Harvard
Ostrom, QT, Coleman, W, Huang, W, Rubin, JB, Lathia, JD, Berens, ME, Speyer, G, Liao, P, Wrensch, MR, Eckel-Passow, JE, Armstrong, G, Rice, T, Wiencke, JK, McCoy, LS, Hansen, HM, Amos, CI, Bernstein, JL, Claus, EB, Houlston, RS, Il'yasova, D, Jenkins, RB
, Johansen, C, Lachance, DH, Lai, RK, Merrell, RT, Olson, SH, Sadetzki, S, Schildkraut, JM, Shete, S, Andersson, U, Rajaraman, P, Chanock, SJ, Linet, MS, Wang, Z, Yeager, M, Melin, B, Bondy, ML, Barnholtz-Sloan, JS & GliomaScan Consortium 2019, '
Sex-specific gene and pathway modeling of inherited glioma risk',
Neuro-Oncology, vol. 21, no. 1, pp. 71-82.
https://doi.org/10.1093/neuonc/noy135APA
Ostrom, Q. T., Coleman, W., Huang, W., Rubin, J. B., Lathia, J. D., Berens, M. E., Speyer, G., Liao, P., Wrensch, M. R., Eckel-Passow, J. E., Armstrong, G., Rice, T., Wiencke, J. K., McCoy, L. S., Hansen, H. M., Amos, C. I., Bernstein, J. L., Claus, E. B., Houlston, R. S., ... GliomaScan Consortium (2019).
Sex-specific gene and pathway modeling of inherited glioma risk.
Neuro-Oncology,
21(1), 71-82.
https://doi.org/10.1093/neuonc/noy135CBE
Ostrom QT, Coleman W, Huang W, Rubin JB, Lathia JD, Berens ME, Speyer G, Liao P, Wrensch MR, Eckel-Passow JE, Armstrong G, Rice T, Wiencke JK, McCoy LS, Hansen HM, Amos CI, Bernstein JL, Claus EB, Houlston RS, Il'yasova D, Jenkins RB
, Johansen C, Lachance DH, Lai RK, Merrell RT, Olson SH, Sadetzki S, Schildkraut JM, Shete S, Andersson U, Rajaraman P, Chanock SJ, Linet MS, Wang Z, Yeager M, Melin B, Bondy ML, Barnholtz-Sloan JS, GliomaScan Consortium. 2019.
Sex-specific gene and pathway modeling of inherited glioma risk.
Neuro-Oncology. 21(1):71-82.
https://doi.org/10.1093/neuonc/noy135MLA
Vancouver
Author
Ostrom, Quinn T ; Coleman, Warren ; Huang, William ; Rubin, Joshua B ; Lathia, Justin D ; Berens, Michael E ; Speyer, Gil ; Liao, Peter ; Wrensch, Margaret R ; Eckel-Passow, Jeanette E ; Armstrong, Georgina ; Rice, Terri ; Wiencke, John K ; McCoy, Lucie S ; Hansen, Helen M ; Amos, Christopher I ; Bernstein, Jonine L ; Claus, Elizabeth B ; Houlston, Richard S ; Il'yasova, Dora ; Jenkins, Robert B
; Johansen, Christoffer ; Lachance, Daniel H ; Lai, Rose K ; Merrell, Ryan T ; Olson, Sara H ; Sadetzki, Siegal ; Schildkraut, Joellen M ; Shete, Sanjay ; Andersson, Ulrika ; Rajaraman, Preetha ; Chanock, Stephen J ; Linet, Martha S ; Wang, Zhaoming ; Yeager, Meredith ; Melin, Beatrice ; Bondy, Melissa L ; Barnholtz-Sloan, Jill S ; GliomaScan Consortium. /
Sex-specific gene and pathway modeling of inherited glioma risk. In:
Neuro-Oncology. 2019 ; Vol. 21, No. 1. pp. 71-82.
Bibtex
@article{aa00356136cd4f739272826d7d9c07ef,
title = "Sex-specific gene and pathway modeling of inherited glioma risk",
abstract = "Background: To date, genome-wide association studies (GWAS) have identified 25 risk variants for glioma, explaining 30% of heritable risk. Most histologies occur with significantly higher incidence in males, and this difference is not explained by currently known risk factors. A previous GWAS identified sex-specific glioma risk variants, and this analysis aims to further elucidate risk variation by sex using gene- and pathway-based approaches.Methods: Results from the Glioma International Case-Control Study were used as a testing set, and results from 3 GWAS were combined via meta-analysis and used as a validation set. Using summary statistics for nominally significant autosomal SNPs (P < 0.01 in a previous meta-analysis) and nominally significant X-chromosome SNPs (P < 0.01), 3 algorithms (Pascal, BimBam, and GATES) were used to generate gene scores, and Pascal was used to generate pathway scores. Results were considered statistically significant in the discovery set when P < 3.3 × 10-6 and in the validation set when P < 0.001 in 2 of 3 algorithms.Results: Twenty-five genes within 5 regions and 19 genes within 6 regions reached statistical significance in at least 2 of 3 algorithms in males and females, respectively. EGFR was significantly associated with all glioma and glioblastoma in males only and a female-specific association in TERT, all of which remained nominally significant after conditioning on known risk loci. There were nominal associations with the BioCarta telomeres pathway in both males and females.Conclusions: These results provide additional evidence that there may be differences by sex in genetic risk for glioma. Additional analyses may further elucidate the biological processes through which this risk is conferred.",
author = "Ostrom, {Quinn T} and Warren Coleman and William Huang and Rubin, {Joshua B} and Lathia, {Justin D} and Berens, {Michael E} and Gil Speyer and Peter Liao and Wrensch, {Margaret R} and Eckel-Passow, {Jeanette E} and Georgina Armstrong and Terri Rice and Wiencke, {John K} and McCoy, {Lucie S} and Hansen, {Helen M} and Amos, {Christopher I} and Bernstein, {Jonine L} and Claus, {Elizabeth B} and Houlston, {Richard S} and Dora Il'yasova and Jenkins, {Robert B} and Christoffer Johansen and Lachance, {Daniel H} and Lai, {Rose K} and Merrell, {Ryan T} and Olson, {Sara H} and Siegal Sadetzki and Schildkraut, {Joellen M} and Sanjay Shete and Ulrika Andersson and Preetha Rajaraman and Chanock, {Stephen J} and Linet, {Martha S} and Zhaoming Wang and Meredith Yeager and Beatrice Melin and Bondy, {Melissa L} and Barnholtz-Sloan, {Jill S} and {GliomaScan Consortium}",
year = "2019",
month = jan,
day = "1",
doi = "10.1093/neuonc/noy135",
language = "English",
volume = "21",
pages = "71--82",
journal = "Neuro-Oncology",
issn = "1522-8517",
publisher = "Oxford University Press",
number = "1",
}
RIS
TY - JOUR
T1 - Sex-specific gene and pathway modeling of inherited glioma risk
AU - Ostrom, Quinn T
AU - Coleman, Warren
AU - Huang, William
AU - Rubin, Joshua B
AU - Lathia, Justin D
AU - Berens, Michael E
AU - Speyer, Gil
AU - Liao, Peter
AU - Wrensch, Margaret R
AU - Eckel-Passow, Jeanette E
AU - Armstrong, Georgina
AU - Rice, Terri
AU - Wiencke, John K
AU - McCoy, Lucie S
AU - Hansen, Helen M
AU - Amos, Christopher I
AU - Bernstein, Jonine L
AU - Claus, Elizabeth B
AU - Houlston, Richard S
AU - Il'yasova, Dora
AU - Jenkins, Robert B
AU - Johansen, Christoffer
AU - Lachance, Daniel H
AU - Lai, Rose K
AU - Merrell, Ryan T
AU - Olson, Sara H
AU - Sadetzki, Siegal
AU - Schildkraut, Joellen M
AU - Shete, Sanjay
AU - Andersson, Ulrika
AU - Rajaraman, Preetha
AU - Chanock, Stephen J
AU - Linet, Martha S
AU - Wang, Zhaoming
AU - Yeager, Meredith
AU - Melin, Beatrice
AU - Bondy, Melissa L
AU - Barnholtz-Sloan, Jill S
AU - GliomaScan Consortium
PY - 2019/1/1
Y1 - 2019/1/1
N2 - Background: To date, genome-wide association studies (GWAS) have identified 25 risk variants for glioma, explaining 30% of heritable risk. Most histologies occur with significantly higher incidence in males, and this difference is not explained by currently known risk factors. A previous GWAS identified sex-specific glioma risk variants, and this analysis aims to further elucidate risk variation by sex using gene- and pathway-based approaches.Methods: Results from the Glioma International Case-Control Study were used as a testing set, and results from 3 GWAS were combined via meta-analysis and used as a validation set. Using summary statistics for nominally significant autosomal SNPs (P < 0.01 in a previous meta-analysis) and nominally significant X-chromosome SNPs (P < 0.01), 3 algorithms (Pascal, BimBam, and GATES) were used to generate gene scores, and Pascal was used to generate pathway scores. Results were considered statistically significant in the discovery set when P < 3.3 × 10-6 and in the validation set when P < 0.001 in 2 of 3 algorithms.Results: Twenty-five genes within 5 regions and 19 genes within 6 regions reached statistical significance in at least 2 of 3 algorithms in males and females, respectively. EGFR was significantly associated with all glioma and glioblastoma in males only and a female-specific association in TERT, all of which remained nominally significant after conditioning on known risk loci. There were nominal associations with the BioCarta telomeres pathway in both males and females.Conclusions: These results provide additional evidence that there may be differences by sex in genetic risk for glioma. Additional analyses may further elucidate the biological processes through which this risk is conferred.
AB - Background: To date, genome-wide association studies (GWAS) have identified 25 risk variants for glioma, explaining 30% of heritable risk. Most histologies occur with significantly higher incidence in males, and this difference is not explained by currently known risk factors. A previous GWAS identified sex-specific glioma risk variants, and this analysis aims to further elucidate risk variation by sex using gene- and pathway-based approaches.Methods: Results from the Glioma International Case-Control Study were used as a testing set, and results from 3 GWAS were combined via meta-analysis and used as a validation set. Using summary statistics for nominally significant autosomal SNPs (P < 0.01 in a previous meta-analysis) and nominally significant X-chromosome SNPs (P < 0.01), 3 algorithms (Pascal, BimBam, and GATES) were used to generate gene scores, and Pascal was used to generate pathway scores. Results were considered statistically significant in the discovery set when P < 3.3 × 10-6 and in the validation set when P < 0.001 in 2 of 3 algorithms.Results: Twenty-five genes within 5 regions and 19 genes within 6 regions reached statistical significance in at least 2 of 3 algorithms in males and females, respectively. EGFR was significantly associated with all glioma and glioblastoma in males only and a female-specific association in TERT, all of which remained nominally significant after conditioning on known risk loci. There were nominal associations with the BioCarta telomeres pathway in both males and females.Conclusions: These results provide additional evidence that there may be differences by sex in genetic risk for glioma. Additional analyses may further elucidate the biological processes through which this risk is conferred.
U2 - 10.1093/neuonc/noy135
DO - 10.1093/neuonc/noy135
M3 - Journal article
C2 - 30124908
VL - 21
SP - 71
EP - 82
JO - Neuro-Oncology
JF - Neuro-Oncology
SN - 1522-8517
IS - 1
ER -
