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@ARTICLE{Hoppe:298978,
author = {R. Hoppe and S. Winter and W.-Y. Lo and K. Michailidou and
M. K. Bolla and R. Keeman and Q. Wang and J. Dennis and M.
Lush and K. R. Kalari and M. P. Goetz and L. Wang and J.
Cairns and R. Weinshilboum and L. Shepherd and B. E. Chen
and L. Häberle and M. Ruebner and M. W. Beckmann and W. He
and N. L. Larson and S. M. Armasu and W. Schroth and B.
Chowbay and C. C. Khor and M. Abubakar and A. C. Antoniou
and T. Brüning and J. E. Castelao and J. Chang-Claude$^*$
and Nbcs Collaborators and T. Dörk and D. M. Eccles and J.
D. Figueroa and M. Gago-Dominguez and J. A. García-Sáenz
and M. Gündert$^*$ and C. C. Hack and U. Hamann$^*$ and S.
Han and M. J. Hooning and H. Huebner and Abctb Investigators
and E. M. John and Y.-D. Ko and V. N. Kristensen and S. Linn
and S. Margolin and D. Mavroudis and H. Nevanlinna and P.
Neven and N. Obi and T.-W. Park-Simon and K. Pylkäs and M.
U. Rashid and A. Romero and E. Saloustros and E. J. Sawyer
and W. J. Tapper and I. Tomlinson and C. Wendt and R.
Winqvist and A. M. Dunning and J. Simard and P. Hall and P.
D. P. Pharoah and M. Schwab and F. J. Couch and K. Czene and
P. A. Fasching and D. F. Easton and M. K. Schmidt and J. N.
Ingle and H. Brauch$^*$},
title = {{L}essons learned from a candidate gene study investigating
aromatase inhibitor treatment outcome in breast cancer.},
journal = {npj Breast cancer},
volume = {11},
number = {1},
issn = {2374-4677},
address = {London},
publisher = {Nature Publ. Group},
reportid = {DKFZ-2025-00398},
pages = {18},
year = {2025},
abstract = {The role of germline genetics in adjuvant aromatase
inhibitor (AI) treatment efficacy in ER-positive breast
cancer is poorly understood. We employed a two-stage
candidate gene approach to examine associations between
survival endpoints and common germline variants in 753
endocrine resistance-related genes. For a discovery cohort,
we screened the Breast Cancer Association Consortium
database (n ≥ 90,000 cases) and retrieved 2789 AI-treated
patients. Cox model-based analysis revealed 125 variants
associated with overall, distant relapse-free, and
relapse-free survival (p-value ≤ 1E-04). In validation
analysis using five independent cohorts (n = 8857), none of
the six selected candidates representing major linkage
blocks at CELA2B/CASP9, NR1I2/GSK3B, LRP1B, and MIR143HG
(CARMN) were validated. We discuss potential reasons for the
failed validation and replication of published findings,
including study/treatment heterogeneity and other
limitations inherent to genomic treatment outcome studies.
For the future, we envision prospective longitudinal studies
with sufficiently long follow-up and endpoints that reflect
the dynamic nature of endocrine resistance.},
cin = {C020 / TU01 / C080 / B072},
ddc = {610},
cid = {I:(DE-He78)C020-20160331 / I:(DE-He78)TU01-20160331 /
I:(DE-He78)C080-20160331 / I:(DE-He78)B072-20160331},
pnm = {313 - Krebsrisikofaktoren und Prävention (POF4-313)},
pid = {G:(DE-HGF)POF4-313},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:39971965},
doi = {10.1038/s41523-025-00733-y},
url = {https://inrepo02.dkfz.de/record/298978},
}