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[Preprint]. 2023 Aug 13:2023.08.08.23293829. [Version 1] doi: 10.1101/2023.08.08.23293829

Unique Capabilities of Genome Sequencing for Rare Disease Diagnosis

Monica H Wojcik, Gabrielle Lemire, Maha S Zaki, Mariel Wissman, Wathone Win, Sue White, Ben Weisburd, Leigh B Waddell, Jeffrey M Verboon, Grace E VanNoy, Ana Töpf, Tiong Yang Tan, Volker Straub, Sarah L Stenton, Hana Snow, Moriel Singer-Berk, Josh Silver, Shirlee Shril, Eleanor G Seaby, Ronen Schneider, Vijay G Sankaran, Alba Sanchis-Juan, Kathryn A Russell, Karit Reinson, Gianina Ravenscroft, Eric A Pierce, Emily M Place, Sander Pajusalu, Lynn Pais, Katrin Õunap, Ikeoluwa Osei-Owusu, Volkan Okur, Kaisa Teele Oja, Melanie O’Leary, Emily O’Heir, Chantal Morel, Rhett G Marchant, Brian E Mangilog, Jill A Madden, Daniel MacArthur, Alysia Lovgren, Jordan P Lerner-Ellis, Jasmine Lin, Nigel Laing, Friedhelm Hildebrandt, Emily Groopman, Julia Goodrich, Joseph G Gleeson, Roula Ghaoui, Casie A Genetti, Hanna T Gazda, Vijay S Ganesh, Mythily Ganapathy, Lyndon Gallacher, Jack Fu, Emily Evangelista, Eleina England, Sandra Donkervoort, Stephanie DiTroia, Sandra T Cooper, Wendy K Chung, John Christodoulou, Katherine R Chao, Liam D Cato, Kinga M Bujakowska, Samantha J Bryen, Harrison Brand, Carsten Bonnemann, Alan H Beggs, Samantha M Baxter, Pankaj B Agrawal, Michael Talkowski, Chrissy Austin-Tse, Heidi L Rehm, Anne O’Donnell-Luria
PMCID: PMC10849673  PMID: 38328047

Abstract

Background

Causal variants underlying rare disorders may remain elusive even after expansive gene panels or exome sequencing (ES). Clinicians and researchers may then turn to genome sequencing (GS), though the added value of this technique and its optimal use remain poorly defined. We therefore investigated the advantages of GS within a phenotypically diverse cohort.

Methods

GS was performed for 744 individuals with rare disease who were genetically undiagnosed. Analysis included review of single nucleotide, indel, structural, and mitochondrial variants.

Results

We successfully solved 218/744 (29.3%) cases using GS, with most solves involving established disease genes (157/218, 72.0%). Of all solved cases, 148 (67.9%) had previously had non-diagnostic ES. We systematically evaluated the 218 causal variants for features requiring GS to identify and 61/218 (28.0%) met these criteria, representing 8.2% of the entire cohort. These included small structural variants (13), copy neutral inversions and complex rearrangements (8), tandem repeat expansions (6), deep intronic variants (15), and coding variants that may be more easily found using GS related to uniformity of coverage (19).

Conclusion

We describe the diagnostic yield of GS in a large and diverse cohort, illustrating several types of pathogenic variation eluding ES or other techniques. Our results reveal a higher diagnostic yield of GS, supporting the utility of a genome-first approach, with consideration of GS as a secondary or tertiary test when higher-resolution structural variant analysis is needed or there is a strong clinical suspicion for a condition and prior targeted genetic testing has been negative.

Full Text Availability

The license terms selected by the author(s) for this preprint version do not permit archiving in PMC. The full text is available from the preprint server.


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