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Cited by 57

The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.

Clonal hematopoiesis in sickle cell disease

Liggett, L. Alexander, Cato, Liam D., Weinstock, Joshua S., Zhang, Yingze, Nouraie, S. Mehdi, Gladwin, Mark T., Garrett, Melanie E., Ashley-Koch, Allison, Telen, Marilyn J., Custer, Brian, Kelly, Shannon, Dinardo, Carla L., Sabino, Ester C., Loureiro, Paula, Carneiro-Proietti, Anna B., Maximo, Cláudia, Reiner, Alexander P., Abecasis, Gonçalo R., Williams, David A., Natarajan, Pradeep, Bick, Alexander G., Sankaran, Vijay G.·2022·Journal of Clinical Investigation
DOI 10.1172/jci156060PMC PMC8843701

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Figures

Figure 1 Prevalence of CH is similar in unaffected and SCD populations. (A) A generalized additive model was used here to fit rates of CH within WGS data from a total of 71,100 individuals unaffected by SCD and 3,090 individuals affected by SCD, which indicates no significantly increased prevalence of CH within individuals affected by SCD (OR = 1.30, P = 0.20). (B) Generalized additive model as in A was used to fit rates of CH using a genetically matched cohort without SCD. The matched cohort was created by selecting the 10 most similar individuals by the first 10 PCs for each individual in the SCD cohort. Resampling of individuals without SCD was permitted. SCD samples without sufficient matches were excluded. (C) Genes ranked by variant load across all individuals separated by SCD status into unaffected (blue) and affected (red). (D) Type of genetic change ranked by prevalence in all individuals separated by SCD status into unaffected (blue) and affected (red).
Figure 1 Prevalence of CH is similar in unaffected and SCD populations. (A) A generalized additive model was used here to fit rates of CH within WGS data from a total of 71,100 individuals unaffected by SCD and 3,090 individuals affected by SCD, which indicates no significantly increased prevalence of CH within individuals affected by SCD (OR = 1.30, P = 0.20). (B) Generalized additive model as in A was used to fit rates of CH using a genetically matched cohort without SCD. The matched cohort was created by selecting the 10 most similar individuals by the first 10 PCs for each individual in the SCD cohort. Resampling of individuals without SCD was permitted. SCD samples without sufficient matches were excluded. (C) Genes ranked by variant load across all individuals separated by SCD status into unaffected (blue) and affected (red). (D) Type of genetic change ranked by prevalence in all individuals separated by SCD status into unaffected (blue) and affected (red).CC BY · PubMed Central
Figure 2 Mutation signatures do not vary in SCD and hydroxyurea (HU) treatment does not impact the rate of CH development. Percentages of total single-base substitutions made up by each possible 96 substitution and trinucleotide context pairs per individual (error is SD across individuals). Signatures are separated into (A) individuals without SCD and (B) individuals with SCD (data represent mean ± SD). (C) A generalized additive model is used here to fit rates of CH within WGS from individuals with SCD separated into never-HU-treated or HU-treated groups. There is no significant difference in the rate of CH in either the HU-treated or untreated groups adjusted for age, age2, sex, study, and the first 10 principal components (OR = 0.58, P = 0.23). (D) Genes ranked by variant load across all individuals with SCD separated by HU treatment status into untreated (green) and (E) treated (purple).
Figure 2 Mutation signatures do not vary in SCD and hydroxyurea (HU) treatment does not impact the rate of CH development. Percentages of total single-base substitutions made up by each possible 96 substitution and trinucleotide context pairs per individual (error is SD across individuals). Signatures are separated into (A) individuals without SCD and (B) individuals with SCD (data represent mean ± SD). (C) A generalized additive model is used here to fit rates of CH within WGS from individuals with SCD separated into never-HU-treated or HU-treated groups. There is no significant difference in the rate of CH in either the HU-treated or untreated groups adjusted for age, age2, sex, study, and the first 10 principal components (OR = 0.58, P = 0.23). (D) Genes ranked by variant load across all individuals with SCD separated by HU treatment status into untreated (green) and (E) treated (purple).CC BY · PubMed Central

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Citations

Cites

Research works printed but not linked: 15

  1. 10.1182/blood-2018-10-880575 · DOI
  2. 10.1038/s41379-019-0325-6 · DOI · Paper page
  3. 10.1182/blood-2017-05-783233 · DOI · Paper page
  4. 10.1177/0141076816651037 · DOI · Paper page
  5. Science. Gene Therapy Trials for Sickle Cell Disease Halted After Two Patients Develop Cancer. https://www.sciencemag.org/news/2021/02/gene-therapy-trials-sickle-cell-disease-halted-after-two-patients-develop-cancer Updated February 16, 2021. Accessed May 7, 2021
  6. 10.1182/bloodadvances.2019001330 · DOI · Paper page
  7. Ghannam, 2020, Baseline TP53 mutations in adults with SCD developing myeloid malignancy following hematopoietic cell transplantation, Blood, 135, 1185
  8. 10.1038/s41591-018-0081-z · DOI · Paper page
  9. 10.1038/s41586-021-03205-y · DOI · Paper page
  10. 10.1016/j.cell.2020.08.030 · DOI · Paper page
  11. 10.1016/S0140-6736(17)30193-9 · DOI
  12. 10.1111/bjh.17323 · DOI
  13. 10.1182/blood.2021011488 · DOI
  14. 10.1182/blood.2021011121 · DOI · Paper page
  15. 10.1186/s12864-019-6041-2 · DOI

Cited by

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Metadata

Authors
Liggett, L. A., Cato, L. D., Weinstock, J. S., Zhang, Y., Nouraie, S. M., Gladwin, M. T., Garrett, M. E., Ashley-Koch, A., Telen, M. J., Custer, B., Kelly, S., Dinardo, C. L., Sabino, E. C., Loureiro, P., Carneiro-Proietti, A. B., Maximo, C., Reiner, A. P., Abecasis, G. R., Williams, D. A., Natarajan, P., Bick, A. G., & Sankaran, V. G.
Venue
Journal of Clinical Investigation
Publisher
American Society for Clinical Investigation
Published
2022-02-15
Volume
132
Issue
4
ISSN
1558-8238
DOI
10.1172/jci156060
PMC
PMC8843701
Cited by
57
References
7
Language
en
Licence
creativecommons.org/licenses/by/4.0/ (vor)
Funders
  • National Institutes of Health (R01 DK103794, R01 HL146500, T32 HL007574)
  • Foundation for the National Institutes of Health (T32 HL066987)

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