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Identifying Novel Susceptibility Genes for Colorectal Cancer Risk From a Transcriptome-Wide Association Study of 125,478 Subjects
X. Guo, W. Lin, W. Wen, J. Huyghe, S. Bien, Q. Cai, T. Harrison, Z. Chen, C. Qu, J. Bao, J. Long, Y. Yuan, F. Wang, M. Bai, GR. Abecasis, D. Albanes, SI. Berndt, S. Bézieau, DT. Bishop, H. Brenner, S. Buch, A. Burnett-Hartman, PT. Campbell, S....
Jazyk angličtina Země Spojené státy americké
Typ dokumentu časopisecké články, Research Support, N.I.H., Extramural, Research Support, N.I.H., Intramural, práce podpořená grantem
Grantová podpora
R01 CA067941
NCI NIH HHS - United States
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R35 CA197735
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C8221/A19170
Cancer Research UK - United Kingdom
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R37 CA227130
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14136
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P30 CA015704
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P30 DK034987
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Department of Health - United Kingdom
P50 CA150964
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R01 CA048998
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U01 CA137088
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U01 CA167552
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HHSN268201100003C
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Z01 CP010200
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U01 CA164930
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R01 CA066635
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U24 CA074806
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U01 CA206110
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1000143
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C490/A16561
Cancer Research UK - United Kingdom
R21 CA191312
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HHSN268201200008C
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R01 CA137178
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U24 CA097735
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U01 CA074794
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P30 CA008748
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HHSN261201300011C
CCR NIH HHS - United States
HHSN261201300012I
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P30 CA014089
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C570/A16491
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R01 CA081488
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N01PC35142
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P01 CA033619
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UM1 CA186107
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MR/M012190/1
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HHSN268201100002C
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HHSN261201300021C
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R01 CA042182
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C588/A19167
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R01 CA060987
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U01 CA097735
NCI NIH HHS - United States
T32 ES013678
NIEHS NIH HHS - United States
R01 CA136726
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P30 CA016058
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UM1 CA167552
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K05 CA152715
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P20 CA252728
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UM1 CA167551
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U01 CA122839
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HHSN261201500005C
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HHSN268201100002I
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U01 CA074783
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U01 CA084968
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KL2 TR000421
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U24 CA074799
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P01 CA196569
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U01 CA074806
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U24 CA074800
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P50 CA127003
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UM1 CA182883
NCI NIH HHS - United States
K07 CA190673
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HHSN268201200008I
NHLBI NIH HHS - United States
HHSN261201000121C
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R01 CA193677
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U01 CA164973
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R37 CA054281
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U01 CA074800
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HHSN268201100001C
WHI NIH HHS - United States
HHSN268201100004C
WHI NIH HHS - United States
R01 CA097325
NCI NIH HHS - United States
U19 CA148107
NCI NIH HHS - United States
N01 CN043302
NCI NIH HHS - United States
NV17-30920A
MZ0
CEP - Centrální evidence projektů
- MeSH
- alely MeSH
- celogenomová asociační studie MeSH
- genetická predispozice k nemoci * MeSH
- genový knockdown MeSH
- jednonukleotidový polymorfismus MeSH
- karcinogeneze genetika MeSH
- kohortové studie MeSH
- kolorektální nádory epidemiologie genetika MeSH
- lidé MeSH
- modely genetické * MeSH
- nádorové biomarkery genetika MeSH
- promotorové oblasti (genetika) genetika MeSH
- rizikové faktory MeSH
- sekvenování transkriptomu MeSH
- studie případů a kontrol MeSH
- xenogenní modely - testy protinádorové aktivity MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Research Support, N.I.H., Extramural MeSH
- Research Support, N.I.H., Intramural MeSH
BACKGROUND AND AIMS: Susceptibility genes and the underlying mechanisms for the majority of risk loci identified by genome-wide association studies (GWAS) for colorectal cancer (CRC) risk remain largely unknown. We conducted a transcriptome-wide association study (TWAS) to identify putative susceptibility genes. METHODS: Gene-expression prediction models were built using transcriptome and genetic data from the 284 normal transverse colon tissues of European descendants from the Genotype-Tissue Expression (GTEx), and model performance was evaluated using data from The Cancer Genome Atlas (n = 355). We applied the gene-expression prediction models and GWAS data to evaluate associations of genetically predicted gene-expression with CRC risk in 58,131 CRC cases and 67,347 controls of European ancestry. Dual-luciferase reporter assays and knockdown experiments in CRC cells and tumor xenografts were conducted. RESULTS: We identified 25 genes associated with CRC risk at a Bonferroni-corrected threshold of P < 9.1 × 10-6, including genes in 4 novel loci, PYGL (14q22.1), RPL28 (19q13.42), CAPN12 (19q13.2), MYH7B (20q11.22), and MAP1L3CA (20q11.22). In 9 known GWAS-identified loci, we uncovered 9 genes that have not been reported previously, whereas 4 genes remained statistically significant after adjusting for the lead risk variant of the locus. Through colocalization analysis in GWAS loci, we additionally identified 12 putative susceptibility genes that were supported by TWAS analysis at P < .01. We showed that risk allele of the lead risk variant rs1741640 affected the promoter activity of CABLES2. Knockdown experiments confirmed that CABLES2 plays a vital role in colorectal carcinogenesis. CONCLUSIONS: Our study reveals new putative susceptibility genes and provides new insight into the biological mechanisms underlying CRC development.
Behavioral and Epidemiology Research Group American Cancer Society Atlanta Georgia
Cancer Epidemiology Division Cancer Council Victoria Melbourne Victoria Australia
Cancer Science Institute of Singapore National University of Singapore Singapore
Center for Public Health Genomics University of Virginia Charlottesville Virginia
CIBER Epidemiología y Salud Pública Madrid Spain
Department of Cancer Epidemiology H Lee Moffitt Cancer Center and Research Institute Tampa Florida
Department of Clinical Genetics Karolinska University Hospital Stockholm Sweden
Department of Community Medicine and Epidemiology Lady Davis Carmel Medical Center Haifa Israel
Department of Epidemiology Johns Hopkins Bloomberg School of Public Health Baltimore Maryland
Department of Epidemiology University of Washington School of Public Health Seattle Washington
Department of Family Medicine University of Virginia Charlottesville Virginia
Department of General Surgery University Hospital Rostock Rostock Germany
Department of Genome Sciences University of Washington Seattle Washington
Department of Hematology Oncology Chonnam National University Hospital Hwasun South Korea
Department of Internal Medicine University of Utah Salt Lake City Utah
Department of Medicine 1 University Hospital Dresden Technische Universität Dresden Dresden Germany
Department of Medicine Weill Cornell Medical College New York New York
Department of Molecular Medicine and Surgery Karolinska Institutet Stockholm Sweden
Department of Public Health and Primary Care University of Cambridge Cambridge United Kingdom
Department of Radiation Sciences Oncology Unit Umeå University Umeå Sweden
Department of Surgery Chonnam National University Hwasun Hospital and Medical School Hwasun Korea
Division of Cancer Epidemiology German Cancer Research Center Heidelberg Germany
Division of Human Nutrition and Health Wageningen University and Research Wageningen the Netherlands
Division of Public Health Sciences Fred Hutchinson Cancer Research Center Seattle Washington
Division of Research Kaiser Permanente Northern California Oakland California
Health Sciences Research Mayo Clinic Scottsdale Arizona
Institute for Health Research Kaiser Permanente Colorado Denver Colorado
Institute of Cancer Research Department of Medicine 1 Medical University Vienna Vienna Austria
Institute of Environmental Medicine Karolinska Institutet Stockholm Sweden
Leeds Institute of Cancer and Pathology University of Leeds Leeds United Kingdom
National University Cancer Institute Singapore
Ruth and Bruce Rappaport Faculty of Medicine Technion Israel Institute of Technology Haifa Israel
School of Public Health University of Washington Seattle Washington
Service de Génétique Médicale Centre Hospitalier Universitaire Nantes France
SWOG Statistical Center Fred Hutchinson Cancer Research Center Seattle Washington
University Medical Centre Hamburg Eppendorf University Cancer Centre Hamburg Hamburg Germany
Citace poskytuje Crossref.org
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- $a Guo, Xingyi $u Division of Epidemiology, Department of Medicine, Vanderbilt Epidemiology Center, and Vanderbilt-Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, Tennessee. Electronic address: xingyi.guo@vumc.org
- 245 10
- $a Identifying Novel Susceptibility Genes for Colorectal Cancer Risk From a Transcriptome-Wide Association Study of 125,478 Subjects / $c X. Guo, W. Lin, W. Wen, J. Huyghe, S. Bien, Q. Cai, T. Harrison, Z. Chen, C. Qu, J. Bao, J. Long, Y. Yuan, F. Wang, M. Bai, GR. Abecasis, D. Albanes, SI. Berndt, S. Bézieau, DT. Bishop, H. Brenner, S. Buch, A. Burnett-Hartman, PT. Campbell, S. Castellví-Bel, AT. Chan, J. Chang-Claude, SJ. Chanock, SH. Cho, DV. Conti, A. Chapelle, EJM. Feskens, SJ. Gallinger, GG. Giles, PJ. Goodman, A. Gsur, M. Guinter, MJ. Gunter, J. Hampe, H. Hampel, RB. Hayes, M. Hoffmeister, E. Kampman, HM. Kang, TO. Keku, HR. Kim, L. Le Marchand, SC. Lee, CI. Li, L. Li, A. Lindblom, N. Lindor, RL. Milne, V. Moreno, N. Murphy, PA. Newcomb, DA. Nickerson, K. Offit, R. Pearlman, PDP. Pharoah, EA. Platz, JD. Potter, G. Rennert, LC. Sakoda, C. Schafmayer, SL. Schmit, RE. Schoen, FR. Schumacher, ML. Slattery, YR. Su, CM. Tangen, CM. Ulrich, FJB. van Duijnhoven, B. Van Guelpen, K. Visvanathan, P. Vodicka, L. Vodickova, V. Vymetalkova, X. Wang, E. White, A. Wolk, MO. Woods, G. Casey, L. Hsu, MA. Jenkins, SB. Gruber, U. Peters, W. Zheng
- 520 9_
- $a BACKGROUND AND AIMS: Susceptibility genes and the underlying mechanisms for the majority of risk loci identified by genome-wide association studies (GWAS) for colorectal cancer (CRC) risk remain largely unknown. We conducted a transcriptome-wide association study (TWAS) to identify putative susceptibility genes. METHODS: Gene-expression prediction models were built using transcriptome and genetic data from the 284 normal transverse colon tissues of European descendants from the Genotype-Tissue Expression (GTEx), and model performance was evaluated using data from The Cancer Genome Atlas (n = 355). We applied the gene-expression prediction models and GWAS data to evaluate associations of genetically predicted gene-expression with CRC risk in 58,131 CRC cases and 67,347 controls of European ancestry. Dual-luciferase reporter assays and knockdown experiments in CRC cells and tumor xenografts were conducted. RESULTS: We identified 25 genes associated with CRC risk at a Bonferroni-corrected threshold of P < 9.1 × 10-6, including genes in 4 novel loci, PYGL (14q22.1), RPL28 (19q13.42), CAPN12 (19q13.2), MYH7B (20q11.22), and MAP1L3CA (20q11.22). In 9 known GWAS-identified loci, we uncovered 9 genes that have not been reported previously, whereas 4 genes remained statistically significant after adjusting for the lead risk variant of the locus. Through colocalization analysis in GWAS loci, we additionally identified 12 putative susceptibility genes that were supported by TWAS analysis at P < .01. We showed that risk allele of the lead risk variant rs1741640 affected the promoter activity of CABLES2. Knockdown experiments confirmed that CABLES2 plays a vital role in colorectal carcinogenesis. CONCLUSIONS: Our study reveals new putative susceptibility genes and provides new insight into the biological mechanisms underlying CRC development.
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