Evidence map›Paper›PMID 33788050›Full record

ArticleJournal, genetic engineering & biotechnology2021

Epigenetic effects toward new insights as potential therapeutic target in B-thalassemia.

Noha Hamdy Eltaweel, Ghada Youssef ElKamah, Rabab Khairat, Hanan Abd Elmawgoud Atia, Khalda S Amr

Abstract read
In one paragraph

Article in Journal, genetic engineering & biotechnology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

10 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Gene editing using gamma modified PNA: HBB gene as a model.Journal, genetic engineering & biotechnology · 2025
    Article
  3. Article
  4. Review
  5. Association ofMolecular genetics and metabolism reports · 2024
    Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Noha Hamdy EltaweelMedical Molecular Genetics Department, Human genetics and genome project Division, National Research Centre, El Buhouth St., Dokki, Cairo, 12622, Egypt.
Ghada Youssef ElKamahClinical Genetics Department, Human genetics and genome project Division, National Research Centre, Cairo, Egypt.
Rabab KhairatMedical Molecular Genetics Department, Human genetics and genome project Division, National Research Centre, El Buhouth St., Dokki, Cairo, 12622, Egypt.
Hanan Abd Elmawgoud AtiaPharmacology and Toxicology Department, College of Pharmacy, Hail University, Hail, Saudi Arabia.
Khalda S AmrMedical Molecular Genetics Department, Human genetics and genome project Division, National Research Centre, El Buhouth St., Dokki, Cairo, 12622, Egypt. khalda_nrc@yahoo.com.ORCID http://orcid.org/0000-0001-8472-5911

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundFetal hemoglobin (HbF) induction has shown promise for the treatment of β-hemoglobinopathies. HbF induction in β-thalassemia could overcome ineffective hematopoiesis and thus terminate transfusion dependency for formerly transfusion dependant patients. Several miRNAs have been found to reactivate γ-globin expression and increase HbF. In this study, we aimed to investigate the expression of 4 miRNAs (miR-15a, miR-16-1, miR-96, and miR-486-3p) in high HbF thalassemia patients and correlate their levels with the patients' HbF levels then, in order to predict the exact role of the studied miRNAs in hematopoiesis, a bioinformatic analysis was carried out. We went through this bioinformatic analysis to determine the network of genes regulated by miRNAs and further investigate the interaction between all of them through their involvement in hematopoiesis. In this study, the differential expression was measured by qRT-PCR for 40 patients with high HbF and compared to 20 healthy controls. Bioinformatics was conducted involving functional annotation and pathway enrichment analyses.

resultsThe studied microRNAs were significantly deregulated in thalassemia patients in correlation with HbF. Functional annotation and pathway enrichment analyses revealed a major role of miR-486-3p and miR-15a in HbF induction.

conclusionMiR-486-3p and miR-15a are crucial for HbF induction. Further validating studies are needed.

Indexed as

HbF inductionMicroRNAmiR-15amiR-16-1miR-486-3pmiR-96Thalassemia therapy

Identifiers

PMID33788050
PMCPMC8012446

What Socratic holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.