Targeted re-sequencing of F8, F9 and VWF : Characterization of Ion Torrent data and clinical implications for mutation screening
(2019) In PLoS ONE 14(4).- Abstract
Mutations are not identified in ~5% of hemophilia A and 10-35% of type 1 VWD patients. The bleeding tendency also varies among patients carrying the same causative mutation, potentially indicating variants in additional genes modifying the phenotype that cannot be identified by routine single-gene analysis. The F8, F9 and VWF genes were analyzed in parallel using an AmpliSeq strategy and Ion Torrent sequencing. Targeting all exonic positions showed an average read depth of >2000X and coverage close to 100% in 24 male patients with known disease-causing mutations. Discrimination between reference alleles and alternative/indel alleles was adequate at a 25% frequency threshold. In F8, F9 and VWF there was an absolute majority of all... (More)
Mutations are not identified in ~5% of hemophilia A and 10-35% of type 1 VWD patients. The bleeding tendency also varies among patients carrying the same causative mutation, potentially indicating variants in additional genes modifying the phenotype that cannot be identified by routine single-gene analysis. The F8, F9 and VWF genes were analyzed in parallel using an AmpliSeq strategy and Ion Torrent sequencing. Targeting all exonic positions showed an average read depth of >2000X and coverage close to 100% in 24 male patients with known disease-causing mutations. Discrimination between reference alleles and alternative/indel alleles was adequate at a 25% frequency threshold. In F8, F9 and VWF there was an absolute majority of all reference alleles at allele frequencies >95% and the average alternative allele and indel frequencies never reached above 10% and 15%, respectively. In VWF, 4-5 regions showed lower reference allele frequencies; in two regions covered by the pseudogene close to the 25% cut-off for reference alleles. All known mutations, including indels, gross deletions and substitutions, were identified. Additional VWF variants were identified in three hemophilia patients. The presence of additional mutations in 2 out of 16 (12%) randomly selected hemophilia patients indicates a potential mutational contribution that may affect the disease phenotype and counseling in these patients. Parallel identification of disease-causing mutations in all three genes not only confirms the deficiency, but differentiates phenotypic overlaps and allows for correct genetic counseling.
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- author
- Manderstedt, Eric LU ; Nilsson, Rosanna ; Lind-Halldén, Christina ; Ljung, Rolf LU ; Astermark, Jan LU and Halldén, Christer LU
- publishing date
- 2019-04-26
- type
- Contribution to journal
- publication status
- published
- subject
- in
- PLoS ONE
- volume
- 14
- issue
- 4
- article number
- e0216179
- publisher
- Public Library of Science (PLoS)
- external identifiers
-
- pmid:31026269
- scopus:85064817851
- ISSN
- 1932-6203
- DOI
- 10.1371/journal.pone.0216179
- language
- English
- LU publication?
- no
- id
- d6986b1f-0892-4aea-b322-c8d667641156
- date added to LUP
- 2019-04-29 15:50:53
- date last changed
- 2024-10-01 21:07:33
@article{d6986b1f-0892-4aea-b322-c8d667641156, abstract = {{<p>Mutations are not identified in ~5% of hemophilia A and 10-35% of type 1 VWD patients. The bleeding tendency also varies among patients carrying the same causative mutation, potentially indicating variants in additional genes modifying the phenotype that cannot be identified by routine single-gene analysis. The F8, F9 and VWF genes were analyzed in parallel using an AmpliSeq strategy and Ion Torrent sequencing. Targeting all exonic positions showed an average read depth of >2000X and coverage close to 100% in 24 male patients with known disease-causing mutations. Discrimination between reference alleles and alternative/indel alleles was adequate at a 25% frequency threshold. In F8, F9 and VWF there was an absolute majority of all reference alleles at allele frequencies >95% and the average alternative allele and indel frequencies never reached above 10% and 15%, respectively. In VWF, 4-5 regions showed lower reference allele frequencies; in two regions covered by the pseudogene close to the 25% cut-off for reference alleles. All known mutations, including indels, gross deletions and substitutions, were identified. Additional VWF variants were identified in three hemophilia patients. The presence of additional mutations in 2 out of 16 (12%) randomly selected hemophilia patients indicates a potential mutational contribution that may affect the disease phenotype and counseling in these patients. Parallel identification of disease-causing mutations in all three genes not only confirms the deficiency, but differentiates phenotypic overlaps and allows for correct genetic counseling.</p>}}, author = {{Manderstedt, Eric and Nilsson, Rosanna and Lind-Halldén, Christina and Ljung, Rolf and Astermark, Jan and Halldén, Christer}}, issn = {{1932-6203}}, language = {{eng}}, month = {{04}}, number = {{4}}, publisher = {{Public Library of Science (PLoS)}}, series = {{PLoS ONE}}, title = {{Targeted re-sequencing of F8, F9 and VWF : Characterization of Ion Torrent data and clinical implications for mutation screening}}, url = {{http://dx.doi.org/10.1371/journal.pone.0216179}}, doi = {{10.1371/journal.pone.0216179}}, volume = {{14}}, year = {{2019}}, }