Genetic variation in the immunosuppression pathway genes and breast cancer susceptibility: a pooled analysis of 42,510 cases and 40,577 controls from the Breast Cancer Association Consortium
Abstract Immunosuppression plays a pivotal role in assisting tumors to evade immune destruction and promoting tumor development. We hypothesized that genetic variation in the immunosuppression pathway genes may be implicated in breast cancer tumorigenesis. We included 42,510 female breast cancer cas...
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E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2015 |
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Enthalten in: Human genetics |
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| Übergeordnetes Werk: |
volume:135 ; year:2015 ; number:1 ; day:30 ; month:11 ; pages:137-154 |
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| DOI / URN: |
10.1007/s00439-015-1616-8 |
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SPR006364381 |
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| 100 | 1 | |a Lei, Jieping |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Genetic variation in the immunosuppression pathway genes and breast cancer susceptibility: a pooled analysis of 42,510 cases and 40,577 controls from the Breast Cancer Association Consortium |
| 264 | 1 | |c 2015 | |
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| 520 | |a Abstract Immunosuppression plays a pivotal role in assisting tumors to evade immune destruction and promoting tumor development. We hypothesized that genetic variation in the immunosuppression pathway genes may be implicated in breast cancer tumorigenesis. We included 42,510 female breast cancer cases and 40,577 controls of European ancestry from 37 studies in the Breast Cancer Association Consortium (2015) with available genotype data for 3595 single nucleotide polymorphisms (SNPs) in 133 candidate genes. Associations between genotyped SNPs and overall breast cancer risk, and secondarily according to estrogen receptor (ER) status, were assessed using multiple logistic regression models. Gene-level associations were assessed based on principal component analysis. Gene expression analyses were conducted using RNA sequencing level 3 data from The Cancer Genome Atlas for 989 breast tumor samples and 113 matched normal tissue samples. SNP rs1905339 (A>G) in the STAT3 region was associated with an increased breast cancer risk (per allele odds ratio 1.05, 95 % confidence interval 1.03–1.08; p value = 1.4 × $ 10^{−6} $). The association did not differ significantly by ER status. On the gene level, in addition to TGFBR2 and CCND1, IL5 and GM-CSF showed the strongest associations with overall breast cancer risk (p value = 1.0 × $ 10^{−3} $ and 7.0 × $ 10^{−3} $, respectively). Furthermore, STAT3 and IL5 but not GM-CSF were differentially expressed between breast tumor tissue and normal tissue (p value = 2.5 × $ 10^{−3} $, 4.5 × $ 10^{−4} $ and 0.63, respectively). Our data provide evidence that the immunosuppression pathway genes STAT3,IL5, and GM-CSF may be novel susceptibility loci for breast cancer in women of European ancestry. | ||
| 650 | 4 | |a Breast Cancer |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Breast Cancer Risk |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Treg Cell |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Linkage Disequilibrium Structure |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Pathway Association |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Rudolph, Anja |e verfasserin |4 aut | |
| 700 | 1 | |a Moysich, Kirsten B. |e verfasserin |4 aut | |
| 700 | 1 | |a Behrens, Sabine |e verfasserin |4 aut | |
| 700 | 1 | |a Goode, Ellen L. |e verfasserin |4 aut | |
| 700 | 1 | |a Bolla, Manjeet K. |e verfasserin |4 aut | |
| 700 | 1 | |a Dennis, Joe |e verfasserin |4 aut | |
| 700 | 1 | |a Dunning, Alison M. |e verfasserin |4 aut | |
| 700 | 1 | |a Easton, Douglas F. |e verfasserin |4 aut | |
| 700 | 1 | |a Wang, Qin |e verfasserin |4 aut | |
| 700 | 1 | |a Benitez, Javier |e verfasserin |4 aut | |
| 700 | 1 | |a Hopper, John L. |e verfasserin |4 aut | |
| 700 | 1 | |a Southey, Melissa C. |e verfasserin |4 aut | |
| 700 | 1 | |a Schmidt, Marjanka K. |e verfasserin |4 aut | |
| 700 | 1 | |a Broeks, Annegien |e verfasserin |4 aut | |
| 700 | 1 | |a Fasching, Peter A. |e verfasserin |4 aut | |
| 700 | 1 | |a Haeberle, Lothar |e verfasserin |4 aut | |
| 700 | 1 | |a Peto, Julian |e verfasserin |4 aut | |
| 700 | 1 | |a dos-Santos-Silva, Isabel |e verfasserin |4 aut | |
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| 700 | 1 | |a Bojesen, Stig E. |e verfasserin |4 aut | |
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| 700 | 1 | |a Nielsen, Sune F. |e verfasserin |4 aut | |
| 700 | 1 | |a Nordestgaard, Børge G. |e verfasserin |4 aut | |
| 700 | 1 | |a González-Neira, Anna |e verfasserin |4 aut | |
| 700 | 1 | |a Menéndez, Primitiva |e verfasserin |4 aut | |
| 700 | 1 | |a Anton-Culver, Hoda |e verfasserin |4 aut | |
| 700 | 1 | |a Neuhausen, Susan L. |e verfasserin |4 aut | |
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| 700 | 1 | |a Beeghly-Fadiel, Alicia |e verfasserin |4 aut | |
| 700 | 1 | |a Winqvist, Robert |e verfasserin |4 aut | |
| 700 | 1 | |a Grip, Mervi |e verfasserin |4 aut | |
| 700 | 1 | |a Andrulis, Irene L. |e verfasserin |4 aut | |
| 700 | 1 | |a Glendon, Gord |e verfasserin |4 aut | |
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10.1007/s00439-015-1616-8 doi (DE-627)SPR006364381 (SPR)s00439-015-1616-8-e DE-627 ger DE-627 rakwb eng 610 ASE 44.48 bkl Lei, Jieping verfasserin aut Genetic variation in the immunosuppression pathway genes and breast cancer susceptibility: a pooled analysis of 42,510 cases and 40,577 controls from the Breast Cancer Association Consortium 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Immunosuppression plays a pivotal role in assisting tumors to evade immune destruction and promoting tumor development. We hypothesized that genetic variation in the immunosuppression pathway genes may be implicated in breast cancer tumorigenesis. We included 42,510 female breast cancer cases and 40,577 controls of European ancestry from 37 studies in the Breast Cancer Association Consortium (2015) with available genotype data for 3595 single nucleotide polymorphisms (SNPs) in 133 candidate genes. Associations between genotyped SNPs and overall breast cancer risk, and secondarily according to estrogen receptor (ER) status, were assessed using multiple logistic regression models. Gene-level associations were assessed based on principal component analysis. Gene expression analyses were conducted using RNA sequencing level 3 data from The Cancer Genome Atlas for 989 breast tumor samples and 113 matched normal tissue samples. SNP rs1905339 (A>G) in the STAT3 region was associated with an increased breast cancer risk (per allele odds ratio 1.05, 95 % confidence interval 1.03–1.08; p value = 1.4 × $ 10^{−6} $). The association did not differ significantly by ER status. On the gene level, in addition to TGFBR2 and CCND1, IL5 and GM-CSF showed the strongest associations with overall breast cancer risk (p value = 1.0 × $ 10^{−3} $ and 7.0 × $ 10^{−3} $, respectively). Furthermore, STAT3 and IL5 but not GM-CSF were differentially expressed between breast tumor tissue and normal tissue (p value = 2.5 × $ 10^{−3} $, 4.5 × $ 10^{−4} $ and 0.63, respectively). Our data provide evidence that the immunosuppression pathway genes STAT3,IL5, and GM-CSF may be novel susceptibility loci for breast cancer in women of European ancestry. Breast Cancer (dpeaa)DE-He213 Breast Cancer Risk (dpeaa)DE-He213 Treg Cell (dpeaa)DE-He213 Linkage Disequilibrium Structure (dpeaa)DE-He213 Pathway Association (dpeaa)DE-He213 Rudolph, Anja verfasserin aut Moysich, Kirsten B. verfasserin aut Behrens, Sabine verfasserin aut Goode, Ellen L. verfasserin aut Bolla, Manjeet K. verfasserin aut Dennis, Joe verfasserin aut Dunning, Alison M. verfasserin aut Easton, Douglas F. verfasserin aut Wang, Qin verfasserin aut Benitez, Javier verfasserin aut Hopper, John L. verfasserin aut Southey, Melissa C. verfasserin aut Schmidt, Marjanka K. verfasserin aut Broeks, Annegien verfasserin aut Fasching, Peter A. verfasserin aut Haeberle, Lothar verfasserin aut Peto, Julian verfasserin aut dos-Santos-Silva, Isabel verfasserin aut Sawyer, Elinor J. verfasserin aut Tomlinson, Ian verfasserin aut Burwinkel, Barbara verfasserin aut Marmé, Frederik verfasserin aut Guénel, Pascal verfasserin aut Truong, Thérèse verfasserin aut Bojesen, Stig E. verfasserin aut Flyger, Henrik verfasserin aut Nielsen, Sune F. verfasserin aut Nordestgaard, Børge G. verfasserin aut González-Neira, Anna verfasserin aut Menéndez, Primitiva verfasserin aut Anton-Culver, Hoda verfasserin aut Neuhausen, Susan L. verfasserin aut Brenner, Hermann verfasserin aut Arndt, Volker verfasserin aut Meindl, Alfons verfasserin aut Schmutzler, Rita K. verfasserin aut Brauch, Hiltrud verfasserin aut Hamann, Ute verfasserin aut Nevanlinna, Heli verfasserin aut Fagerholm, Rainer verfasserin aut Dörk, Thilo verfasserin aut Bogdanova, Natalia V. verfasserin aut Mannermaa, Arto verfasserin aut Hartikainen, Jaana M. verfasserin aut Van Dijck, Laurien verfasserin aut Smeets, Ann verfasserin aut Flesch-Janys, Dieter verfasserin aut Eilber, Ursula verfasserin aut Radice, Paolo verfasserin aut Peterlongo, Paolo verfasserin aut Couch, Fergus J. verfasserin aut Hallberg, Emily verfasserin aut Giles, Graham G. verfasserin aut Milne, Roger L. verfasserin aut Haiman, Christopher A. verfasserin aut Schumacher, Fredrick verfasserin aut Simard, Jacques verfasserin aut Goldberg, Mark S. verfasserin aut Kristensen, Vessela verfasserin aut Borresen-Dale, Anne-Lise verfasserin aut Zheng, Wei verfasserin aut Beeghly-Fadiel, Alicia verfasserin aut Winqvist, Robert verfasserin aut Grip, Mervi verfasserin aut Andrulis, Irene L. verfasserin aut Glendon, Gord verfasserin aut García-Closas, Montserrat verfasserin aut Figueroa, Jonine verfasserin aut Czene, Kamila verfasserin aut Brand, Judith S. verfasserin aut Darabi, Hatef verfasserin aut Eriksson, Mikael verfasserin aut Hall, Per verfasserin aut Li, Jingmei verfasserin aut Cox, Angela verfasserin aut Cross, Simon S. verfasserin aut Pharoah, Paul D. P. verfasserin aut Shah, Mitul verfasserin aut Kabisch, Maria verfasserin aut Torres, Diana verfasserin aut Jakubowska, Anna verfasserin aut Lubinski, Jan verfasserin aut Ademuyiwa, Foluso verfasserin aut Ambrosone, Christine B. verfasserin aut Swerdlow, Anthony verfasserin aut Jones, Michael verfasserin aut Chang-Claude, Jenny verfasserin aut Enthalten in Human genetics <Berlin> Berlin : Springer, 1964 135(2015), 1 vom: 30. Nov., Seite 137-154 (DE-627)253723973 (DE-600)1459188-1 1432-1203 nnns volume:135 year:2015 number:1 day:30 month:11 pages:137-154 https://dx.doi.org/10.1007/s00439-015-1616-8 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_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_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 44.48 ASE AR 135 2015 1 30 11 137-154 |
| spelling |
10.1007/s00439-015-1616-8 doi (DE-627)SPR006364381 (SPR)s00439-015-1616-8-e DE-627 ger DE-627 rakwb eng 610 ASE 44.48 bkl Lei, Jieping verfasserin aut Genetic variation in the immunosuppression pathway genes and breast cancer susceptibility: a pooled analysis of 42,510 cases and 40,577 controls from the Breast Cancer Association Consortium 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Immunosuppression plays a pivotal role in assisting tumors to evade immune destruction and promoting tumor development. We hypothesized that genetic variation in the immunosuppression pathway genes may be implicated in breast cancer tumorigenesis. We included 42,510 female breast cancer cases and 40,577 controls of European ancestry from 37 studies in the Breast Cancer Association Consortium (2015) with available genotype data for 3595 single nucleotide polymorphisms (SNPs) in 133 candidate genes. Associations between genotyped SNPs and overall breast cancer risk, and secondarily according to estrogen receptor (ER) status, were assessed using multiple logistic regression models. Gene-level associations were assessed based on principal component analysis. Gene expression analyses were conducted using RNA sequencing level 3 data from The Cancer Genome Atlas for 989 breast tumor samples and 113 matched normal tissue samples. SNP rs1905339 (A>G) in the STAT3 region was associated with an increased breast cancer risk (per allele odds ratio 1.05, 95 % confidence interval 1.03–1.08; p value = 1.4 × $ 10^{−6} $). The association did not differ significantly by ER status. On the gene level, in addition to TGFBR2 and CCND1, IL5 and GM-CSF showed the strongest associations with overall breast cancer risk (p value = 1.0 × $ 10^{−3} $ and 7.0 × $ 10^{−3} $, respectively). Furthermore, STAT3 and IL5 but not GM-CSF were differentially expressed between breast tumor tissue and normal tissue (p value = 2.5 × $ 10^{−3} $, 4.5 × $ 10^{−4} $ and 0.63, respectively). Our data provide evidence that the immunosuppression pathway genes STAT3,IL5, and GM-CSF may be novel susceptibility loci for breast cancer in women of European ancestry. Breast Cancer (dpeaa)DE-He213 Breast Cancer Risk (dpeaa)DE-He213 Treg Cell (dpeaa)DE-He213 Linkage Disequilibrium Structure (dpeaa)DE-He213 Pathway Association (dpeaa)DE-He213 Rudolph, Anja verfasserin aut Moysich, Kirsten B. verfasserin aut Behrens, Sabine verfasserin aut Goode, Ellen L. verfasserin aut Bolla, Manjeet K. verfasserin aut Dennis, Joe verfasserin aut Dunning, Alison M. verfasserin aut Easton, Douglas F. verfasserin aut Wang, Qin verfasserin aut Benitez, Javier verfasserin aut Hopper, John L. verfasserin aut Southey, Melissa C. verfasserin aut Schmidt, Marjanka K. verfasserin aut Broeks, Annegien verfasserin aut Fasching, Peter A. verfasserin aut Haeberle, Lothar verfasserin aut Peto, Julian verfasserin aut dos-Santos-Silva, Isabel verfasserin aut Sawyer, Elinor J. verfasserin aut Tomlinson, Ian verfasserin aut Burwinkel, Barbara verfasserin aut Marmé, Frederik verfasserin aut Guénel, Pascal verfasserin aut Truong, Thérèse verfasserin aut Bojesen, Stig E. verfasserin aut Flyger, Henrik verfasserin aut Nielsen, Sune F. verfasserin aut Nordestgaard, Børge G. verfasserin aut González-Neira, Anna verfasserin aut Menéndez, Primitiva verfasserin aut Anton-Culver, Hoda verfasserin aut Neuhausen, Susan L. verfasserin aut Brenner, Hermann verfasserin aut Arndt, Volker verfasserin aut Meindl, Alfons verfasserin aut Schmutzler, Rita K. verfasserin aut Brauch, Hiltrud verfasserin aut Hamann, Ute verfasserin aut Nevanlinna, Heli verfasserin aut Fagerholm, Rainer verfasserin aut Dörk, Thilo verfasserin aut Bogdanova, Natalia V. verfasserin aut Mannermaa, Arto verfasserin aut Hartikainen, Jaana M. verfasserin aut Van Dijck, Laurien verfasserin aut Smeets, Ann verfasserin aut Flesch-Janys, Dieter verfasserin aut Eilber, Ursula verfasserin aut Radice, Paolo verfasserin aut Peterlongo, Paolo verfasserin aut Couch, Fergus J. verfasserin aut Hallberg, Emily verfasserin aut Giles, Graham G. verfasserin aut Milne, Roger L. verfasserin aut Haiman, Christopher A. verfasserin aut Schumacher, Fredrick verfasserin aut Simard, Jacques verfasserin aut Goldberg, Mark S. verfasserin aut Kristensen, Vessela verfasserin aut Borresen-Dale, Anne-Lise verfasserin aut Zheng, Wei verfasserin aut Beeghly-Fadiel, Alicia verfasserin aut Winqvist, Robert verfasserin aut Grip, Mervi verfasserin aut Andrulis, Irene L. verfasserin aut Glendon, Gord verfasserin aut García-Closas, Montserrat verfasserin aut Figueroa, Jonine verfasserin aut Czene, Kamila verfasserin aut Brand, Judith S. verfasserin aut Darabi, Hatef verfasserin aut Eriksson, Mikael verfasserin aut Hall, Per verfasserin aut Li, Jingmei verfasserin aut Cox, Angela verfasserin aut Cross, Simon S. verfasserin aut Pharoah, Paul D. P. verfasserin aut Shah, Mitul verfasserin aut Kabisch, Maria verfasserin aut Torres, Diana verfasserin aut Jakubowska, Anna verfasserin aut Lubinski, Jan verfasserin aut Ademuyiwa, Foluso verfasserin aut Ambrosone, Christine B. verfasserin aut Swerdlow, Anthony verfasserin aut Jones, Michael verfasserin aut Chang-Claude, Jenny verfasserin aut Enthalten in Human genetics <Berlin> Berlin : Springer, 1964 135(2015), 1 vom: 30. Nov., Seite 137-154 (DE-627)253723973 (DE-600)1459188-1 1432-1203 nnns volume:135 year:2015 number:1 day:30 month:11 pages:137-154 https://dx.doi.org/10.1007/s00439-015-1616-8 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_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_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 44.48 ASE AR 135 2015 1 30 11 137-154 |
| allfields_unstemmed |
10.1007/s00439-015-1616-8 doi (DE-627)SPR006364381 (SPR)s00439-015-1616-8-e DE-627 ger DE-627 rakwb eng 610 ASE 44.48 bkl Lei, Jieping verfasserin aut Genetic variation in the immunosuppression pathway genes and breast cancer susceptibility: a pooled analysis of 42,510 cases and 40,577 controls from the Breast Cancer Association Consortium 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Immunosuppression plays a pivotal role in assisting tumors to evade immune destruction and promoting tumor development. We hypothesized that genetic variation in the immunosuppression pathway genes may be implicated in breast cancer tumorigenesis. We included 42,510 female breast cancer cases and 40,577 controls of European ancestry from 37 studies in the Breast Cancer Association Consortium (2015) with available genotype data for 3595 single nucleotide polymorphisms (SNPs) in 133 candidate genes. Associations between genotyped SNPs and overall breast cancer risk, and secondarily according to estrogen receptor (ER) status, were assessed using multiple logistic regression models. Gene-level associations were assessed based on principal component analysis. Gene expression analyses were conducted using RNA sequencing level 3 data from The Cancer Genome Atlas for 989 breast tumor samples and 113 matched normal tissue samples. SNP rs1905339 (A>G) in the STAT3 region was associated with an increased breast cancer risk (per allele odds ratio 1.05, 95 % confidence interval 1.03–1.08; p value = 1.4 × $ 10^{−6} $). The association did not differ significantly by ER status. On the gene level, in addition to TGFBR2 and CCND1, IL5 and GM-CSF showed the strongest associations with overall breast cancer risk (p value = 1.0 × $ 10^{−3} $ and 7.0 × $ 10^{−3} $, respectively). Furthermore, STAT3 and IL5 but not GM-CSF were differentially expressed between breast tumor tissue and normal tissue (p value = 2.5 × $ 10^{−3} $, 4.5 × $ 10^{−4} $ and 0.63, respectively). Our data provide evidence that the immunosuppression pathway genes STAT3,IL5, and GM-CSF may be novel susceptibility loci for breast cancer in women of European ancestry. Breast Cancer (dpeaa)DE-He213 Breast Cancer Risk (dpeaa)DE-He213 Treg Cell (dpeaa)DE-He213 Linkage Disequilibrium Structure (dpeaa)DE-He213 Pathway Association (dpeaa)DE-He213 Rudolph, Anja verfasserin aut Moysich, Kirsten B. verfasserin aut Behrens, Sabine verfasserin aut Goode, Ellen L. verfasserin aut Bolla, Manjeet K. verfasserin aut Dennis, Joe verfasserin aut Dunning, Alison M. verfasserin aut Easton, Douglas F. verfasserin aut Wang, Qin verfasserin aut Benitez, Javier verfasserin aut Hopper, John L. verfasserin aut Southey, Melissa C. verfasserin aut Schmidt, Marjanka K. verfasserin aut Broeks, Annegien verfasserin aut Fasching, Peter A. verfasserin aut Haeberle, Lothar verfasserin aut Peto, Julian verfasserin aut dos-Santos-Silva, Isabel verfasserin aut Sawyer, Elinor J. verfasserin aut Tomlinson, Ian verfasserin aut Burwinkel, Barbara verfasserin aut Marmé, Frederik verfasserin aut Guénel, Pascal verfasserin aut Truong, Thérèse verfasserin aut Bojesen, Stig E. verfasserin aut Flyger, Henrik verfasserin aut Nielsen, Sune F. verfasserin aut Nordestgaard, Børge G. verfasserin aut González-Neira, Anna verfasserin aut Menéndez, Primitiva verfasserin aut Anton-Culver, Hoda verfasserin aut Neuhausen, Susan L. verfasserin aut Brenner, Hermann verfasserin aut Arndt, Volker verfasserin aut Meindl, Alfons verfasserin aut Schmutzler, Rita K. verfasserin aut Brauch, Hiltrud verfasserin aut Hamann, Ute verfasserin aut Nevanlinna, Heli verfasserin aut Fagerholm, Rainer verfasserin aut Dörk, Thilo verfasserin aut Bogdanova, Natalia V. verfasserin aut Mannermaa, Arto verfasserin aut Hartikainen, Jaana M. verfasserin aut Van Dijck, Laurien verfasserin aut Smeets, Ann verfasserin aut Flesch-Janys, Dieter verfasserin aut Eilber, Ursula verfasserin aut Radice, Paolo verfasserin aut Peterlongo, Paolo verfasserin aut Couch, Fergus J. verfasserin aut Hallberg, Emily verfasserin aut Giles, Graham G. verfasserin aut Milne, Roger L. verfasserin aut Haiman, Christopher A. verfasserin aut Schumacher, Fredrick verfasserin aut Simard, Jacques verfasserin aut Goldberg, Mark S. verfasserin aut Kristensen, Vessela verfasserin aut Borresen-Dale, Anne-Lise verfasserin aut Zheng, Wei verfasserin aut Beeghly-Fadiel, Alicia verfasserin aut Winqvist, Robert verfasserin aut Grip, Mervi verfasserin aut Andrulis, Irene L. verfasserin aut Glendon, Gord verfasserin aut García-Closas, Montserrat verfasserin aut Figueroa, Jonine verfasserin aut Czene, Kamila verfasserin aut Brand, Judith S. verfasserin aut Darabi, Hatef verfasserin aut Eriksson, Mikael verfasserin aut Hall, Per verfasserin aut Li, Jingmei verfasserin aut Cox, Angela verfasserin aut Cross, Simon S. verfasserin aut Pharoah, Paul D. P. verfasserin aut Shah, Mitul verfasserin aut Kabisch, Maria verfasserin aut Torres, Diana verfasserin aut Jakubowska, Anna verfasserin aut Lubinski, Jan verfasserin aut Ademuyiwa, Foluso verfasserin aut Ambrosone, Christine B. verfasserin aut Swerdlow, Anthony verfasserin aut Jones, Michael verfasserin aut Chang-Claude, Jenny verfasserin aut Enthalten in Human genetics <Berlin> Berlin : Springer, 1964 135(2015), 1 vom: 30. Nov., Seite 137-154 (DE-627)253723973 (DE-600)1459188-1 1432-1203 nnns volume:135 year:2015 number:1 day:30 month:11 pages:137-154 https://dx.doi.org/10.1007/s00439-015-1616-8 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_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_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 44.48 ASE AR 135 2015 1 30 11 137-154 |
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10.1007/s00439-015-1616-8 doi (DE-627)SPR006364381 (SPR)s00439-015-1616-8-e DE-627 ger DE-627 rakwb eng 610 ASE 44.48 bkl Lei, Jieping verfasserin aut Genetic variation in the immunosuppression pathway genes and breast cancer susceptibility: a pooled analysis of 42,510 cases and 40,577 controls from the Breast Cancer Association Consortium 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Immunosuppression plays a pivotal role in assisting tumors to evade immune destruction and promoting tumor development. We hypothesized that genetic variation in the immunosuppression pathway genes may be implicated in breast cancer tumorigenesis. We included 42,510 female breast cancer cases and 40,577 controls of European ancestry from 37 studies in the Breast Cancer Association Consortium (2015) with available genotype data for 3595 single nucleotide polymorphisms (SNPs) in 133 candidate genes. Associations between genotyped SNPs and overall breast cancer risk, and secondarily according to estrogen receptor (ER) status, were assessed using multiple logistic regression models. Gene-level associations were assessed based on principal component analysis. Gene expression analyses were conducted using RNA sequencing level 3 data from The Cancer Genome Atlas for 989 breast tumor samples and 113 matched normal tissue samples. SNP rs1905339 (A>G) in the STAT3 region was associated with an increased breast cancer risk (per allele odds ratio 1.05, 95 % confidence interval 1.03–1.08; p value = 1.4 × $ 10^{−6} $). The association did not differ significantly by ER status. On the gene level, in addition to TGFBR2 and CCND1, IL5 and GM-CSF showed the strongest associations with overall breast cancer risk (p value = 1.0 × $ 10^{−3} $ and 7.0 × $ 10^{−3} $, respectively). Furthermore, STAT3 and IL5 but not GM-CSF were differentially expressed between breast tumor tissue and normal tissue (p value = 2.5 × $ 10^{−3} $, 4.5 × $ 10^{−4} $ and 0.63, respectively). Our data provide evidence that the immunosuppression pathway genes STAT3,IL5, and GM-CSF may be novel susceptibility loci for breast cancer in women of European ancestry. Breast Cancer (dpeaa)DE-He213 Breast Cancer Risk (dpeaa)DE-He213 Treg Cell (dpeaa)DE-He213 Linkage Disequilibrium Structure (dpeaa)DE-He213 Pathway Association (dpeaa)DE-He213 Rudolph, Anja verfasserin aut Moysich, Kirsten B. verfasserin aut Behrens, Sabine verfasserin aut Goode, Ellen L. verfasserin aut Bolla, Manjeet K. verfasserin aut Dennis, Joe verfasserin aut Dunning, Alison M. verfasserin aut Easton, Douglas F. verfasserin aut Wang, Qin verfasserin aut Benitez, Javier verfasserin aut Hopper, John L. verfasserin aut Southey, Melissa C. verfasserin aut Schmidt, Marjanka K. verfasserin aut Broeks, Annegien verfasserin aut Fasching, Peter A. verfasserin aut Haeberle, Lothar verfasserin aut Peto, Julian verfasserin aut dos-Santos-Silva, Isabel verfasserin aut Sawyer, Elinor J. verfasserin aut Tomlinson, Ian verfasserin aut Burwinkel, Barbara verfasserin aut Marmé, Frederik verfasserin aut Guénel, Pascal verfasserin aut Truong, Thérèse verfasserin aut Bojesen, Stig E. verfasserin aut Flyger, Henrik verfasserin aut Nielsen, Sune F. verfasserin aut Nordestgaard, Børge G. verfasserin aut González-Neira, Anna verfasserin aut Menéndez, Primitiva verfasserin aut Anton-Culver, Hoda verfasserin aut Neuhausen, Susan L. verfasserin aut Brenner, Hermann verfasserin aut Arndt, Volker verfasserin aut Meindl, Alfons verfasserin aut Schmutzler, Rita K. verfasserin aut Brauch, Hiltrud verfasserin aut Hamann, Ute verfasserin aut Nevanlinna, Heli verfasserin aut Fagerholm, Rainer verfasserin aut Dörk, Thilo verfasserin aut Bogdanova, Natalia V. verfasserin aut Mannermaa, Arto verfasserin aut Hartikainen, Jaana M. verfasserin aut Van Dijck, Laurien verfasserin aut Smeets, Ann verfasserin aut Flesch-Janys, Dieter verfasserin aut Eilber, Ursula verfasserin aut Radice, Paolo verfasserin aut Peterlongo, Paolo verfasserin aut Couch, Fergus J. verfasserin aut Hallberg, Emily verfasserin aut Giles, Graham G. verfasserin aut Milne, Roger L. verfasserin aut Haiman, Christopher A. verfasserin aut Schumacher, Fredrick verfasserin aut Simard, Jacques verfasserin aut Goldberg, Mark S. verfasserin aut Kristensen, Vessela verfasserin aut Borresen-Dale, Anne-Lise verfasserin aut Zheng, Wei verfasserin aut Beeghly-Fadiel, Alicia verfasserin aut Winqvist, Robert verfasserin aut Grip, Mervi verfasserin aut Andrulis, Irene L. verfasserin aut Glendon, Gord verfasserin aut García-Closas, Montserrat verfasserin aut Figueroa, Jonine verfasserin aut Czene, Kamila verfasserin aut Brand, Judith S. verfasserin aut Darabi, Hatef verfasserin aut Eriksson, Mikael verfasserin aut Hall, Per verfasserin aut Li, Jingmei verfasserin aut Cox, Angela verfasserin aut Cross, Simon S. verfasserin aut Pharoah, Paul D. P. verfasserin aut Shah, Mitul verfasserin aut Kabisch, Maria verfasserin aut Torres, Diana verfasserin aut Jakubowska, Anna verfasserin aut Lubinski, Jan verfasserin aut Ademuyiwa, Foluso verfasserin aut Ambrosone, Christine B. verfasserin aut Swerdlow, Anthony verfasserin aut Jones, Michael verfasserin aut Chang-Claude, Jenny verfasserin aut Enthalten in Human genetics <Berlin> Berlin : Springer, 1964 135(2015), 1 vom: 30. Nov., Seite 137-154 (DE-627)253723973 (DE-600)1459188-1 1432-1203 nnns volume:135 year:2015 number:1 day:30 month:11 pages:137-154 https://dx.doi.org/10.1007/s00439-015-1616-8 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_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_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 44.48 ASE AR 135 2015 1 30 11 137-154 |
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10.1007/s00439-015-1616-8 doi (DE-627)SPR006364381 (SPR)s00439-015-1616-8-e DE-627 ger DE-627 rakwb eng 610 ASE 44.48 bkl Lei, Jieping verfasserin aut Genetic variation in the immunosuppression pathway genes and breast cancer susceptibility: a pooled analysis of 42,510 cases and 40,577 controls from the Breast Cancer Association Consortium 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Immunosuppression plays a pivotal role in assisting tumors to evade immune destruction and promoting tumor development. We hypothesized that genetic variation in the immunosuppression pathway genes may be implicated in breast cancer tumorigenesis. We included 42,510 female breast cancer cases and 40,577 controls of European ancestry from 37 studies in the Breast Cancer Association Consortium (2015) with available genotype data for 3595 single nucleotide polymorphisms (SNPs) in 133 candidate genes. Associations between genotyped SNPs and overall breast cancer risk, and secondarily according to estrogen receptor (ER) status, were assessed using multiple logistic regression models. Gene-level associations were assessed based on principal component analysis. Gene expression analyses were conducted using RNA sequencing level 3 data from The Cancer Genome Atlas for 989 breast tumor samples and 113 matched normal tissue samples. SNP rs1905339 (A>G) in the STAT3 region was associated with an increased breast cancer risk (per allele odds ratio 1.05, 95 % confidence interval 1.03–1.08; p value = 1.4 × $ 10^{−6} $). The association did not differ significantly by ER status. On the gene level, in addition to TGFBR2 and CCND1, IL5 and GM-CSF showed the strongest associations with overall breast cancer risk (p value = 1.0 × $ 10^{−3} $ and 7.0 × $ 10^{−3} $, respectively). Furthermore, STAT3 and IL5 but not GM-CSF were differentially expressed between breast tumor tissue and normal tissue (p value = 2.5 × $ 10^{−3} $, 4.5 × $ 10^{−4} $ and 0.63, respectively). Our data provide evidence that the immunosuppression pathway genes STAT3,IL5, and GM-CSF may be novel susceptibility loci for breast cancer in women of European ancestry. Breast Cancer (dpeaa)DE-He213 Breast Cancer Risk (dpeaa)DE-He213 Treg Cell (dpeaa)DE-He213 Linkage Disequilibrium Structure (dpeaa)DE-He213 Pathway Association (dpeaa)DE-He213 Rudolph, Anja verfasserin aut Moysich, Kirsten B. verfasserin aut Behrens, Sabine verfasserin aut Goode, Ellen L. verfasserin aut Bolla, Manjeet K. verfasserin aut Dennis, Joe verfasserin aut Dunning, Alison M. verfasserin aut Easton, Douglas F. verfasserin aut Wang, Qin verfasserin aut Benitez, Javier verfasserin aut Hopper, John L. verfasserin aut Southey, Melissa C. verfasserin aut Schmidt, Marjanka K. verfasserin aut Broeks, Annegien verfasserin aut Fasching, Peter A. verfasserin aut Haeberle, Lothar verfasserin aut Peto, Julian verfasserin aut dos-Santos-Silva, Isabel verfasserin aut Sawyer, Elinor J. verfasserin aut Tomlinson, Ian verfasserin aut Burwinkel, Barbara verfasserin aut Marmé, Frederik verfasserin aut Guénel, Pascal verfasserin aut Truong, Thérèse verfasserin aut Bojesen, Stig E. verfasserin aut Flyger, Henrik verfasserin aut Nielsen, Sune F. verfasserin aut Nordestgaard, Børge G. verfasserin aut González-Neira, Anna verfasserin aut Menéndez, Primitiva verfasserin aut Anton-Culver, Hoda verfasserin aut Neuhausen, Susan L. verfasserin aut Brenner, Hermann verfasserin aut Arndt, Volker verfasserin aut Meindl, Alfons verfasserin aut Schmutzler, Rita K. verfasserin aut Brauch, Hiltrud verfasserin aut Hamann, Ute verfasserin aut Nevanlinna, Heli verfasserin aut Fagerholm, Rainer verfasserin aut Dörk, Thilo verfasserin aut Bogdanova, Natalia V. verfasserin aut Mannermaa, Arto verfasserin aut Hartikainen, Jaana M. verfasserin aut Van Dijck, Laurien verfasserin aut Smeets, Ann verfasserin aut Flesch-Janys, Dieter verfasserin aut Eilber, Ursula verfasserin aut Radice, Paolo verfasserin aut Peterlongo, Paolo verfasserin aut Couch, Fergus J. verfasserin aut Hallberg, Emily verfasserin aut Giles, Graham G. verfasserin aut Milne, Roger L. verfasserin aut Haiman, Christopher A. verfasserin aut Schumacher, Fredrick verfasserin aut Simard, Jacques verfasserin aut Goldberg, Mark S. verfasserin aut Kristensen, Vessela verfasserin aut Borresen-Dale, Anne-Lise verfasserin aut Zheng, Wei verfasserin aut Beeghly-Fadiel, Alicia verfasserin aut Winqvist, Robert verfasserin aut Grip, Mervi verfasserin aut Andrulis, Irene L. verfasserin aut Glendon, Gord verfasserin aut García-Closas, Montserrat verfasserin aut Figueroa, Jonine verfasserin aut Czene, Kamila verfasserin aut Brand, Judith S. verfasserin aut Darabi, Hatef verfasserin aut Eriksson, Mikael verfasserin aut Hall, Per verfasserin aut Li, Jingmei verfasserin aut Cox, Angela verfasserin aut Cross, Simon S. verfasserin aut Pharoah, Paul D. P. verfasserin aut Shah, Mitul verfasserin aut Kabisch, Maria verfasserin aut Torres, Diana verfasserin aut Jakubowska, Anna verfasserin aut Lubinski, Jan verfasserin aut Ademuyiwa, Foluso verfasserin aut Ambrosone, Christine B. verfasserin aut Swerdlow, Anthony verfasserin aut Jones, Michael verfasserin aut Chang-Claude, Jenny verfasserin aut Enthalten in Human genetics <Berlin> Berlin : Springer, 1964 135(2015), 1 vom: 30. Nov., Seite 137-154 (DE-627)253723973 (DE-600)1459188-1 1432-1203 nnns volume:135 year:2015 number:1 day:30 month:11 pages:137-154 https://dx.doi.org/10.1007/s00439-015-1616-8 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_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_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 44.48 ASE AR 135 2015 1 30 11 137-154 |
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Enthalten in Human genetics <Berlin> 135(2015), 1 vom: 30. Nov., Seite 137-154 volume:135 year:2015 number:1 day:30 month:11 pages:137-154 |
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Lei, Jieping @@aut@@ Rudolph, Anja @@aut@@ Moysich, Kirsten B. @@aut@@ Behrens, Sabine @@aut@@ Goode, Ellen L. @@aut@@ Bolla, Manjeet K. @@aut@@ Dennis, Joe @@aut@@ Dunning, Alison M. @@aut@@ Easton, Douglas F. @@aut@@ Wang, Qin @@aut@@ Benitez, Javier @@aut@@ Hopper, John L. @@aut@@ Southey, Melissa C. @@aut@@ Schmidt, Marjanka K. @@aut@@ Broeks, Annegien @@aut@@ Fasching, Peter A. @@aut@@ Haeberle, Lothar @@aut@@ Peto, Julian @@aut@@ dos-Santos-Silva, Isabel @@aut@@ Sawyer, Elinor J. @@aut@@ Tomlinson, Ian @@aut@@ Burwinkel, Barbara @@aut@@ Marmé, Frederik @@aut@@ Guénel, Pascal @@aut@@ Truong, Thérèse @@aut@@ Bojesen, Stig E. @@aut@@ Flyger, Henrik @@aut@@ Nielsen, Sune F. @@aut@@ Nordestgaard, Børge G. @@aut@@ González-Neira, Anna @@aut@@ Menéndez, Primitiva @@aut@@ Anton-Culver, Hoda @@aut@@ Neuhausen, Susan L. @@aut@@ Brenner, Hermann @@aut@@ Arndt, Volker @@aut@@ Meindl, Alfons @@aut@@ Schmutzler, Rita K. @@aut@@ Brauch, Hiltrud @@aut@@ Hamann, Ute @@aut@@ Nevanlinna, Heli @@aut@@ Fagerholm, Rainer @@aut@@ Dörk, Thilo @@aut@@ Bogdanova, Natalia V. @@aut@@ Mannermaa, Arto @@aut@@ Hartikainen, Jaana M. @@aut@@ Van Dijck, Laurien @@aut@@ Smeets, Ann @@aut@@ Flesch-Janys, Dieter @@aut@@ Eilber, Ursula @@aut@@ Radice, Paolo @@aut@@ Peterlongo, Paolo @@aut@@ Couch, Fergus J. @@aut@@ Hallberg, Emily @@aut@@ Giles, Graham G. @@aut@@ Milne, Roger L. @@aut@@ Haiman, Christopher A. @@aut@@ Schumacher, Fredrick @@aut@@ Simard, Jacques @@aut@@ Goldberg, Mark S. @@aut@@ Kristensen, Vessela @@aut@@ Borresen-Dale, Anne-Lise @@aut@@ Zheng, Wei @@aut@@ Beeghly-Fadiel, Alicia @@aut@@ Winqvist, Robert @@aut@@ Grip, Mervi @@aut@@ Andrulis, Irene L. @@aut@@ Glendon, Gord @@aut@@ García-Closas, Montserrat @@aut@@ Figueroa, Jonine @@aut@@ Czene, Kamila @@aut@@ Brand, Judith S. @@aut@@ Darabi, Hatef @@aut@@ Eriksson, Mikael @@aut@@ Hall, Per @@aut@@ Li, Jingmei @@aut@@ Cox, Angela @@aut@@ Cross, Simon S. @@aut@@ Pharoah, Paul D. P. @@aut@@ Shah, Mitul @@aut@@ Kabisch, Maria @@aut@@ Torres, Diana @@aut@@ Jakubowska, Anna @@aut@@ Lubinski, Jan @@aut@@ Ademuyiwa, Foluso @@aut@@ Ambrosone, Christine B. @@aut@@ Swerdlow, Anthony @@aut@@ Jones, Michael @@aut@@ Chang-Claude, Jenny @@aut@@ |
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SNP rs1905339 (A>G) in the STAT3 region was associated with an increased breast cancer risk (per allele odds ratio 1.05, 95 % confidence interval 1.03–1.08; p value = 1.4 × $ 10^{−6} $). The association did not differ significantly by ER status. On the gene level, in addition to TGFBR2 and CCND1, IL5 and GM-CSF showed the strongest associations with overall breast cancer risk (p value = 1.0 × $ 10^{−3} $ and 7.0 × $ 10^{−3} $, respectively). Furthermore, STAT3 and IL5 but not GM-CSF were differentially expressed between breast tumor tissue and normal tissue (p value = 2.5 × $ 10^{−3} $, 4.5 × $ 10^{−4} $ and 0.63, respectively). 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Lei, Jieping |
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Lei, Jieping ddc 610 bkl 44.48 misc Breast Cancer misc Breast Cancer Risk misc Treg Cell misc Linkage Disequilibrium Structure misc Pathway Association Genetic variation in the immunosuppression pathway genes and breast cancer susceptibility: a pooled analysis of 42,510 cases and 40,577 controls from the Breast Cancer Association Consortium |
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610 ASE 44.48 bkl Genetic variation in the immunosuppression pathway genes and breast cancer susceptibility: a pooled analysis of 42,510 cases and 40,577 controls from the Breast Cancer Association Consortium Breast Cancer (dpeaa)DE-He213 Breast Cancer Risk (dpeaa)DE-He213 Treg Cell (dpeaa)DE-He213 Linkage Disequilibrium Structure (dpeaa)DE-He213 Pathway Association (dpeaa)DE-He213 |
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ddc 610 bkl 44.48 misc Breast Cancer misc Breast Cancer Risk misc Treg Cell misc Linkage Disequilibrium Structure misc Pathway Association |
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Genetic variation in the immunosuppression pathway genes and breast cancer susceptibility: a pooled analysis of 42,510 cases and 40,577 controls from the Breast Cancer Association Consortium |
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Genetic variation in the immunosuppression pathway genes and breast cancer susceptibility: a pooled analysis of 42,510 cases and 40,577 controls from the Breast Cancer Association Consortium |
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Lei, Jieping Rudolph, Anja Moysich, Kirsten B. Behrens, Sabine Goode, Ellen L. Bolla, Manjeet K. Dennis, Joe Dunning, Alison M. Easton, Douglas F. Wang, Qin Benitez, Javier Hopper, John L. Southey, Melissa C. Schmidt, Marjanka K. Broeks, Annegien Fasching, Peter A. Haeberle, Lothar Peto, Julian dos-Santos-Silva, Isabel Sawyer, Elinor J. Tomlinson, Ian Burwinkel, Barbara Marmé, Frederik Guénel, Pascal Truong, Thérèse Bojesen, Stig E. Flyger, Henrik Nielsen, Sune F. Nordestgaard, Børge G. González-Neira, Anna Menéndez, Primitiva Anton-Culver, Hoda Neuhausen, Susan L. Brenner, Hermann Arndt, Volker Meindl, Alfons Schmutzler, Rita K. Brauch, Hiltrud Hamann, Ute Nevanlinna, Heli Fagerholm, Rainer Dörk, Thilo Bogdanova, Natalia V. Mannermaa, Arto Hartikainen, Jaana M. Van Dijck, Laurien Smeets, Ann Flesch-Janys, Dieter Eilber, Ursula Radice, Paolo Peterlongo, Paolo Couch, Fergus J. Hallberg, Emily Giles, Graham G. Milne, Roger L. Haiman, Christopher A. Schumacher, Fredrick Simard, Jacques Goldberg, Mark S. Kristensen, Vessela Borresen-Dale, Anne-Lise Zheng, Wei Beeghly-Fadiel, Alicia Winqvist, Robert Grip, Mervi Andrulis, Irene L. Glendon, Gord García-Closas, Montserrat Figueroa, Jonine Czene, Kamila Brand, Judith S. Darabi, Hatef Eriksson, Mikael Hall, Per Li, Jingmei Cox, Angela Cross, Simon S. Pharoah, Paul D. P. Shah, Mitul Kabisch, Maria Torres, Diana Jakubowska, Anna Lubinski, Jan Ademuyiwa, Foluso Ambrosone, Christine B. Swerdlow, Anthony Jones, Michael Chang-Claude, Jenny |
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genetic variation in the immunosuppression pathway genes and breast cancer susceptibility: a pooled analysis of 42,510 cases and 40,577 controls from the breast cancer association consortium |
| title_auth |
Genetic variation in the immunosuppression pathway genes and breast cancer susceptibility: a pooled analysis of 42,510 cases and 40,577 controls from the Breast Cancer Association Consortium |
| abstract |
Abstract Immunosuppression plays a pivotal role in assisting tumors to evade immune destruction and promoting tumor development. We hypothesized that genetic variation in the immunosuppression pathway genes may be implicated in breast cancer tumorigenesis. We included 42,510 female breast cancer cases and 40,577 controls of European ancestry from 37 studies in the Breast Cancer Association Consortium (2015) with available genotype data for 3595 single nucleotide polymorphisms (SNPs) in 133 candidate genes. Associations between genotyped SNPs and overall breast cancer risk, and secondarily according to estrogen receptor (ER) status, were assessed using multiple logistic regression models. Gene-level associations were assessed based on principal component analysis. Gene expression analyses were conducted using RNA sequencing level 3 data from The Cancer Genome Atlas for 989 breast tumor samples and 113 matched normal tissue samples. SNP rs1905339 (A>G) in the STAT3 region was associated with an increased breast cancer risk (per allele odds ratio 1.05, 95 % confidence interval 1.03–1.08; p value = 1.4 × $ 10^{−6} $). The association did not differ significantly by ER status. On the gene level, in addition to TGFBR2 and CCND1, IL5 and GM-CSF showed the strongest associations with overall breast cancer risk (p value = 1.0 × $ 10^{−3} $ and 7.0 × $ 10^{−3} $, respectively). Furthermore, STAT3 and IL5 but not GM-CSF were differentially expressed between breast tumor tissue and normal tissue (p value = 2.5 × $ 10^{−3} $, 4.5 × $ 10^{−4} $ and 0.63, respectively). Our data provide evidence that the immunosuppression pathway genes STAT3,IL5, and GM-CSF may be novel susceptibility loci for breast cancer in women of European ancestry. |
| abstractGer |
Abstract Immunosuppression plays a pivotal role in assisting tumors to evade immune destruction and promoting tumor development. We hypothesized that genetic variation in the immunosuppression pathway genes may be implicated in breast cancer tumorigenesis. We included 42,510 female breast cancer cases and 40,577 controls of European ancestry from 37 studies in the Breast Cancer Association Consortium (2015) with available genotype data for 3595 single nucleotide polymorphisms (SNPs) in 133 candidate genes. Associations between genotyped SNPs and overall breast cancer risk, and secondarily according to estrogen receptor (ER) status, were assessed using multiple logistic regression models. Gene-level associations were assessed based on principal component analysis. Gene expression analyses were conducted using RNA sequencing level 3 data from The Cancer Genome Atlas for 989 breast tumor samples and 113 matched normal tissue samples. SNP rs1905339 (A>G) in the STAT3 region was associated with an increased breast cancer risk (per allele odds ratio 1.05, 95 % confidence interval 1.03–1.08; p value = 1.4 × $ 10^{−6} $). The association did not differ significantly by ER status. On the gene level, in addition to TGFBR2 and CCND1, IL5 and GM-CSF showed the strongest associations with overall breast cancer risk (p value = 1.0 × $ 10^{−3} $ and 7.0 × $ 10^{−3} $, respectively). Furthermore, STAT3 and IL5 but not GM-CSF were differentially expressed between breast tumor tissue and normal tissue (p value = 2.5 × $ 10^{−3} $, 4.5 × $ 10^{−4} $ and 0.63, respectively). Our data provide evidence that the immunosuppression pathway genes STAT3,IL5, and GM-CSF may be novel susceptibility loci for breast cancer in women of European ancestry. |
| abstract_unstemmed |
Abstract Immunosuppression plays a pivotal role in assisting tumors to evade immune destruction and promoting tumor development. We hypothesized that genetic variation in the immunosuppression pathway genes may be implicated in breast cancer tumorigenesis. We included 42,510 female breast cancer cases and 40,577 controls of European ancestry from 37 studies in the Breast Cancer Association Consortium (2015) with available genotype data for 3595 single nucleotide polymorphisms (SNPs) in 133 candidate genes. Associations between genotyped SNPs and overall breast cancer risk, and secondarily according to estrogen receptor (ER) status, were assessed using multiple logistic regression models. Gene-level associations were assessed based on principal component analysis. Gene expression analyses were conducted using RNA sequencing level 3 data from The Cancer Genome Atlas for 989 breast tumor samples and 113 matched normal tissue samples. SNP rs1905339 (A>G) in the STAT3 region was associated with an increased breast cancer risk (per allele odds ratio 1.05, 95 % confidence interval 1.03–1.08; p value = 1.4 × $ 10^{−6} $). The association did not differ significantly by ER status. On the gene level, in addition to TGFBR2 and CCND1, IL5 and GM-CSF showed the strongest associations with overall breast cancer risk (p value = 1.0 × $ 10^{−3} $ and 7.0 × $ 10^{−3} $, respectively). Furthermore, STAT3 and IL5 but not GM-CSF were differentially expressed between breast tumor tissue and normal tissue (p value = 2.5 × $ 10^{−3} $, 4.5 × $ 10^{−4} $ and 0.63, respectively). Our data provide evidence that the immunosuppression pathway genes STAT3,IL5, and GM-CSF may be novel susceptibility loci for breast cancer in women of European ancestry. |
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Genetic variation in the immunosuppression pathway genes and breast cancer susceptibility: a pooled analysis of 42,510 cases and 40,577 controls from the Breast Cancer Association Consortium |
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Rudolph, Anja Moysich, Kirsten B. Behrens, Sabine Goode, Ellen L. Bolla, Manjeet K. Dennis, Joe Dunning, Alison M. Easton, Douglas F. Wang, Qin Benitez, Javier Hopper, John L. Southey, Melissa C. Schmidt, Marjanka K. Broeks, Annegien Fasching, Peter A. Haeberle, Lothar Peto, Julian dos-Santos-Silva, Isabel Sawyer, Elinor J. Tomlinson, Ian Burwinkel, Barbara Marmé, Frederik Guénel, Pascal Truong, Thérèse Bojesen, Stig E. Flyger, Henrik Nielsen, Sune F. Nordestgaard, Børge G. González-Neira, Anna Menéndez, Primitiva Anton-Culver, Hoda Neuhausen, Susan L. Brenner, Hermann Arndt, Volker Meindl, Alfons Schmutzler, Rita K. Brauch, Hiltrud Hamann, Ute Nevanlinna, Heli Fagerholm, Rainer Dörk, Thilo Bogdanova, Natalia V. Mannermaa, Arto Hartikainen, Jaana M. Van Dijck, Laurien Smeets, Ann Flesch-Janys, Dieter Eilber, Ursula Radice, Paolo Peterlongo, Paolo Couch, Fergus J. Hallberg, Emily Giles, Graham G. Milne, Roger L. Haiman, Christopher A. Schumacher, Fredrick Simard, Jacques Goldberg, Mark S. Kristensen, Vessela Borresen-Dale, Anne-Lise Zheng, Wei Beeghly-Fadiel, Alicia Winqvist, Robert Grip, Mervi Andrulis, Irene L. Glendon, Gord García-Closas, Montserrat Figueroa, Jonine Czene, Kamila Brand, Judith S. Darabi, Hatef Eriksson, Mikael Hall, Per Li, Jingmei Cox, Angela Cross, Simon S. Pharoah, Paul D. P. Shah, Mitul Kabisch, Maria Torres, Diana Jakubowska, Anna Lubinski, Jan Ademuyiwa, Foluso Ambrosone, Christine B. Swerdlow, Anthony Jones, Michael Chang-Claude, Jenny |
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Rudolph, Anja Moysich, Kirsten B. Behrens, Sabine Goode, Ellen L. Bolla, Manjeet K. Dennis, Joe Dunning, Alison M. Easton, Douglas F. Wang, Qin Benitez, Javier Hopper, John L. Southey, Melissa C. Schmidt, Marjanka K. Broeks, Annegien Fasching, Peter A. Haeberle, Lothar Peto, Julian dos-Santos-Silva, Isabel Sawyer, Elinor J. Tomlinson, Ian Burwinkel, Barbara Marmé, Frederik Guénel, Pascal Truong, Thérèse Bojesen, Stig E. Flyger, Henrik Nielsen, Sune F. Nordestgaard, Børge G. González-Neira, Anna Menéndez, Primitiva Anton-Culver, Hoda Neuhausen, Susan L. Brenner, Hermann Arndt, Volker Meindl, Alfons Schmutzler, Rita K. Brauch, Hiltrud Hamann, Ute Nevanlinna, Heli Fagerholm, Rainer Dörk, Thilo Bogdanova, Natalia V. Mannermaa, Arto Hartikainen, Jaana M. Van Dijck, Laurien Smeets, Ann Flesch-Janys, Dieter Eilber, Ursula Radice, Paolo Peterlongo, Paolo Couch, Fergus J. Hallberg, Emily Giles, Graham G. Milne, Roger L. Haiman, Christopher A. Schumacher, Fredrick Simard, Jacques Goldberg, Mark S. Kristensen, Vessela Borresen-Dale, Anne-Lise Zheng, Wei Beeghly-Fadiel, Alicia Winqvist, Robert Grip, Mervi Andrulis, Irene L. Glendon, Gord García-Closas, Montserrat Figueroa, Jonine Czene, Kamila Brand, Judith S. Darabi, Hatef Eriksson, Mikael Hall, Per Li, Jingmei Cox, Angela Cross, Simon S. Pharoah, Paul D. P. Shah, Mitul Kabisch, Maria Torres, Diana Jakubowska, Anna Lubinski, Jan Ademuyiwa, Foluso Ambrosone, Christine B. Swerdlow, Anthony Jones, Michael Chang-Claude, Jenny |
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| doi_str |
10.1007/s00439-015-1616-8 |
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2024-07-03T22:35:42.417Z |
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We hypothesized that genetic variation in the immunosuppression pathway genes may be implicated in breast cancer tumorigenesis. We included 42,510 female breast cancer cases and 40,577 controls of European ancestry from 37 studies in the Breast Cancer Association Consortium (2015) with available genotype data for 3595 single nucleotide polymorphisms (SNPs) in 133 candidate genes. Associations between genotyped SNPs and overall breast cancer risk, and secondarily according to estrogen receptor (ER) status, were assessed using multiple logistic regression models. Gene-level associations were assessed based on principal component analysis. Gene expression analyses were conducted using RNA sequencing level 3 data from The Cancer Genome Atlas for 989 breast tumor samples and 113 matched normal tissue samples. SNP rs1905339 (A>G) in the STAT3 region was associated with an increased breast cancer risk (per allele odds ratio 1.05, 95 % confidence interval 1.03–1.08; p value = 1.4 × $ 10^{−6} $). The association did not differ significantly by ER status. On the gene level, in addition to TGFBR2 and CCND1, IL5 and GM-CSF showed the strongest associations with overall breast cancer risk (p value = 1.0 × $ 10^{−3} $ and 7.0 × $ 10^{−3} $, respectively). Furthermore, STAT3 and IL5 but not GM-CSF were differentially expressed between breast tumor tissue and normal tissue (p value = 2.5 × $ 10^{−3} $, 4.5 × $ 10^{−4} $ and 0.63, respectively). 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