Re: Association between endothelin receptor B nonsynonymous variants and melanoma risk
The known genetic risk factors for malignant melanoma, besides CDKN2A and CDK4 mutations, include variant alleles of the melanocortin-1 receptor (MC1R) gene ( 1 ) . Recently, Soufir et al. ( 2 ) in a study that was based on 137 malignant melanoma patients and 131 ethnically matched control subje...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Thirumaran, Ranjit Kumar - 1978- [verfasserIn] Figl, Adina - 1975- [verfasserIn] Ugurel, Selma - 1971- [verfasserIn] Hemminki, Kari - 1947- [verfasserIn] Schadendorf, Dirk - 1960- [verfasserIn] Kumar, Rajiv - 1955- [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
06 September 2006 |
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| Anmerkung: |
Gesehen am 05.02.2021 |
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| Umfang: |
2 |
| Übergeordnetes Werk: |
Enthalten in: Journal of the National Cancer Institute - National Cancer Institute, Oxford : Oxford Univ. Press, 1941, 98(2006), 17, Seite 1252-1253 |
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| Übergeordnetes Werk: |
volume:98 ; year:2006 ; number:17 ; pages:1252-1253 ; extent:2 |
| Links: |
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| DOI / URN: |
10.1093/jnci/djj336 |
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| Katalog-ID: |
1747635618 |
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| 100 | 1 | |a Thirumaran, Ranjit Kumar |d 1978- |e verfasserin |0 (DE-588)132214466 |0 (DE-627)519239571 |0 (DE-576)299010074 |4 aut | |
| 245 | 1 | 0 | |a Re: Association between endothelin receptor B nonsynonymous variants and melanoma risk |c Ranjit K. Thirumaran, Adina Thoelke, Selma Ugurel, Kari Hemminki, Dirk Schadendorf, Rajiv Kumar |
| 264 | 1 | |c 06 September 2006 | |
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| 500 | |a Gesehen am 05.02.2021 | ||
| 520 | |a The known genetic risk factors for malignant melanoma, besides CDKN2A and CDK4 mutations, include variant alleles of the melanocortin-1 receptor (MC1R) gene ( 1 ) . Recently, Soufir et al. ( 2 ) in a study that was based on 137 malignant melanoma patients and 131 ethnically matched control subjects reported an association between nonsynonymous variants in the endothelin receptor B (EDNRB) gene and increased risk of melanoma. They reported six nonsynonymous EDNRB variants in 15 patients compared with two variants in four control subjects. EDNRB promotes migration and proliferation of melanocyte precursors during embryonic development ( 3 ) . The overexpression of EDNRB in most human melanomas and the shrinkage of tumors in immunocompromised mice and induction of apoptosis upon inhibition of EDNRB suggest a role in disease progression ( 4 , 5 ) . Mutations in the gene are associated with several genetic disorders. The most common variant detected by Soufir et al. in 12 melanoma patients and three control subjects, S305N, has previously been reported in Hirschsprung disease ( 2 , 6 ) . | ||
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06 September 2006 |
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2006 |
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10.1093/jnci/djj336 doi (DE-627)1747635618 (DE-599)KXP1747635618 (OCoLC)1341391735 DE-627 ger DE-627 rda eng Thirumaran, Ranjit Kumar 1978- verfasserin (DE-588)132214466 (DE-627)519239571 (DE-576)299010074 aut Re: Association between endothelin receptor B nonsynonymous variants and melanoma risk Ranjit K. Thirumaran, Adina Thoelke, Selma Ugurel, Kari Hemminki, Dirk Schadendorf, Rajiv Kumar 06 September 2006 2 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Gesehen am 05.02.2021 The known genetic risk factors for malignant melanoma, besides CDKN2A and CDK4 mutations, include variant alleles of the melanocortin-1 receptor (MC1R) gene ( 1 ) . Recently, Soufir et al. ( 2 ) in a study that was based on 137 malignant melanoma patients and 131 ethnically matched control subjects reported an association between nonsynonymous variants in the endothelin receptor B (EDNRB) gene and increased risk of melanoma. They reported six nonsynonymous EDNRB variants in 15 patients compared with two variants in four control subjects. EDNRB promotes migration and proliferation of melanocyte precursors during embryonic development ( 3 ) . The overexpression of EDNRB in most human melanomas and the shrinkage of tumors in immunocompromised mice and induction of apoptosis upon inhibition of EDNRB suggest a role in disease progression ( 4 , 5 ) . Mutations in the gene are associated with several genetic disorders. The most common variant detected by Soufir et al. in 12 melanoma patients and three control subjects, S305N, has previously been reported in Hirschsprung disease ( 2 , 6 ) . Figl, Adina 1975- verfasserin (DE-588)1146398816 (DE-627)1005834245 (DE-576)186024819 aut Ugurel, Selma 1971- verfasserin (DE-588)122030923 (DE-627)081693532 (DE-576)293057567 aut Hemminki, Kari 1947- verfasserin (DE-588)1150735872 (DE-627)1010964402 (DE-576)172043751 aut Schadendorf, Dirk 1960- verfasserin (DE-588)11142576X (DE-627)499566076 (DE-576)289702275 aut Kumar, Rajiv 1955- verfasserin (DE-588)1164253425 (DE-627)1028811942 (DE-576)508469805 aut Enthalten in National Cancer Institute Journal of the National Cancer Institute Oxford : Oxford Univ. Press, 1941 98(2006), 17, Seite 1252-1253 (DE-627)265780713 (DE-600)1465951-7 (DE-576)074959581 1460-2105 nnns volume:98 year:2006 number:17 pages:1252-1253 extent:2 https://doi.org/10.1093/jnci/djj336 Verlag Resolving-System lizenzpflichtig Volltext GBV_USEFLAG_U GBV_ILN_2013 ISIL_DE-16-250 SYSFLAG_1 GBV_KXP 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_121 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_374 GBV_ILN_602 GBV_ILN_636 GBV_ILN_647 GBV_ILN_702 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_2018 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_2043 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2098 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_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2145 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2158 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_2810 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_4277 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_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4346 GBV_ILN_4367 GBV_ILN_4392 GBV_ILN_4393 GBV_ILN_4700 GBV_ILN_4753 AR 98 2006 17 1252-1253 2 2013 01 DE-16-250 3849400859 00 --%%-- --%%-- --%%-- --%%-- l01 05-02-21 2013 01 DE-16-250 00 s hd2006 2013 01 DE-16-250 01 s (DE-627)1410508463 wissenschaftlicher Artikel (Zeitschrift) 2013 01 DE-16-250 02 s per_6 2013 01 DE-16-250 03 s s_2 2013 01 DE-16-250 04 p (DE-627)1742696414 Figl, Adina 2013 01 DE-16-250 04 k (DE-627)1416535500 Fakultät für Biowissenschaften 2013 01 DE-16-250 04 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 04 s pos_2 2013 01 DE-16-250 05 p (DE-627)1581218141 Ugurel, Selma 2013 01 DE-16-250 05 k (DE-627)1416466967 Medizinische Fakultät Heidelberg 2013 01 DE-16-250 05 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 05 s pos_3 2013 01 DE-16-250 06 p (DE-627)1567234704 Hemminki, Kari 2013 01 DE-16-250 06 k (DE-627)1416466967 Medizinische Fakultät Heidelberg 2013 01 DE-16-250 06 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 06 s pos_4 2013 01 DE-16-250 07 p (DE-627)1582286639 Schadendorf, Dirk 2013 01 DE-16-250 07 k (DE-627)1416466967 Medizinische Fakultät Heidelberg 2013 01 DE-16-250 07 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 07 s pos_5 2013 01 DE-16-250 08 p (DE-627)1578469856 Kumar, Rajiv 2013 01 DE-16-250 08 k (DE-627)1416822720 Extern 2013 01 DE-16-250 08 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 08 s pos_6 |
| spelling |
10.1093/jnci/djj336 doi (DE-627)1747635618 (DE-599)KXP1747635618 (OCoLC)1341391735 DE-627 ger DE-627 rda eng Thirumaran, Ranjit Kumar 1978- verfasserin (DE-588)132214466 (DE-627)519239571 (DE-576)299010074 aut Re: Association between endothelin receptor B nonsynonymous variants and melanoma risk Ranjit K. Thirumaran, Adina Thoelke, Selma Ugurel, Kari Hemminki, Dirk Schadendorf, Rajiv Kumar 06 September 2006 2 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Gesehen am 05.02.2021 The known genetic risk factors for malignant melanoma, besides CDKN2A and CDK4 mutations, include variant alleles of the melanocortin-1 receptor (MC1R) gene ( 1 ) . Recently, Soufir et al. ( 2 ) in a study that was based on 137 malignant melanoma patients and 131 ethnically matched control subjects reported an association between nonsynonymous variants in the endothelin receptor B (EDNRB) gene and increased risk of melanoma. They reported six nonsynonymous EDNRB variants in 15 patients compared with two variants in four control subjects. EDNRB promotes migration and proliferation of melanocyte precursors during embryonic development ( 3 ) . The overexpression of EDNRB in most human melanomas and the shrinkage of tumors in immunocompromised mice and induction of apoptosis upon inhibition of EDNRB suggest a role in disease progression ( 4 , 5 ) . Mutations in the gene are associated with several genetic disorders. The most common variant detected by Soufir et al. in 12 melanoma patients and three control subjects, S305N, has previously been reported in Hirschsprung disease ( 2 , 6 ) . Figl, Adina 1975- verfasserin (DE-588)1146398816 (DE-627)1005834245 (DE-576)186024819 aut Ugurel, Selma 1971- verfasserin (DE-588)122030923 (DE-627)081693532 (DE-576)293057567 aut Hemminki, Kari 1947- verfasserin (DE-588)1150735872 (DE-627)1010964402 (DE-576)172043751 aut Schadendorf, Dirk 1960- verfasserin (DE-588)11142576X (DE-627)499566076 (DE-576)289702275 aut Kumar, Rajiv 1955- verfasserin (DE-588)1164253425 (DE-627)1028811942 (DE-576)508469805 aut Enthalten in National Cancer Institute Journal of the National Cancer Institute Oxford : Oxford Univ. Press, 1941 98(2006), 17, Seite 1252-1253 (DE-627)265780713 (DE-600)1465951-7 (DE-576)074959581 1460-2105 nnns volume:98 year:2006 number:17 pages:1252-1253 extent:2 https://doi.org/10.1093/jnci/djj336 Verlag Resolving-System lizenzpflichtig Volltext GBV_USEFLAG_U GBV_ILN_2013 ISIL_DE-16-250 SYSFLAG_1 GBV_KXP 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_121 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_374 GBV_ILN_602 GBV_ILN_636 GBV_ILN_647 GBV_ILN_702 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_2018 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_2043 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2098 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_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2145 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2158 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_2810 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_4277 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_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4346 GBV_ILN_4367 GBV_ILN_4392 GBV_ILN_4393 GBV_ILN_4700 GBV_ILN_4753 AR 98 2006 17 1252-1253 2 2013 01 DE-16-250 3849400859 00 --%%-- --%%-- --%%-- --%%-- l01 05-02-21 2013 01 DE-16-250 00 s hd2006 2013 01 DE-16-250 01 s (DE-627)1410508463 wissenschaftlicher Artikel (Zeitschrift) 2013 01 DE-16-250 02 s per_6 2013 01 DE-16-250 03 s s_2 2013 01 DE-16-250 04 p (DE-627)1742696414 Figl, Adina 2013 01 DE-16-250 04 k (DE-627)1416535500 Fakultät für Biowissenschaften 2013 01 DE-16-250 04 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 04 s pos_2 2013 01 DE-16-250 05 p (DE-627)1581218141 Ugurel, Selma 2013 01 DE-16-250 05 k (DE-627)1416466967 Medizinische Fakultät Heidelberg 2013 01 DE-16-250 05 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 05 s pos_3 2013 01 DE-16-250 06 p (DE-627)1567234704 Hemminki, Kari 2013 01 DE-16-250 06 k (DE-627)1416466967 Medizinische Fakultät Heidelberg 2013 01 DE-16-250 06 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 06 s pos_4 2013 01 DE-16-250 07 p (DE-627)1582286639 Schadendorf, Dirk 2013 01 DE-16-250 07 k (DE-627)1416466967 Medizinische Fakultät Heidelberg 2013 01 DE-16-250 07 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 07 s pos_5 2013 01 DE-16-250 08 p (DE-627)1578469856 Kumar, Rajiv 2013 01 DE-16-250 08 k (DE-627)1416822720 Extern 2013 01 DE-16-250 08 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 08 s pos_6 |
| allfields_unstemmed |
10.1093/jnci/djj336 doi (DE-627)1747635618 (DE-599)KXP1747635618 (OCoLC)1341391735 DE-627 ger DE-627 rda eng Thirumaran, Ranjit Kumar 1978- verfasserin (DE-588)132214466 (DE-627)519239571 (DE-576)299010074 aut Re: Association between endothelin receptor B nonsynonymous variants and melanoma risk Ranjit K. Thirumaran, Adina Thoelke, Selma Ugurel, Kari Hemminki, Dirk Schadendorf, Rajiv Kumar 06 September 2006 2 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Gesehen am 05.02.2021 The known genetic risk factors for malignant melanoma, besides CDKN2A and CDK4 mutations, include variant alleles of the melanocortin-1 receptor (MC1R) gene ( 1 ) . Recently, Soufir et al. ( 2 ) in a study that was based on 137 malignant melanoma patients and 131 ethnically matched control subjects reported an association between nonsynonymous variants in the endothelin receptor B (EDNRB) gene and increased risk of melanoma. They reported six nonsynonymous EDNRB variants in 15 patients compared with two variants in four control subjects. EDNRB promotes migration and proliferation of melanocyte precursors during embryonic development ( 3 ) . The overexpression of EDNRB in most human melanomas and the shrinkage of tumors in immunocompromised mice and induction of apoptosis upon inhibition of EDNRB suggest a role in disease progression ( 4 , 5 ) . Mutations in the gene are associated with several genetic disorders. The most common variant detected by Soufir et al. in 12 melanoma patients and three control subjects, S305N, has previously been reported in Hirschsprung disease ( 2 , 6 ) . Figl, Adina 1975- verfasserin (DE-588)1146398816 (DE-627)1005834245 (DE-576)186024819 aut Ugurel, Selma 1971- verfasserin (DE-588)122030923 (DE-627)081693532 (DE-576)293057567 aut Hemminki, Kari 1947- verfasserin (DE-588)1150735872 (DE-627)1010964402 (DE-576)172043751 aut Schadendorf, Dirk 1960- verfasserin (DE-588)11142576X (DE-627)499566076 (DE-576)289702275 aut Kumar, Rajiv 1955- verfasserin (DE-588)1164253425 (DE-627)1028811942 (DE-576)508469805 aut Enthalten in National Cancer Institute Journal of the National Cancer Institute Oxford : Oxford Univ. Press, 1941 98(2006), 17, Seite 1252-1253 (DE-627)265780713 (DE-600)1465951-7 (DE-576)074959581 1460-2105 nnns volume:98 year:2006 number:17 pages:1252-1253 extent:2 https://doi.org/10.1093/jnci/djj336 Verlag Resolving-System lizenzpflichtig Volltext GBV_USEFLAG_U GBV_ILN_2013 ISIL_DE-16-250 SYSFLAG_1 GBV_KXP 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_121 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_374 GBV_ILN_602 GBV_ILN_636 GBV_ILN_647 GBV_ILN_702 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_2018 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_2043 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2098 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_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2145 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2158 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_2810 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_4277 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_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4346 GBV_ILN_4367 GBV_ILN_4392 GBV_ILN_4393 GBV_ILN_4700 GBV_ILN_4753 AR 98 2006 17 1252-1253 2 2013 01 DE-16-250 3849400859 00 --%%-- --%%-- --%%-- --%%-- l01 05-02-21 2013 01 DE-16-250 00 s hd2006 2013 01 DE-16-250 01 s (DE-627)1410508463 wissenschaftlicher Artikel (Zeitschrift) 2013 01 DE-16-250 02 s per_6 2013 01 DE-16-250 03 s s_2 2013 01 DE-16-250 04 p (DE-627)1742696414 Figl, Adina 2013 01 DE-16-250 04 k (DE-627)1416535500 Fakultät für Biowissenschaften 2013 01 DE-16-250 04 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 04 s pos_2 2013 01 DE-16-250 05 p (DE-627)1581218141 Ugurel, Selma 2013 01 DE-16-250 05 k (DE-627)1416466967 Medizinische Fakultät Heidelberg 2013 01 DE-16-250 05 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 05 s pos_3 2013 01 DE-16-250 06 p (DE-627)1567234704 Hemminki, Kari 2013 01 DE-16-250 06 k (DE-627)1416466967 Medizinische Fakultät Heidelberg 2013 01 DE-16-250 06 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 06 s pos_4 2013 01 DE-16-250 07 p (DE-627)1582286639 Schadendorf, Dirk 2013 01 DE-16-250 07 k (DE-627)1416466967 Medizinische Fakultät Heidelberg 2013 01 DE-16-250 07 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 07 s pos_5 2013 01 DE-16-250 08 p (DE-627)1578469856 Kumar, Rajiv 2013 01 DE-16-250 08 k (DE-627)1416822720 Extern 2013 01 DE-16-250 08 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 08 s pos_6 |
| allfieldsGer |
10.1093/jnci/djj336 doi (DE-627)1747635618 (DE-599)KXP1747635618 (OCoLC)1341391735 DE-627 ger DE-627 rda eng Thirumaran, Ranjit Kumar 1978- verfasserin (DE-588)132214466 (DE-627)519239571 (DE-576)299010074 aut Re: Association between endothelin receptor B nonsynonymous variants and melanoma risk Ranjit K. Thirumaran, Adina Thoelke, Selma Ugurel, Kari Hemminki, Dirk Schadendorf, Rajiv Kumar 06 September 2006 2 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Gesehen am 05.02.2021 The known genetic risk factors for malignant melanoma, besides CDKN2A and CDK4 mutations, include variant alleles of the melanocortin-1 receptor (MC1R) gene ( 1 ) . Recently, Soufir et al. ( 2 ) in a study that was based on 137 malignant melanoma patients and 131 ethnically matched control subjects reported an association between nonsynonymous variants in the endothelin receptor B (EDNRB) gene and increased risk of melanoma. They reported six nonsynonymous EDNRB variants in 15 patients compared with two variants in four control subjects. EDNRB promotes migration and proliferation of melanocyte precursors during embryonic development ( 3 ) . The overexpression of EDNRB in most human melanomas and the shrinkage of tumors in immunocompromised mice and induction of apoptosis upon inhibition of EDNRB suggest a role in disease progression ( 4 , 5 ) . Mutations in the gene are associated with several genetic disorders. The most common variant detected by Soufir et al. in 12 melanoma patients and three control subjects, S305N, has previously been reported in Hirschsprung disease ( 2 , 6 ) . Figl, Adina 1975- verfasserin (DE-588)1146398816 (DE-627)1005834245 (DE-576)186024819 aut Ugurel, Selma 1971- verfasserin (DE-588)122030923 (DE-627)081693532 (DE-576)293057567 aut Hemminki, Kari 1947- verfasserin (DE-588)1150735872 (DE-627)1010964402 (DE-576)172043751 aut Schadendorf, Dirk 1960- verfasserin (DE-588)11142576X (DE-627)499566076 (DE-576)289702275 aut Kumar, Rajiv 1955- verfasserin (DE-588)1164253425 (DE-627)1028811942 (DE-576)508469805 aut Enthalten in National Cancer Institute Journal of the National Cancer Institute Oxford : Oxford Univ. 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10.1093/jnci/djj336 doi (DE-627)1747635618 (DE-599)KXP1747635618 (OCoLC)1341391735 DE-627 ger DE-627 rda eng Thirumaran, Ranjit Kumar 1978- verfasserin (DE-588)132214466 (DE-627)519239571 (DE-576)299010074 aut Re: Association between endothelin receptor B nonsynonymous variants and melanoma risk Ranjit K. Thirumaran, Adina Thoelke, Selma Ugurel, Kari Hemminki, Dirk Schadendorf, Rajiv Kumar 06 September 2006 2 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Gesehen am 05.02.2021 The known genetic risk factors for malignant melanoma, besides CDKN2A and CDK4 mutations, include variant alleles of the melanocortin-1 receptor (MC1R) gene ( 1 ) . Recently, Soufir et al. ( 2 ) in a study that was based on 137 malignant melanoma patients and 131 ethnically matched control subjects reported an association between nonsynonymous variants in the endothelin receptor B (EDNRB) gene and increased risk of melanoma. They reported six nonsynonymous EDNRB variants in 15 patients compared with two variants in four control subjects. EDNRB promotes migration and proliferation of melanocyte precursors during embryonic development ( 3 ) . The overexpression of EDNRB in most human melanomas and the shrinkage of tumors in immunocompromised mice and induction of apoptosis upon inhibition of EDNRB suggest a role in disease progression ( 4 , 5 ) . Mutations in the gene are associated with several genetic disorders. The most common variant detected by Soufir et al. in 12 melanoma patients and three control subjects, S305N, has previously been reported in Hirschsprung disease ( 2 , 6 ) . Figl, Adina 1975- verfasserin (DE-588)1146398816 (DE-627)1005834245 (DE-576)186024819 aut Ugurel, Selma 1971- verfasserin (DE-588)122030923 (DE-627)081693532 (DE-576)293057567 aut Hemminki, Kari 1947- verfasserin (DE-588)1150735872 (DE-627)1010964402 (DE-576)172043751 aut Schadendorf, Dirk 1960- verfasserin (DE-588)11142576X (DE-627)499566076 (DE-576)289702275 aut Kumar, Rajiv 1955- verfasserin (DE-588)1164253425 (DE-627)1028811942 (DE-576)508469805 aut Enthalten in National Cancer Institute Journal of the National Cancer Institute Oxford : Oxford Univ. Press, 1941 98(2006), 17, Seite 1252-1253 (DE-627)265780713 (DE-600)1465951-7 (DE-576)074959581 1460-2105 nnns volume:98 year:2006 number:17 pages:1252-1253 extent:2 https://doi.org/10.1093/jnci/djj336 Verlag Resolving-System lizenzpflichtig Volltext GBV_USEFLAG_U GBV_ILN_2013 ISIL_DE-16-250 SYSFLAG_1 GBV_KXP 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_121 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_374 GBV_ILN_602 GBV_ILN_636 GBV_ILN_647 GBV_ILN_702 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_2018 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_2043 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2098 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_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2145 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2158 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_2810 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_4277 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_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4346 GBV_ILN_4367 GBV_ILN_4392 GBV_ILN_4393 GBV_ILN_4700 GBV_ILN_4753 AR 98 2006 17 1252-1253 2 2013 01 DE-16-250 3849400859 00 --%%-- --%%-- --%%-- --%%-- l01 05-02-21 2013 01 DE-16-250 00 s hd2006 2013 01 DE-16-250 01 s (DE-627)1410508463 wissenschaftlicher Artikel (Zeitschrift) 2013 01 DE-16-250 02 s per_6 2013 01 DE-16-250 03 s s_2 2013 01 DE-16-250 04 p (DE-627)1742696414 Figl, Adina 2013 01 DE-16-250 04 k (DE-627)1416535500 Fakultät für Biowissenschaften 2013 01 DE-16-250 04 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 04 s pos_2 2013 01 DE-16-250 05 p (DE-627)1581218141 Ugurel, Selma 2013 01 DE-16-250 05 k (DE-627)1416466967 Medizinische Fakultät Heidelberg 2013 01 DE-16-250 05 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 05 s pos_3 2013 01 DE-16-250 06 p (DE-627)1567234704 Hemminki, Kari 2013 01 DE-16-250 06 k (DE-627)1416466967 Medizinische Fakultät Heidelberg 2013 01 DE-16-250 06 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 06 s pos_4 2013 01 DE-16-250 07 p (DE-627)1582286639 Schadendorf, Dirk 2013 01 DE-16-250 07 k (DE-627)1416466967 Medizinische Fakultät Heidelberg 2013 01 DE-16-250 07 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 07 s pos_5 2013 01 DE-16-250 08 p (DE-627)1578469856 Kumar, Rajiv 2013 01 DE-16-250 08 k (DE-627)1416822720 Extern 2013 01 DE-16-250 08 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 08 s pos_6 |
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The known genetic risk factors for malignant melanoma, besides CDKN2A and CDK4 mutations, include variant alleles of the melanocortin-1 receptor (MC1R) gene ( 1 ) . Recently, Soufir et al. ( 2 ) in a study that was based on 137 malignant melanoma patients and 131 ethnically matched control subjects reported an association between nonsynonymous variants in the endothelin receptor B (EDNRB) gene and increased risk of melanoma. They reported six nonsynonymous EDNRB variants in 15 patients compared with two variants in four control subjects. EDNRB promotes migration and proliferation of melanocyte precursors during embryonic development ( 3 ) . The overexpression of EDNRB in most human melanomas and the shrinkage of tumors in immunocompromised mice and induction of apoptosis upon inhibition of EDNRB suggest a role in disease progression ( 4 , 5 ) . Mutations in the gene are associated with several genetic disorders. The most common variant detected by Soufir et al. in 12 melanoma patients and three control subjects, S305N, has previously been reported in Hirschsprung disease ( 2 , 6 ) . Gesehen am 05.02.2021 |
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The known genetic risk factors for malignant melanoma, besides CDKN2A and CDK4 mutations, include variant alleles of the melanocortin-1 receptor (MC1R) gene ( 1 ) . Recently, Soufir et al. ( 2 ) in a study that was based on 137 malignant melanoma patients and 131 ethnically matched control subjects reported an association between nonsynonymous variants in the endothelin receptor B (EDNRB) gene and increased risk of melanoma. They reported six nonsynonymous EDNRB variants in 15 patients compared with two variants in four control subjects. EDNRB promotes migration and proliferation of melanocyte precursors during embryonic development ( 3 ) . The overexpression of EDNRB in most human melanomas and the shrinkage of tumors in immunocompromised mice and induction of apoptosis upon inhibition of EDNRB suggest a role in disease progression ( 4 , 5 ) . Mutations in the gene are associated with several genetic disorders. The most common variant detected by Soufir et al. in 12 melanoma patients and three control subjects, S305N, has previously been reported in Hirschsprung disease ( 2 , 6 ) . Gesehen am 05.02.2021 |
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The known genetic risk factors for malignant melanoma, besides CDKN2A and CDK4 mutations, include variant alleles of the melanocortin-1 receptor (MC1R) gene ( 1 ) . Recently, Soufir et al. ( 2 ) in a study that was based on 137 malignant melanoma patients and 131 ethnically matched control subjects reported an association between nonsynonymous variants in the endothelin receptor B (EDNRB) gene and increased risk of melanoma. They reported six nonsynonymous EDNRB variants in 15 patients compared with two variants in four control subjects. EDNRB promotes migration and proliferation of melanocyte precursors during embryonic development ( 3 ) . The overexpression of EDNRB in most human melanomas and the shrinkage of tumors in immunocompromised mice and induction of apoptosis upon inhibition of EDNRB suggest a role in disease progression ( 4 , 5 ) . Mutations in the gene are associated with several genetic disorders. The most common variant detected by Soufir et al. in 12 melanoma patients and three control subjects, S305N, has previously been reported in Hirschsprung disease ( 2 , 6 ) . Gesehen am 05.02.2021 |
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Thirumaran, Adina Thoelke, Selma Ugurel, Kari Hemminki, Dirk Schadendorf, Rajiv Kumar</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">06 September 2006</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">2</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="500" ind1=" " ind2=" "><subfield code="a">Gesehen am 05.02.2021</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">The known genetic risk factors for malignant melanoma, besides CDKN2A and CDK4 mutations, include variant alleles of the melanocortin-1 receptor (MC1R) gene ( 1 ) . Recently, Soufir et al. ( 2 ) in a study that was based on 137 malignant melanoma patients and 131 ethnically matched control subjects reported an association between nonsynonymous variants in the endothelin receptor B (EDNRB) gene and increased risk of melanoma. They reported six nonsynonymous EDNRB variants in 15 patients compared with two variants in four control subjects. EDNRB promotes migration and proliferation of melanocyte precursors during embryonic development ( 3 ) . The overexpression of EDNRB in most human melanomas and the shrinkage of tumors in immunocompromised mice and induction of apoptosis upon inhibition of EDNRB suggest a role in disease progression ( 4 , 5 ) . Mutations in the gene are associated with several genetic disorders. The most common variant detected by Soufir et al. in 12 melanoma patients and three control subjects, S305N, has previously been reported in Hirschsprung disease ( 2 , 6 ) .</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Figl, Adina</subfield><subfield code="d">1975-</subfield><subfield code="e">verfasserin</subfield><subfield code="0">(DE-588)1146398816</subfield><subfield code="0">(DE-627)1005834245</subfield><subfield code="0">(DE-576)186024819</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Ugurel, Selma</subfield><subfield code="d">1971-</subfield><subfield code="e">verfasserin</subfield><subfield code="0">(DE-588)122030923</subfield><subfield code="0">(DE-627)081693532</subfield><subfield code="0">(DE-576)293057567</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Hemminki, Kari</subfield><subfield code="d">1947-</subfield><subfield code="e">verfasserin</subfield><subfield code="0">(DE-588)1150735872</subfield><subfield code="0">(DE-627)1010964402</subfield><subfield code="0">(DE-576)172043751</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Schadendorf, Dirk</subfield><subfield code="d">1960-</subfield><subfield code="e">verfasserin</subfield><subfield code="0">(DE-588)11142576X</subfield><subfield code="0">(DE-627)499566076</subfield><subfield code="0">(DE-576)289702275</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Kumar, Rajiv</subfield><subfield code="d">1955-</subfield><subfield code="e">verfasserin</subfield><subfield code="0">(DE-588)1164253425</subfield><subfield code="0">(DE-627)1028811942</subfield><subfield code="0">(DE-576)508469805</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="a">National Cancer Institute</subfield><subfield code="t">Journal of the National Cancer Institute</subfield><subfield code="d">Oxford : Oxford Univ. 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