DNA methylation status of REIC/Dkk-3 gene in human malignancies
Purpose The REIC (reduced expression in immortalized cells)/Dkk-3 is down-regulated in various cancers and considered to be a tumor suppressor gene. REIC/Dkk-3 mRNA has two isoforms (type-a,b). REIC type-a mRNA has shown to be a major transcript in various cancer cells, and its promoter activity was...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Hayashi, Tatsuro [verfasserIn] Asano, Hiroaki [verfasserIn] Toyooka, Shinichi [verfasserIn] Tsukuda, Kazunori [verfasserIn] Soh, Junichi [verfasserIn] Shien, Tadahiko [verfasserIn] Taira, Naruto [verfasserIn] Maki, Yuho [verfasserIn] Tanaka, Norimitsu [verfasserIn] Doihara, Hiroyoshi [verfasserIn] Nasu, Yasutomo [verfasserIn] Huh, Nam-ho [verfasserIn] Miyoshi, Shinichiro [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2012 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: Journal of cancer research and clinical oncology - Berlin : Springer, 1904, 138(2012), 5 vom: 25. Jan., Seite 799-809 |
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| Übergeordnetes Werk: |
volume:138 ; year:2012 ; number:5 ; day:25 ; month:01 ; pages:799-809 |
| Links: |
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| DOI / URN: |
10.1007/s00432-012-1158-6 |
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| Katalog-ID: |
SPR00584911X |
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| 024 | 7 | |a 10.1007/s00432-012-1158-6 |2 doi | |
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| 100 | 1 | |a Hayashi, Tatsuro |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a DNA methylation status of REIC/Dkk-3 gene in human malignancies |
| 264 | 1 | |c 2012 | |
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| 520 | |a Purpose The REIC (reduced expression in immortalized cells)/Dkk-3 is down-regulated in various cancers and considered to be a tumor suppressor gene. REIC/Dkk-3 mRNA has two isoforms (type-a,b). REIC type-a mRNA has shown to be a major transcript in various cancer cells, and its promoter activity was much stronger than that of type-b. In this study, we examined the methylation status of REIC/Dkk-3 type-a in a broad range of human malignancies. Methods We examined REIC/Dkk-3 type-a methylation in breast cancers, non-small-cell lung cancers, gastric cancers, colorectal cancers, and malignant pleural mesotheliomas using a quantitative combined bisulfite restriction analysis assay and bisulfate sequencing. REIC/Dkk-3 type-a and type-b expression was examined using reverse transcriptional PCR. The relationships between the methylation and clinicopathological factors were analyzed. Results The rate of REIC/Dkk-3 type-a methylation ranged from 26.2 to 50.0% in the various primary tumors that were examined. REIC/Dkk-3 type-a methylation in breast cancer cells was significantly heavier than that in the other cell lines that we tested. REIC/Dkk-3 type-a methylation was inversely correlated with REIC/Dkk-3 type-a expression. There was a correlation between REIC/Dkk-3 type-a and type-b mRNA expression. REIC/Dkk-3 type-a expression was restored in MDA-MB-231 cells using 5-aza-2′-deoxycytidine treatment. We found that estrogen receptor–positive breast cancers were significantly more common among the methylated group than among the non-methylated group. Conclusions REIC/Dkk-3 type-a methylation was frequently detected in a broad range of cancers and appeared to play a key role in silencing REIC/Dkk-3 type-a expression in these malignancies. | ||
| 650 | 4 | |a DNA methylation |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a - |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Breast cancer |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Lung cancer |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Mesothelioma |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Asano, Hiroaki |e verfasserin |4 aut | |
| 700 | 1 | |a Toyooka, Shinichi |e verfasserin |4 aut | |
| 700 | 1 | |a Tsukuda, Kazunori |e verfasserin |4 aut | |
| 700 | 1 | |a Soh, Junichi |e verfasserin |4 aut | |
| 700 | 1 | |a Shien, Tadahiko |e verfasserin |4 aut | |
| 700 | 1 | |a Taira, Naruto |e verfasserin |4 aut | |
| 700 | 1 | |a Maki, Yuho |e verfasserin |4 aut | |
| 700 | 1 | |a Tanaka, Norimitsu |e verfasserin |4 aut | |
| 700 | 1 | |a Doihara, Hiroyoshi |e verfasserin |4 aut | |
| 700 | 1 | |a Nasu, Yasutomo |e verfasserin |4 aut | |
| 700 | 1 | |a Huh, Nam-ho |e verfasserin |4 aut | |
| 700 | 1 | |a Miyoshi, Shinichiro |e verfasserin |4 aut | |
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10.1007/s00432-012-1158-6 doi (DE-627)SPR00584911X (SPR)s00432-012-1158-6-e DE-627 ger DE-627 rakwb eng 610 ASE 44.81 bkl Hayashi, Tatsuro verfasserin aut DNA methylation status of REIC/Dkk-3 gene in human malignancies 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Purpose The REIC (reduced expression in immortalized cells)/Dkk-3 is down-regulated in various cancers and considered to be a tumor suppressor gene. REIC/Dkk-3 mRNA has two isoforms (type-a,b). REIC type-a mRNA has shown to be a major transcript in various cancer cells, and its promoter activity was much stronger than that of type-b. In this study, we examined the methylation status of REIC/Dkk-3 type-a in a broad range of human malignancies. Methods We examined REIC/Dkk-3 type-a methylation in breast cancers, non-small-cell lung cancers, gastric cancers, colorectal cancers, and malignant pleural mesotheliomas using a quantitative combined bisulfite restriction analysis assay and bisulfate sequencing. REIC/Dkk-3 type-a and type-b expression was examined using reverse transcriptional PCR. The relationships between the methylation and clinicopathological factors were analyzed. Results The rate of REIC/Dkk-3 type-a methylation ranged from 26.2 to 50.0% in the various primary tumors that were examined. REIC/Dkk-3 type-a methylation in breast cancer cells was significantly heavier than that in the other cell lines that we tested. REIC/Dkk-3 type-a methylation was inversely correlated with REIC/Dkk-3 type-a expression. There was a correlation between REIC/Dkk-3 type-a and type-b mRNA expression. REIC/Dkk-3 type-a expression was restored in MDA-MB-231 cells using 5-aza-2′-deoxycytidine treatment. We found that estrogen receptor–positive breast cancers were significantly more common among the methylated group than among the non-methylated group. Conclusions REIC/Dkk-3 type-a methylation was frequently detected in a broad range of cancers and appeared to play a key role in silencing REIC/Dkk-3 type-a expression in these malignancies. DNA methylation (dpeaa)DE-He213 - (dpeaa)DE-He213 Breast cancer (dpeaa)DE-He213 Lung cancer (dpeaa)DE-He213 Mesothelioma (dpeaa)DE-He213 Asano, Hiroaki verfasserin aut Toyooka, Shinichi verfasserin aut Tsukuda, Kazunori verfasserin aut Soh, Junichi verfasserin aut Shien, Tadahiko verfasserin aut Taira, Naruto verfasserin aut Maki, Yuho verfasserin aut Tanaka, Norimitsu verfasserin aut Doihara, Hiroyoshi verfasserin aut Nasu, Yasutomo verfasserin aut Huh, Nam-ho verfasserin aut Miyoshi, Shinichiro verfasserin aut Enthalten in Journal of cancer research and clinical oncology Berlin : Springer, 1904 138(2012), 5 vom: 25. Jan., Seite 799-809 (DE-627)253769515 (DE-600)1459285-X 1432-1335 nnns volume:138 year:2012 number:5 day:25 month:01 pages:799-809 https://dx.doi.org/10.1007/s00432-012-1158-6 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.81 ASE AR 138 2012 5 25 01 799-809 |
| spelling |
10.1007/s00432-012-1158-6 doi (DE-627)SPR00584911X (SPR)s00432-012-1158-6-e DE-627 ger DE-627 rakwb eng 610 ASE 44.81 bkl Hayashi, Tatsuro verfasserin aut DNA methylation status of REIC/Dkk-3 gene in human malignancies 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Purpose The REIC (reduced expression in immortalized cells)/Dkk-3 is down-regulated in various cancers and considered to be a tumor suppressor gene. REIC/Dkk-3 mRNA has two isoforms (type-a,b). REIC type-a mRNA has shown to be a major transcript in various cancer cells, and its promoter activity was much stronger than that of type-b. In this study, we examined the methylation status of REIC/Dkk-3 type-a in a broad range of human malignancies. Methods We examined REIC/Dkk-3 type-a methylation in breast cancers, non-small-cell lung cancers, gastric cancers, colorectal cancers, and malignant pleural mesotheliomas using a quantitative combined bisulfite restriction analysis assay and bisulfate sequencing. REIC/Dkk-3 type-a and type-b expression was examined using reverse transcriptional PCR. The relationships between the methylation and clinicopathological factors were analyzed. Results The rate of REIC/Dkk-3 type-a methylation ranged from 26.2 to 50.0% in the various primary tumors that were examined. REIC/Dkk-3 type-a methylation in breast cancer cells was significantly heavier than that in the other cell lines that we tested. REIC/Dkk-3 type-a methylation was inversely correlated with REIC/Dkk-3 type-a expression. There was a correlation between REIC/Dkk-3 type-a and type-b mRNA expression. REIC/Dkk-3 type-a expression was restored in MDA-MB-231 cells using 5-aza-2′-deoxycytidine treatment. We found that estrogen receptor–positive breast cancers were significantly more common among the methylated group than among the non-methylated group. Conclusions REIC/Dkk-3 type-a methylation was frequently detected in a broad range of cancers and appeared to play a key role in silencing REIC/Dkk-3 type-a expression in these malignancies. DNA methylation (dpeaa)DE-He213 - (dpeaa)DE-He213 Breast cancer (dpeaa)DE-He213 Lung cancer (dpeaa)DE-He213 Mesothelioma (dpeaa)DE-He213 Asano, Hiroaki verfasserin aut Toyooka, Shinichi verfasserin aut Tsukuda, Kazunori verfasserin aut Soh, Junichi verfasserin aut Shien, Tadahiko verfasserin aut Taira, Naruto verfasserin aut Maki, Yuho verfasserin aut Tanaka, Norimitsu verfasserin aut Doihara, Hiroyoshi verfasserin aut Nasu, Yasutomo verfasserin aut Huh, Nam-ho verfasserin aut Miyoshi, Shinichiro verfasserin aut Enthalten in Journal of cancer research and clinical oncology Berlin : Springer, 1904 138(2012), 5 vom: 25. Jan., Seite 799-809 (DE-627)253769515 (DE-600)1459285-X 1432-1335 nnns volume:138 year:2012 number:5 day:25 month:01 pages:799-809 https://dx.doi.org/10.1007/s00432-012-1158-6 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.81 ASE AR 138 2012 5 25 01 799-809 |
| allfields_unstemmed |
10.1007/s00432-012-1158-6 doi (DE-627)SPR00584911X (SPR)s00432-012-1158-6-e DE-627 ger DE-627 rakwb eng 610 ASE 44.81 bkl Hayashi, Tatsuro verfasserin aut DNA methylation status of REIC/Dkk-3 gene in human malignancies 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Purpose The REIC (reduced expression in immortalized cells)/Dkk-3 is down-regulated in various cancers and considered to be a tumor suppressor gene. REIC/Dkk-3 mRNA has two isoforms (type-a,b). REIC type-a mRNA has shown to be a major transcript in various cancer cells, and its promoter activity was much stronger than that of type-b. In this study, we examined the methylation status of REIC/Dkk-3 type-a in a broad range of human malignancies. Methods We examined REIC/Dkk-3 type-a methylation in breast cancers, non-small-cell lung cancers, gastric cancers, colorectal cancers, and malignant pleural mesotheliomas using a quantitative combined bisulfite restriction analysis assay and bisulfate sequencing. REIC/Dkk-3 type-a and type-b expression was examined using reverse transcriptional PCR. The relationships between the methylation and clinicopathological factors were analyzed. Results The rate of REIC/Dkk-3 type-a methylation ranged from 26.2 to 50.0% in the various primary tumors that were examined. REIC/Dkk-3 type-a methylation in breast cancer cells was significantly heavier than that in the other cell lines that we tested. REIC/Dkk-3 type-a methylation was inversely correlated with REIC/Dkk-3 type-a expression. There was a correlation between REIC/Dkk-3 type-a and type-b mRNA expression. REIC/Dkk-3 type-a expression was restored in MDA-MB-231 cells using 5-aza-2′-deoxycytidine treatment. We found that estrogen receptor–positive breast cancers were significantly more common among the methylated group than among the non-methylated group. Conclusions REIC/Dkk-3 type-a methylation was frequently detected in a broad range of cancers and appeared to play a key role in silencing REIC/Dkk-3 type-a expression in these malignancies. DNA methylation (dpeaa)DE-He213 - (dpeaa)DE-He213 Breast cancer (dpeaa)DE-He213 Lung cancer (dpeaa)DE-He213 Mesothelioma (dpeaa)DE-He213 Asano, Hiroaki verfasserin aut Toyooka, Shinichi verfasserin aut Tsukuda, Kazunori verfasserin aut Soh, Junichi verfasserin aut Shien, Tadahiko verfasserin aut Taira, Naruto verfasserin aut Maki, Yuho verfasserin aut Tanaka, Norimitsu verfasserin aut Doihara, Hiroyoshi verfasserin aut Nasu, Yasutomo verfasserin aut Huh, Nam-ho verfasserin aut Miyoshi, Shinichiro verfasserin aut Enthalten in Journal of cancer research and clinical oncology Berlin : Springer, 1904 138(2012), 5 vom: 25. Jan., Seite 799-809 (DE-627)253769515 (DE-600)1459285-X 1432-1335 nnns volume:138 year:2012 number:5 day:25 month:01 pages:799-809 https://dx.doi.org/10.1007/s00432-012-1158-6 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.81 ASE AR 138 2012 5 25 01 799-809 |
| allfieldsGer |
10.1007/s00432-012-1158-6 doi (DE-627)SPR00584911X (SPR)s00432-012-1158-6-e DE-627 ger DE-627 rakwb eng 610 ASE 44.81 bkl Hayashi, Tatsuro verfasserin aut DNA methylation status of REIC/Dkk-3 gene in human malignancies 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Purpose The REIC (reduced expression in immortalized cells)/Dkk-3 is down-regulated in various cancers and considered to be a tumor suppressor gene. REIC/Dkk-3 mRNA has two isoforms (type-a,b). REIC type-a mRNA has shown to be a major transcript in various cancer cells, and its promoter activity was much stronger than that of type-b. In this study, we examined the methylation status of REIC/Dkk-3 type-a in a broad range of human malignancies. Methods We examined REIC/Dkk-3 type-a methylation in breast cancers, non-small-cell lung cancers, gastric cancers, colorectal cancers, and malignant pleural mesotheliomas using a quantitative combined bisulfite restriction analysis assay and bisulfate sequencing. REIC/Dkk-3 type-a and type-b expression was examined using reverse transcriptional PCR. The relationships between the methylation and clinicopathological factors were analyzed. Results The rate of REIC/Dkk-3 type-a methylation ranged from 26.2 to 50.0% in the various primary tumors that were examined. REIC/Dkk-3 type-a methylation in breast cancer cells was significantly heavier than that in the other cell lines that we tested. REIC/Dkk-3 type-a methylation was inversely correlated with REIC/Dkk-3 type-a expression. There was a correlation between REIC/Dkk-3 type-a and type-b mRNA expression. REIC/Dkk-3 type-a expression was restored in MDA-MB-231 cells using 5-aza-2′-deoxycytidine treatment. We found that estrogen receptor–positive breast cancers were significantly more common among the methylated group than among the non-methylated group. Conclusions REIC/Dkk-3 type-a methylation was frequently detected in a broad range of cancers and appeared to play a key role in silencing REIC/Dkk-3 type-a expression in these malignancies. DNA methylation (dpeaa)DE-He213 - (dpeaa)DE-He213 Breast cancer (dpeaa)DE-He213 Lung cancer (dpeaa)DE-He213 Mesothelioma (dpeaa)DE-He213 Asano, Hiroaki verfasserin aut Toyooka, Shinichi verfasserin aut Tsukuda, Kazunori verfasserin aut Soh, Junichi verfasserin aut Shien, Tadahiko verfasserin aut Taira, Naruto verfasserin aut Maki, Yuho verfasserin aut Tanaka, Norimitsu verfasserin aut Doihara, Hiroyoshi verfasserin aut Nasu, Yasutomo verfasserin aut Huh, Nam-ho verfasserin aut Miyoshi, Shinichiro verfasserin aut Enthalten in Journal of cancer research and clinical oncology Berlin : Springer, 1904 138(2012), 5 vom: 25. Jan., Seite 799-809 (DE-627)253769515 (DE-600)1459285-X 1432-1335 nnns volume:138 year:2012 number:5 day:25 month:01 pages:799-809 https://dx.doi.org/10.1007/s00432-012-1158-6 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.81 ASE AR 138 2012 5 25 01 799-809 |
| allfieldsSound |
10.1007/s00432-012-1158-6 doi (DE-627)SPR00584911X (SPR)s00432-012-1158-6-e DE-627 ger DE-627 rakwb eng 610 ASE 44.81 bkl Hayashi, Tatsuro verfasserin aut DNA methylation status of REIC/Dkk-3 gene in human malignancies 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Purpose The REIC (reduced expression in immortalized cells)/Dkk-3 is down-regulated in various cancers and considered to be a tumor suppressor gene. REIC/Dkk-3 mRNA has two isoforms (type-a,b). REIC type-a mRNA has shown to be a major transcript in various cancer cells, and its promoter activity was much stronger than that of type-b. In this study, we examined the methylation status of REIC/Dkk-3 type-a in a broad range of human malignancies. Methods We examined REIC/Dkk-3 type-a methylation in breast cancers, non-small-cell lung cancers, gastric cancers, colorectal cancers, and malignant pleural mesotheliomas using a quantitative combined bisulfite restriction analysis assay and bisulfate sequencing. REIC/Dkk-3 type-a and type-b expression was examined using reverse transcriptional PCR. The relationships between the methylation and clinicopathological factors were analyzed. Results The rate of REIC/Dkk-3 type-a methylation ranged from 26.2 to 50.0% in the various primary tumors that were examined. REIC/Dkk-3 type-a methylation in breast cancer cells was significantly heavier than that in the other cell lines that we tested. REIC/Dkk-3 type-a methylation was inversely correlated with REIC/Dkk-3 type-a expression. There was a correlation between REIC/Dkk-3 type-a and type-b mRNA expression. REIC/Dkk-3 type-a expression was restored in MDA-MB-231 cells using 5-aza-2′-deoxycytidine treatment. We found that estrogen receptor–positive breast cancers were significantly more common among the methylated group than among the non-methylated group. Conclusions REIC/Dkk-3 type-a methylation was frequently detected in a broad range of cancers and appeared to play a key role in silencing REIC/Dkk-3 type-a expression in these malignancies. DNA methylation (dpeaa)DE-He213 - (dpeaa)DE-He213 Breast cancer (dpeaa)DE-He213 Lung cancer (dpeaa)DE-He213 Mesothelioma (dpeaa)DE-He213 Asano, Hiroaki verfasserin aut Toyooka, Shinichi verfasserin aut Tsukuda, Kazunori verfasserin aut Soh, Junichi verfasserin aut Shien, Tadahiko verfasserin aut Taira, Naruto verfasserin aut Maki, Yuho verfasserin aut Tanaka, Norimitsu verfasserin aut Doihara, Hiroyoshi verfasserin aut Nasu, Yasutomo verfasserin aut Huh, Nam-ho verfasserin aut Miyoshi, Shinichiro verfasserin aut Enthalten in Journal of cancer research and clinical oncology Berlin : Springer, 1904 138(2012), 5 vom: 25. Jan., Seite 799-809 (DE-627)253769515 (DE-600)1459285-X 1432-1335 nnns volume:138 year:2012 number:5 day:25 month:01 pages:799-809 https://dx.doi.org/10.1007/s00432-012-1158-6 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.81 ASE AR 138 2012 5 25 01 799-809 |
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Enthalten in Journal of cancer research and clinical oncology 138(2012), 5 vom: 25. Jan., Seite 799-809 volume:138 year:2012 number:5 day:25 month:01 pages:799-809 |
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Enthalten in Journal of cancer research and clinical oncology 138(2012), 5 vom: 25. Jan., Seite 799-809 volume:138 year:2012 number:5 day:25 month:01 pages:799-809 |
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DNA methylation - Breast cancer Lung cancer Mesothelioma |
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Journal of cancer research and clinical oncology |
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Hayashi, Tatsuro @@aut@@ Asano, Hiroaki @@aut@@ Toyooka, Shinichi @@aut@@ Tsukuda, Kazunori @@aut@@ Soh, Junichi @@aut@@ Shien, Tadahiko @@aut@@ Taira, Naruto @@aut@@ Maki, Yuho @@aut@@ Tanaka, Norimitsu @@aut@@ Doihara, Hiroyoshi @@aut@@ Nasu, Yasutomo @@aut@@ Huh, Nam-ho @@aut@@ Miyoshi, Shinichiro @@aut@@ |
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2012-01-25T00:00:00Z |
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REIC/Dkk-3 mRNA has two isoforms (type-a,b). REIC type-a mRNA has shown to be a major transcript in various cancer cells, and its promoter activity was much stronger than that of type-b. In this study, we examined the methylation status of REIC/Dkk-3 type-a in a broad range of human malignancies. Methods We examined REIC/Dkk-3 type-a methylation in breast cancers, non-small-cell lung cancers, gastric cancers, colorectal cancers, and malignant pleural mesotheliomas using a quantitative combined bisulfite restriction analysis assay and bisulfate sequencing. REIC/Dkk-3 type-a and type-b expression was examined using reverse transcriptional PCR. The relationships between the methylation and clinicopathological factors were analyzed. Results The rate of REIC/Dkk-3 type-a methylation ranged from 26.2 to 50.0% in the various primary tumors that were examined. REIC/Dkk-3 type-a methylation in breast cancer cells was significantly heavier than that in the other cell lines that we tested. REIC/Dkk-3 type-a methylation was inversely correlated with REIC/Dkk-3 type-a expression. There was a correlation between REIC/Dkk-3 type-a and type-b mRNA expression. REIC/Dkk-3 type-a expression was restored in MDA-MB-231 cells using 5-aza-2′-deoxycytidine treatment. We found that estrogen receptor–positive breast cancers were significantly more common among the methylated group than among the non-methylated group. 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| author |
Hayashi, Tatsuro |
| spellingShingle |
Hayashi, Tatsuro ddc 610 bkl 44.81 misc DNA methylation misc - misc Breast cancer misc Lung cancer misc Mesothelioma DNA methylation status of REIC/Dkk-3 gene in human malignancies |
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Hayashi, Tatsuro |
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610 - Medicine & health |
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1432-1335 |
| topic_title |
610 ASE 44.81 bkl DNA methylation status of REIC/Dkk-3 gene in human malignancies DNA methylation (dpeaa)DE-He213 - (dpeaa)DE-He213 Breast cancer (dpeaa)DE-He213 Lung cancer (dpeaa)DE-He213 Mesothelioma (dpeaa)DE-He213 |
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ddc 610 bkl 44.81 misc DNA methylation misc - misc Breast cancer misc Lung cancer misc Mesothelioma |
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ddc 610 bkl 44.81 misc DNA methylation misc - misc Breast cancer misc Lung cancer misc Mesothelioma |
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ddc 610 bkl 44.81 misc DNA methylation misc - misc Breast cancer misc Lung cancer misc Mesothelioma |
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Journal of cancer research and clinical oncology |
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Journal of cancer research and clinical oncology |
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DNA methylation status of REIC/Dkk-3 gene in human malignancies |
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(DE-627)SPR00584911X (SPR)s00432-012-1158-6-e |
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DNA methylation status of REIC/Dkk-3 gene in human malignancies |
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Hayashi, Tatsuro |
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Journal of cancer research and clinical oncology |
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Journal of cancer research and clinical oncology |
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eng |
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2012 |
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Hayashi, Tatsuro Asano, Hiroaki Toyooka, Shinichi Tsukuda, Kazunori Soh, Junichi Shien, Tadahiko Taira, Naruto Maki, Yuho Tanaka, Norimitsu Doihara, Hiroyoshi Nasu, Yasutomo Huh, Nam-ho Miyoshi, Shinichiro |
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138 |
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610 ASE 44.81 bkl |
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Elektronische Aufsätze |
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Hayashi, Tatsuro |
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10.1007/s00432-012-1158-6 |
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610 |
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verfasserin |
| title_sort |
dna methylation status of reic/dkk-3 gene in human malignancies |
| title_auth |
DNA methylation status of REIC/Dkk-3 gene in human malignancies |
| abstract |
Purpose The REIC (reduced expression in immortalized cells)/Dkk-3 is down-regulated in various cancers and considered to be a tumor suppressor gene. REIC/Dkk-3 mRNA has two isoforms (type-a,b). REIC type-a mRNA has shown to be a major transcript in various cancer cells, and its promoter activity was much stronger than that of type-b. In this study, we examined the methylation status of REIC/Dkk-3 type-a in a broad range of human malignancies. Methods We examined REIC/Dkk-3 type-a methylation in breast cancers, non-small-cell lung cancers, gastric cancers, colorectal cancers, and malignant pleural mesotheliomas using a quantitative combined bisulfite restriction analysis assay and bisulfate sequencing. REIC/Dkk-3 type-a and type-b expression was examined using reverse transcriptional PCR. The relationships between the methylation and clinicopathological factors were analyzed. Results The rate of REIC/Dkk-3 type-a methylation ranged from 26.2 to 50.0% in the various primary tumors that were examined. REIC/Dkk-3 type-a methylation in breast cancer cells was significantly heavier than that in the other cell lines that we tested. REIC/Dkk-3 type-a methylation was inversely correlated with REIC/Dkk-3 type-a expression. There was a correlation between REIC/Dkk-3 type-a and type-b mRNA expression. REIC/Dkk-3 type-a expression was restored in MDA-MB-231 cells using 5-aza-2′-deoxycytidine treatment. We found that estrogen receptor–positive breast cancers were significantly more common among the methylated group than among the non-methylated group. Conclusions REIC/Dkk-3 type-a methylation was frequently detected in a broad range of cancers and appeared to play a key role in silencing REIC/Dkk-3 type-a expression in these malignancies. |
| abstractGer |
Purpose The REIC (reduced expression in immortalized cells)/Dkk-3 is down-regulated in various cancers and considered to be a tumor suppressor gene. REIC/Dkk-3 mRNA has two isoforms (type-a,b). REIC type-a mRNA has shown to be a major transcript in various cancer cells, and its promoter activity was much stronger than that of type-b. In this study, we examined the methylation status of REIC/Dkk-3 type-a in a broad range of human malignancies. Methods We examined REIC/Dkk-3 type-a methylation in breast cancers, non-small-cell lung cancers, gastric cancers, colorectal cancers, and malignant pleural mesotheliomas using a quantitative combined bisulfite restriction analysis assay and bisulfate sequencing. REIC/Dkk-3 type-a and type-b expression was examined using reverse transcriptional PCR. The relationships between the methylation and clinicopathological factors were analyzed. Results The rate of REIC/Dkk-3 type-a methylation ranged from 26.2 to 50.0% in the various primary tumors that were examined. REIC/Dkk-3 type-a methylation in breast cancer cells was significantly heavier than that in the other cell lines that we tested. REIC/Dkk-3 type-a methylation was inversely correlated with REIC/Dkk-3 type-a expression. There was a correlation between REIC/Dkk-3 type-a and type-b mRNA expression. REIC/Dkk-3 type-a expression was restored in MDA-MB-231 cells using 5-aza-2′-deoxycytidine treatment. We found that estrogen receptor–positive breast cancers were significantly more common among the methylated group than among the non-methylated group. Conclusions REIC/Dkk-3 type-a methylation was frequently detected in a broad range of cancers and appeared to play a key role in silencing REIC/Dkk-3 type-a expression in these malignancies. |
| abstract_unstemmed |
Purpose The REIC (reduced expression in immortalized cells)/Dkk-3 is down-regulated in various cancers and considered to be a tumor suppressor gene. REIC/Dkk-3 mRNA has two isoforms (type-a,b). REIC type-a mRNA has shown to be a major transcript in various cancer cells, and its promoter activity was much stronger than that of type-b. In this study, we examined the methylation status of REIC/Dkk-3 type-a in a broad range of human malignancies. Methods We examined REIC/Dkk-3 type-a methylation in breast cancers, non-small-cell lung cancers, gastric cancers, colorectal cancers, and malignant pleural mesotheliomas using a quantitative combined bisulfite restriction analysis assay and bisulfate sequencing. REIC/Dkk-3 type-a and type-b expression was examined using reverse transcriptional PCR. The relationships between the methylation and clinicopathological factors were analyzed. Results The rate of REIC/Dkk-3 type-a methylation ranged from 26.2 to 50.0% in the various primary tumors that were examined. REIC/Dkk-3 type-a methylation in breast cancer cells was significantly heavier than that in the other cell lines that we tested. REIC/Dkk-3 type-a methylation was inversely correlated with REIC/Dkk-3 type-a expression. There was a correlation between REIC/Dkk-3 type-a and type-b mRNA expression. REIC/Dkk-3 type-a expression was restored in MDA-MB-231 cells using 5-aza-2′-deoxycytidine treatment. We found that estrogen receptor–positive breast cancers were significantly more common among the methylated group than among the non-methylated group. Conclusions REIC/Dkk-3 type-a methylation was frequently detected in a broad range of cancers and appeared to play a key role in silencing REIC/Dkk-3 type-a expression in these malignancies. |
| collection_details |
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| title_short |
DNA methylation status of REIC/Dkk-3 gene in human malignancies |
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https://dx.doi.org/10.1007/s00432-012-1158-6 |
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Asano, Hiroaki Toyooka, Shinichi Tsukuda, Kazunori Soh, Junichi Shien, Tadahiko Taira, Naruto Maki, Yuho Tanaka, Norimitsu Doihara, Hiroyoshi Nasu, Yasutomo Huh, Nam-ho Miyoshi, Shinichiro |
| author2Str |
Asano, Hiroaki Toyooka, Shinichi Tsukuda, Kazunori Soh, Junichi Shien, Tadahiko Taira, Naruto Maki, Yuho Tanaka, Norimitsu Doihara, Hiroyoshi Nasu, Yasutomo Huh, Nam-ho Miyoshi, Shinichiro |
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| doi_str |
10.1007/s00432-012-1158-6 |
| up_date |
2024-07-03T19:07:02.866Z |
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1803585976136630272 |
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REIC/Dkk-3 type-a methylation was inversely correlated with REIC/Dkk-3 type-a expression. There was a correlation between REIC/Dkk-3 type-a and type-b mRNA expression. REIC/Dkk-3 type-a expression was restored in MDA-MB-231 cells using 5-aza-2′-deoxycytidine treatment. We found that estrogen receptor–positive breast cancers were significantly more common among the methylated group than among the non-methylated group. 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| score |
7.401598 |