Common variants in breast cancer risk loci predispose to distinct tumor subtypes. Breast cancer research : BCR Ahearn, T. U., Zhang, H., Michailidou, K., Milne, R. L., Bolla, M. K., Dennis, J., Dunning, A. M., Lush, M., Wang, Q., Andrulis, I. L., Anton-Culver, H., Arndt, V., Aronson, K. J., Auer, P. L., Augustinsson, A., Baten, A., Becher, H., Behrens, S., Benitez, J., Bermisheva, M., Blomqvist, C., Bojesen, S. E., Bonanni, B., Børresen-Dale, A. L., Brauch, H., Brenner, H., Brooks-Wilson, A., Brüning, T., Burwinkel, B., Buys, S. S., Canzian, F., Castelao, J. E., Chang-Claude, J., Chanock, S. J., Chenevix-Trench, G., Clarke, C. L., Collée, J. M., Cox, A., Cross, S. S., Czene, K., Daly, M. B., Devilee, P., Dörk, T., Dwek, M., Eccles, D. M., Evans, D. G., Fasching, P. A., Figueroa, J., Floris, G., Gago-Dominguez, M., Gapstur, S. M., García-Sáenz, J. A., Gaudet, M. M., Giles, G. G., Goldberg, M. S., González-Neira, A., Alnæs, G. I., Grip, M., Guénel, P., Haiman, C. A., Hall, P., Hamann, U., Harkness, E. F., Heemskerk-Gerritsen, B. A., Holleczek, B., Hollestelle, A., Hooning, M. J., Hoover, R. N., Hopper, J. L., Howell, A., Jakimovska, M., Jakubowska, A., John, E. M., Jones, M. E., Jung, A., Kaaks, R., Kauppila, S., Keeman, R., Khusnutdinova, E., Kitahara, C. M., Ko, Y. D., Koutros, S., Kristensen, V. N., Krüger, U., Kubelka-Sabit, K., Kurian, A. W., Kyriacou, K., Lambrechts, D., Lee, D. G., Lindblom, A., Linet, M., Lissowska, J., Llaneza, A., Lo, W. Y., MacInnis, R. J., Mannermaa, A., Manoochehri, M., Margolin, S., Martinez, M. E., McLean, C., Meindl, A., Menon, U., Nevanlinna, H., Newman, W. G., Nodora, J., Offit, K., Olsson, H., Orr, N., Park-Simon, T. W., Patel, A. V., Peto, J., Pita, G., Plaseska-Karanfilska, D., Prentice, R., Punie, K., Pylkäs, K., Radice, P., Rennert, G., Romero, A., Rüdiger, T., Saloustros, E., Sampson, S., Sandler, D. P., Sawyer, E. J., Schmutzler, R. K., Schoemaker, M. J., Schöttker, B., Sherman, M. E., Shu, X. O., Smichkoska, S., Southey, M. C., Spinelli, J. J., Swerdlow, A. J., Tamimi, R. M., Tapper, W. J., Taylor, J. A., Teras, L. R., Terry, M. B., Torres, D., Troester, M. A., Vachon, C. M., van Deurzen, C. H., van Veen, E. M., Wagner, P., Weinberg, C. R., Wendt, C., Wesseling, J., Winqvist, R., Wolk, A., Yang, X. R., Zheng, W., Couch, F. J., Simard, J., Kraft, P., Easton, D. F., Pharoah, P. D., Schmidt, M. K., García-Closas, M., Chatterjee, N. 2022; 24 (1): 2
Abstract
Genome-wide association studies (GWAS) have identified multiple common breast cancer susceptibility variants. Many of these variants have differential associations by estrogen receptor (ER) status, but how these variants relate with other tumor features and intrinsic molecular subtypes is unclear.Among 106,571 invasive breast cancer cases and 95,762 controls of European ancestry with data on 173 breast cancer variants identified in previous GWAS, we used novel two-stage polytomous logistic regression models to evaluate variants in relation to multiple tumor features (ER, progesterone receptor (PR), human epidermal growth factor receptor 2 (HER2) and grade) adjusting for each other, and to intrinsic-like subtypes.Eighty-five of 173 variants were associated with at least one tumor feature (false discovery rate?
View details for DOI 10.1186/s13058-021-01484-x
View details for PubMedID 34983606
