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A Precision Medicine Tool for Measurement and Monitoring of Hemoglobin S in Sickle Cell Disease Patients Receiving Transfusion Therapy
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Whole Blood Transcriptomic Analysis of Sickle Cell Trait.

Mari Johnson1, Yanwei Cai1, Ana Gabriela Vasconcelos2

  • 1Division of Public Health Sciences, Fred Hutchinson Cancer Center, Seattle, Washington, USA.

European Journal of Haematology
|January 13, 2026
PubMed
Summary
This summary is machine-generated.

Sickle cell trait (SCT) is linked to altered gene expression, particularly involving erythropoiesis and ubiquitin pathways. These changes may explain some adverse health outcomes associated with SCT.

Keywords:
chronic kidney diseaseerythropoiesissickle cell diseasesickle cell traitubiquitination

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Area of Science:

  • Genomics
  • Hematology
  • Molecular Biology

Background:

  • Sickle cell trait (SCT) is the carrier state for the sickle cell disease (SCD) gene.
  • SCT is associated with increased risks of venous thromboembolism and chronic kidney disease.
  • Previous studies suggest SCT alters clinical laboratory parameters.

Purpose of the Study:

  • To investigate differential gene expression in individuals with SCT compared to non-carriers.
  • To identify specific genes and pathways affected by SCT.
  • To explore potential mechanisms linking SCT to adverse health outcomes.

Main Methods:

  • RNA sequencing was performed on whole blood samples from 805 African American women (143 SCT, 660 controls).
  • Differential gene expression analysis was conducted to identify genes with significant expression changes in SCT.
  • Pathway enrichment analysis was used to determine biological processes affected by SCT.

Main Results:

  • 226 differentially expressed genes (DEGs) were identified in SCT compared to controls (FDR < 0.05).
  • Enriched pathways included erythropoiesis, hemoglobin synthesis, and proteasomal degradation.
  • SCT-associated DEGs showed patterns similar to those in SCD, including upregulated ubiquitin-related genes.

Conclusions:

  • SCT is associated with significant differential gene expression in whole blood.
  • The identified DEGs and pathways suggest potential links between SCT, hemolysis, erythropoiesis, and kidney injury.
  • Further research, including single-cell transcriptomics, is warranted to elucidate SCT's mechanisms for adverse health outcomes.