bib11) 2007; 102 Kaise (2022061702412192400_bib12) 2008; 13 Llorente (2022061702412192400_bib37) 1996; 24 Nakajima (2022061702412192400_bib45) 2009; 124 Cheng (2022061702412192400_bib21) 1984; 86 Ushijima (2022061702412192400_bib29) 2003; 13 Mihm (2022061702412192400_bib39) 1997; 26 Chan (2022061702412192400_bib41) 2007; 56 Issa (2022061702412192400_bib4) 2001; 61 Nozaki (2022061702412192400_bib19) 2005; 96 Wong (2022061702412192400_bib18) 2004; 291 Song (2022061702412192400_bib31) 2002; 21 De Smet (2022061702412192400_bib30) 2004; 24 Ushijima (2022061702412192400_bib23) 1997; 94 Kass (2022061702412192400_bib26) 1997; 99 Kondo (2022061702412192400_bib3) 2000; 32 Weisenberger (2022061702412192400_bib27) 2005; 33 Hatakeyama (2022061702412192400_bib34) 2004; 4 Leung (2022061702412192400_bib14) 2006; 12 Nakajima (2022061702412192400_bib47) 2006; 9 Fukase (2022061702412192400_bib17) 2008; 372 Shimizu (2022061702412192400_bib20) 2000; 60 Nozaki (2022061702412192400_bib16) 2003; 94 Takeshima (2022061702412192400_bib48) 2009; 19 Jones (2022061702412192400_bib1) 2007; 128 Moss (2022061702412192400_bib8) 2005; 2 Cappello (2022061702412192400_bib36) 1992; 33 El-Omar (2022061702412192400_bib40) 2000; 404 Tatematsu (2022061702412192400_bib15) 2005; 10 Vitkute (2022061702412192400_bib35) 2001; 183 Moriguchi (2022061702412192400_bib46) 2007; 249 Hmadcha (2022061702412192400_bib42) 1999; 190 Ushijima (2022061702412192400_bib32) 2005; 96 |
References_xml | – volume: 357 start-page: 695 year: 1992 ident: 2022061702412192400_bib28 article-title: Identification of calcineurin as a key signalling enzyme in T-lymphocyte activation publication-title: Nature doi: 10.1038/357695a0 – volume: 60 start-page: 1512 year: 2000 ident: 2022061702412192400_bib20 article-title: Eradication diminishes enhancing effects of Helicobacter pylori infection on glandular stomach carcinogenesis in Mongolian gerbils publication-title: Cancer Res – volume: 175 start-page: 49 year: 1976 ident: 2022061702412192400_bib43 article-title: Tritiated thymidine autoradiographic study of cell migration and renewal in the pyloric mucosa of golden hamsters publication-title: Cell Tissue Res doi: 10.1007/BF00220822 – volume: 124 start-page: 905 year: 2009 ident: 2022061702412192400_bib45 article-title: The presence of a methylation fingerprint of Helicobacter pylori infection in human gastric mucosae publication-title: Int J Cancer doi: 10.1002/ijc.24018 – volume: 33 start-page: 1214 year: 1992 ident: 2022061702412192400_bib36 article-title: Detection of mRNAs for macrophage products in inflammatory bowel disease by in situ hybridisation publication-title: Gut doi: 10.1136/gut.33.9.1214 – volume: 128 start-page: 683 year: 2007 ident: 2022061702412192400_bib1 article-title: The epigenomics of cancer publication-title: Cell doi: 10.1016/j.cell.2007.01.029 – volume: 15 start-page: 2317 year: 2006 ident: 2022061702412192400_bib10 article-title: Higher methylation levels in gastric mucosae significantly correlate with higher risk of gastric cancers publication-title: Cancer Epidemiol Biomarkers Prev doi: 10.1158/1055-9965.EPI-06-0436 – volume: 24 start-page: 4781 year: 2004 ident: 2022061702412192400_bib30 article-title: Promoter-dependent mechanism leading to selective hypomethylation within the 5′ region of gene MAGE-A1 in tumor cells publication-title: Mol Cell Biol doi: 10.1128/MCB.24.11.4781-4790.2004 – volume: 56 start-page: 595 year: 2007 ident: 2022061702412192400_bib41 article-title: Association between Helicobacter pylori infection and interleukin 1β polymorphism predispose to CpG island methylation in gastric cancer publication-title: Gut doi: 10.1136/gut.2006.113258 – volume: 181 start-page: 87 year: 1997 ident: 2022061702412192400_bib38 article-title: Interleukin-8 and inducible nitric oxide synthase mRNA levels in inflammatory bowel disease at first presentation publication-title: J Pathol doi: 10.1002/(SICI)1096-9896(199701)181:1<87::AID-PATH736>3.0.CO;2-J – volume: 19 start-page: 1974 year: 2009 ident: 2022061702412192400_bib48 article-title: The presence of RNA polymerase II, active or stalled, predicts epigenetic fate of promoter CpG islands publication-title: Genome Res doi: 10.1101/gr.093310.109 – volume: 183 start-page: 443 year: 2001 ident: 2022061702412192400_bib35 article-title: Specificities of eleven different DNA methyltransferases of Helicobacter pylori strain 26695 publication-title: J Bacteriol doi: 10.1128/JB.183.2.443-450.2001 – volume: 55 start-page: 463 year: 2006 ident: 2022061702412192400_bib13 article-title: Eradication of Helicobacter pylori infection reverses E-cadherin promoter hypermethylation publication-title: Gut doi: 10.1136/gut.2005.077776 – volume: 94 start-page: 2284 year: 1997 ident: 2022061702412192400_bib23 article-title: Establishment of methylation-sensitive-representational difference analysis and isolation of hypo- and hypermethylated genomic fragments in mouse liver tumors publication-title: Proc Natl Acad Sci U S A doi: 10.1073/pnas.94.6.2284 – volume: 28 start-page: 2434 year: 2007 ident: 2022061702412192400_bib33 article-title: Alterations of DNA methylation associated with abnormalities of DNA methyltransferases in human cancers during transition from a precancerous to a malignant state publication-title: Carcinogenesis doi: 10.1093/carcin/bgm206 – volume: 32 start-page: 970 year: 2000 ident: 2022061702412192400_bib3 article-title: Genetic instability and aberrant DNA methylation in chronic hepatitis and cirrhosis—a comprehensive study of loss of heterozygosity and microsatellite instability at 39 loci and DNA hypermethylation on 8 CpG islands in microdissected specimens from patients with hepatocellular carcinoma publication-title: Hepatology doi: 10.1053/jhep.2000.19797 – volume: 372 start-page: 392 year: 2008 ident: 2022061702412192400_bib17 article-title: Effect of eradication of Helicobacter pylori on incidence of metachronous gastric carcinoma after endoscopic resection of early gastric cancer: an open-label, randomised controlled trial publication-title: Lancet doi: 10.1016/S0140-6736(08)61159-9 – volume: 12 start-page: 3216 year: 2006 ident: 2022061702412192400_bib14 article-title: Effects of Helicobacter pylori eradication on methylation status of E-cadherin gene in noncancerous stomach publication-title: Clin Cancer Res doi: 10.1158/1078-0432.CCR-05-2442 – volume: 24 start-page: 555 year: 1996 ident: 2022061702412192400_bib37 article-title: Cytokine gene expression in cirrhotic and non-cirrhotic human liver publication-title: J Hepatol doi: 10.1016/S0168-8278(96)80140-1 – volume: 96 start-page: 206 year: 2005 ident: 2022061702412192400_bib32 article-title: Aberrant methylations in cancer cells: where do they come from? publication-title: Cancer Sci doi: 10.1111/j.1349-7006.2005.00035.x – volume: 9 start-page: 93 year: 2006 ident: 2022061702412192400_bib47 article-title: Metachronous gastric cancers after endoscopic resection: how effective is annual endoscopic surveillance? publication-title: Gastric Cancer doi: 10.1007/s10120-006-0372-9 – volume: 61 start-page: 3573 year: 2001 ident: 2022061702412192400_bib4 article-title: Accelerated age-related CpG island methylation in ulcerative colitis publication-title: Cancer Res – volume: 68 start-page: 2112 year: 2008 ident: 2022061702412192400_bib22 article-title: Methylation silencing of transforming growth factor-β receptor type II in rat prostate cancers publication-title: Cancer Res doi: 10.1158/0008-5472.CAN-07-5282 – volume: 21 start-page: 1048 year: 2002 ident: 2022061702412192400_bib31 article-title: Hypermethylation trigger of the glutathione-S-transferase gene (GSTP1) in prostate cancer cells publication-title: Oncogene doi: 10.1038/sj.onc.1205153 – volume: 249 start-page: 178 year: 2007 ident: 2022061702412192400_bib46 article-title: Larger numbers of silenced genes in cancer cell lines with increased de novo methylation of scattered CpG sites publication-title: Cancer Lett doi: 10.1016/j.canlet.2006.08.014 – volume: 2 start-page: 90 year: 2005 ident: 2022061702412192400_bib8 article-title: Mechanisms of disease: inflammation and the origins of cancer publication-title: Nat Clin Pract Oncol doi: 10.1038/ncponc0081 – volume: 96 start-page: 170 year: 2005 ident: 2022061702412192400_bib19 article-title: Helicobacter pylori-dependent NF-κB activation in newly established Mongolian gerbil gastric cancer cell lines publication-title: Cancer Sci doi: 10.1111/j.1349-7006.2005.00030.x – volume: 86 start-page: 78 year: 1984 ident: 2022061702412192400_bib21 article-title: Methods for the determination of epithelial cell kinetic parameters of human colonic epithelium isolated from surgical and biopsy specimens publication-title: Gastroenterology doi: 10.1016/0016-5085(84)90592-4 – volume: 4 start-page: 221 year: 2006 ident: 2022061702412192400_bib2 article-title: Inflammation, a key event in cancer development publication-title: Mol Cancer Res doi: 10.1158/1541-7786.MCR-05-0261 – volume: 345 start-page: 784 year: 2001 ident: 2022061702412192400_bib9 article-title: Helicobacter pylori infection and the development of gastric cancer publication-title: N Engl J Med doi: 10.1056/NEJMoa001999 – volume: 10 start-page: 97 year: 2005 ident: 2022061702412192400_bib15 article-title: Role of Helicobacter pylori in gastric carcinogenesis: the origin of gastric cancers and heterotopic proliferative glands in Mongolian gerbils publication-title: Helicobacter doi: 10.1111/j.1523-5378.2005.00305.x – volume: 99 start-page: 1 year: 1997 ident: 2022061702412192400_bib26 article-title: Evolution of B2 repeats: the muroid explosion publication-title: Genetica doi: 10.1007/BF02259494 – volume: 172 start-page: 225 year: 1985 ident: 2022061702412192400_bib44 article-title: Dynamic histology of the antral epithelium in the mouse stomach: III. Ultrastructure and renewal of pit cells publication-title: Am J Anat doi: 10.1002/aja.1001720305 – volume: 12 start-page: 989 year: 2006 ident: 2022061702412192400_bib5 article-title: High levels of aberrant DNA methylation in Helicobacter pylori-infected gastric mucosae and its possible association with gastric cancer risk publication-title: Clin Cancer Res doi: 10.1158/1078-0432.CCR-05-2096 – volume: 37 Suppl 14 start-page: 97 year: 2002 ident: 2022061702412192400_bib6 article-title: DNA methylation changes in gastrointestinal disease publication-title: J Gastroenterol doi: 10.1007/BF03326425 – volume: 4 start-page: 688 year: 2004 ident: 2022061702412192400_bib34 article-title: Oncogenic mechanisms of the Helicobacter pylori CagA protein publication-title: Nat Rev Cancer doi: 10.1038/nrc1433 – volume: 33 start-page: 6823 year: 2005 ident: 2022061702412192400_bib27 article-title: Analysis of repetitive element DNA methylation by MethyLight publication-title: Nucleic Acids Res doi: 10.1093/nar/gki987 – volume: 404 start-page: 398 year: 2000 ident: 2022061702412192400_bib40 article-title: Interleukin-1 polymorphisms associated with increased risk of gastric cancer publication-title: Nature doi: 10.1038/35006081 – volume: 190 start-page: 1595 year: 1999 ident: 2022061702412192400_bib42 article-title: Methylation-dependent gene silencing induced by interleukin 1β via nitric oxide production publication-title: J Exp Med doi: 10.1084/jem.190.11.1595 – volume: 94 start-page: 235 year: 2003 ident: 2022061702412192400_bib16 article-title: Effect of early eradication on Helicobacter pylori-related gastric carcinogenesis in Mongolian gerbils publication-title: Cancer Sci doi: 10.1111/j.1349-7006.2003.tb01426.x – volume: 13 start-page: 868 year: 2003 ident: 2022061702412192400_bib29 article-title: Fidelity of the methylation pattern and its variation in the genome publication-title: Genome Res doi: 10.1101/gr.969603 – volume: 40 start-page: 142 year: 2007 ident: 2022061702412192400_bib7 article-title: Epigenetic field for cancerization publication-title: J Biochem Mol Biol – volume: 96 start-page: 409 year: 2005 ident: 2022061702412192400_bib25 article-title: Whole-genome analyses of loss of heterozygosity and methylation analysis of four tumor-suppressor genes in N-methyl-N′-nitro-N-nitrosoguanidine-induced rat stomach carcinomas publication-title: Cancer Sci doi: 10.1111/j.1349-7006.2005.00068.x – volume: 26 start-page: 451 year: 1997 ident: 2022061702412192400_bib39 article-title: Hepatic expression of inducible nitric oxide synthase transcripts in chronic hepatitis C virus infection: relation to hepatic viral load and liver injury publication-title: Hepatology doi: 10.1002/hep.510260228 – volume: 13 start-page: 35 year: 2008 ident: 2022061702412192400_bib12 article-title: CpG island hypermethylation of tumor-suppressor genes in H. pylori-infected non-neoplastic gastric mucosa is linked with gastric cancer risk publication-title: Helicobacter doi: 10.1111/j.1523-5378.2008.00572.x – volume: 291 start-page: 187 year: 2004 ident: 2022061702412192400_bib18 article-title: Helicobacter pylori eradication to prevent gastric cancer in a high-risk region of China: a randomized controlled trial publication-title: JAMA doi: 10.1001/jama.291.2.187 – volume: 62 start-page: 6645 year: 2002 ident: 2022061702412192400_bib24 article-title: Identification of silencing of nine genes in human gastric cancers publication-title: Cancer Res – volume: 102 start-page: 1361 year: 2007 ident: 2022061702412192400_bib11 article-title: Aberrant DNA methylation in non-neoplastic gastric mucosa of H. pylori infected patients and effect of eradication publication-title: Am J Gastroenterol doi: 10.1111/j.1572-0241.2007.01284.x |
SSID | ssj0005105 |
Score | 2.481798 |
Snippet | Altered patterns of DNA methylation associated with Helicobacter pylori (HP) infection of gastric epithelial cells are thought to contribute to gastric cancer... |
SourceID | proquest pubmed pascalfrancis crossref |
SourceType | Aggregation Database Index Database Enrichment Source |
StartPage | 1430 |
SubjectTerms | Adult Aged Animals Antineoplastic agents Bacterial diseases Bacterial diseases of the digestive system and abdomen Biological and medical sciences Carcinoma - etiology Carcinoma - genetics Cells, Cultured DNA Methylation - drug effects Epithelial Cells - drug effects Epithelial Cells - metabolism Female Gastritis - etiology Gastritis - genetics Gastritis - pathology Gerbillinae Helicobacter Infections - complications Helicobacter Infections - genetics Helicobacter Infections - metabolism Helicobacter Infections - pathology Helicobacter pylori - physiology Human bacterial diseases Humans Infectious diseases Inflammation - genetics Inflammation - metabolism Inflammation - pathology Inflammation Mediators - metabolism Inflammation Mediators - pharmacology Male Medical sciences Middle Aged Pharmacology. Drug treatments Risk Factors Stomach - metabolism Stomach - pathology Stomach Neoplasms - etiology Stomach Neoplasms - genetics Tumors Young Adult |
Title | Inflammatory Processes Triggered by Helicobacter pylori Infection Cause Aberrant DNA Methylation in Gastric Epithelial Cells |
URI | https://www.ncbi.nlm.nih.gov/pubmed/20124475 https://www.proquest.com/docview/733858681 |
Volume | 70 |
hasFullText | 1 |
inHoldings | 1 |
isFullTextHit | |
isPrint | |
link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV1bi9NAFB7qCiKIeLdelnnwLaROk8llH0tdXZUWhCzsW5jJTGxpTEqTIBX_nv_LczJpmkq9rC-hBM4k9Hw59wshr0LhSO6LwNbumNvcd85skWDHsquYGIfSSyUG9Gdz_-KSf7jyrgaDH72qpbqSo-Tb0b6S_-Eq3AO-YpfsNTjbHQo34DfwF67AYbj-E4_f5ykw9ItJlLcl_7q0IvC4P-MOTrQtQa8As2UzlNlao3u-BKFgKrByaypqnEwi9QZ0VmW9mU-smQbemQo5DIa8E7jZI7HO19i9kWGAfaqzrOxbtVOEzsZqBwctmsywKfFoRFCWjXoBh_nya2OwRsViU3eBg7JeCUBNQxDpqqy3nb6Iim2hDIlY6XKx7EBSmDb5yWq5KvrhC8y8O7Zp4OxEcmh73OzvGem9FA64mTO5E9Nmv0gLR96TuWDxsZ7-xmz1cd3ghaaY0jxvNJ1glMp2AjMn-HAW9y86sqtcbHwmL8ScfRjjMTEcE7OzGI-5QW464K3gIo2Pn_ZD6722knb35LaRDI55ffRtDkykO2tRwteamjUrv_eDGnsoukfuto4MnRhU3icDnT8gt2ZtqcZD8r0PTtqBk3bgpHJL--CkBpy0AydtwEl34KQATtoDJ13mtAUn3YOTNuB8RC7fnkfTC7td9WEn3A0qW6rAk9o_c0H3psJRTCoWpEwzX0qmFU9dodyx8pTvSu6kSeoLL9DBGLwJpdlYuI_JSV7k-imhXDkCTtNcMLC80EUPfemgJ60cJngyJHz378ZJOwcf17Fk8R95OySjjmxtBsH8jeD0gHUdFRjNOESSDQnd8TIGmY6JOpHroi7jwMV0vR-Oh-SJ4fGemKFBHnjPrvs6z8nt_ef3gpxUm1q_BHu6kqcNWn8C5rnFKw |
linkProvider | Colorado Alliance of Research Libraries |
openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Inflammatory+Processes+Triggered+by+Helicobacter+pylori+Infection+Cause+Aberrant+DNA+Methylation+in+Gastric+Epithelial+Cells&rft.jtitle=Cancer+research+%28Chicago%2C+Ill.%29&rft.au=Niwa%2C+Tohru&rft.au=Tsukamoto%2C+Tetsuya&rft.au=Toyoda%2C+Takeshi&rft.au=Mori%2C+Akiko&rft.date=2010-02-15&rft.issn=0008-5472&rft.eissn=1538-7445&rft.volume=70&rft.issue=4&rft.spage=1430&rft.epage=1440&rft_id=info:doi/10.1158%2F0008-5472.CAN-09-2755&rft.externalDBID=n%2Fa&rft.externalDocID=10_1158_0008_5472_CAN_09_2755 |
thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=0008-5472&client=summon |
thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=0008-5472&client=summon |
thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=0008-5472&client=summon |