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@ARTICLE{Cheerie:283022,
author = {Cheerie, David and Lauffer, Marlen C and Newton, Logan and
Amburgey, Kimberly and Beijer, Danique and Haque, Bushra and
Kalish, Brian T and Meserve, Margaret M and Oh, Rachel Y and
Pan, Amy Y and Reuter, Miriam S and Szego, Michael J and
Szuto, Anna and Aartsma-Rus, Annemieke and Axford, Michelle
M and Deshwar, Ashish R and Dowling, James J and Marshall,
Christian R and Ivakine, Zhenya and Synofzik, Matthis and
Yu, Timothy W and Costain, Gregory},
collaboration = {N={1 Collaborative}},
othercontributors = {Taylor Tavares, Ana Lisa and Aartsma-Rus, Annemieke and
Verran, Aubrie Soucy and Kaiwar, Charu and Beijer, Danique
and Cheerie, David and Sherrill, Emma and Costain, Gregory
and Newton, Logan and Meserve, Margaret M and Lauffer,
Marlen C and Synofzik, Matthis and Nolen, Nicole and
Leonard, Stefanie and Sanders, Stephan J and Yu, Timothy W},
title = {{S}creening rare genetic diagnoses for amenability to
bespoke antisense oligonucleotide therapy development: {A}
retrospective cohort study.},
journal = {Genetics in medicine},
volume = {28},
number = {1},
issn = {1098-3600},
address = {Amsterdam},
publisher = {Elsevier},
reportid = {DZNE-2025-01434},
pages = {101597},
year = {2025},
abstract = {To estimate the proportion of molecular genetic diagnoses
in a real-world, phenotypically heterogeneous patient cohort
that are amenable to antisense oligonucleotide (ASO)
treatment.We retrospectively applied the N=1 Collaborative's
Variant Assessments toward Eligibility for Antisense
Oligonucleotide Treatment guidelines to all diagnostic
variants found by clinical genome-wide sequencing at a
single pediatric hospital in 532 patients over a 6-year
period. Variants were classified as either 'eligible,'
'likely eligible,' 'unlikely eligible,' or 'not eligible' in
relation to the different ASO approaches, or 'unable to
assess.'In total, 25 unique variants across 26 patients
$(4.9\%$ of 532 patients) were eligible or likely eligible
for ASO treatment at a molecular genetic level, via
canonical exon skipping (4), splice correction (3), or
messenger RNA knockdown (19). Only 8 of these molecular
genetic diagnoses were made within a year of symptom onset.
After considering disease and delivery related factors, 11
diagnoses were still considered candidates for bespoke ASO
development.A meaningful proportion of genetic diagnoses
identified by genome-wide sequencing may be amenable to ASO
treatment. These results underscore the importance of timely
diagnosis, and the proactive identification and accelerated
functional testing of genetic variants amenable to ASO
treatments.},
keywords = {Antisense oligonucleotides (Other) / Experimental therapy
(Other) / Inborn genetic disease (Other) / Rare disease
(Other)},
cin = {AG Gasser},
ddc = {610},
cid = {I:(DE-2719)1210000},
pnm = {353 - Clinical and Health Care Research (POF4-353)},
pid = {G:(DE-HGF)POF4-353},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:41090344},
doi = {10.1016/j.gim.2025.101597},
url = {https://pub.dzne.de/record/283022},
}