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April 1, 2026Annals of Medicine and SurgeryOpen Access

CRISPR-directed epigenetic reprogramming of the FLT1 locus: a novel strategy for reversing fetal hemoglobin silencing in β-thalassemia minor

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Authors

MNMaheen NazIsra UniversityMBMaryam BatoolCMH Lahore Medical College and Institute of DentistrySSSyed Abdullah ShahKing Edward Medical University

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Implication

This intervention reveals potential for improving hemoglobin levels in beta-thalassemia minor, indicating a novel therapeutic avenue.

Key Points

  • To explore FLT1-directed epigenetic reprogramming as a method for reactivating fetal hemoglobin in β-thalassemia minor.
  • Leveraging CRISPR/Cas9 technology to target FLT1 regulatory elements.
  • Analyzing the genetic variants associated with HbF in African populations.
  • Evaluating the functional role of FLT1 variants in HbF regulation.
  • FLT1 variants were identified that account for approximately 3-3.5% of HbF variation.
  • Individuals with minor alleles exhibited elevated HbF levels, suggesting their role in hemoglobin regulation.
  • FLT1 reprogramming shows promise for safer HbF induction compared to traditional approaches.

Cite This Study

Naz et al. (2026) studied this question.

synapsesocial.com/papers/69ccb71716edfba7beb88e7ehttps://doi.org/10.1097/ms9.0000000000004847
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Also Consider

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