ArticleBlood2011
Pomalidomide augments fetal hemoglobin production without the myelosuppressive effects of hydroxyurea in transgenic sickle cell mice.
Article in Blood, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
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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.
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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.
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Who cites it
40 citing papers in PubMed, 85 citations in OpenAlex.
- Safety and efficacy of thalidomide in patients with transfusion-dependent β-thalassemia: a randomized clinical trial.Signal transduction and targeted therapy · 2021Trial
- A case of SCD controlled by IMiDs and hydroxyurea.International journal of hematology · 2026Article
- Regulation of BCL11A DNA binding and expression in human erythrocyte precursor HUDEP-2 cells.bioRxiv : the preprint server for biology · 2026Article
- Comprehensive Review of Genetic and Epigenetic Regulation of Fetal Hemoglobin in β-Hemoglobinopathies: From Molecular Mechanisms to Clinical Applications.Mediterranean journal of hematology and infectious diseases · 2026Review
- Selective AMPKβ1 activation induces fetal hemoglobin in human erythroid cells and sickle cell mice via the noncanonical NRF2 pathway.Science advances · 2025Article
- Hydroxyurea Mitigates Heme-Induced Inflammation and Kidney Injury in Humanized Sickle Cell Mice.International journal of molecular sciences · 2025Article
- A cellular reporter system to evaluate endogenous fetal hemoglobin induction and screen for therapeutic compounds.HemaSphere · 2024Article
- C2H2 Zinc Finger Transcription Factors Associated with Hemoglobinopathies.Journal of molecular biology · 2024Review
- Identification of small molecule agonists of fetal hemoglobin expression for the treatment of sickle cell disease.PloS one · 2024Article
- Article
- Pharmacological Induction of Fetal Hemoglobin in β-Thalassemia and Sickle Cell Disease: An Updated Perspective.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Fetal hemoglobin rescues ineffective erythropoiesis in sickle cell disease.Haematologica · 2021Article
- Synthesis and pharmacological evaluation of pomalidomide derivatives useful for sickle cell disease treatment.Bioorganic chemistry · 2021Article
- Manipulation of Developmental Gamma-Globin Gene Expression: an Approach for Healing Hemoglobinopathies.Molecular and cellular biology · 2020Review
- Targeted Protein Degradation as a Promising Tool for Epigenetic Upregulation of Fetal Hemoglobin.ChemMedChem · 2020Review
- HRI depletion cooperates with pharmacologic inducers to elevate fetal hemoglobin and reduce sickle cell formation.Blood advances · 2020Article
- Article
- Drug Therapies for the Management of Sickle Cell Disease.F1000Research · 2020Review
- The Evolving Pharmacotherapeutic Landscape for the Treatment of Sickle Cell Disease.Mediterranean journal of hematology and infectious diseases · 2020Review
- The E3 ligase adaptor molecule SPOP regulates fetal hemoglobin levels in adult erythroid cells.Blood advances · 2019Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Pharmacologic induction of fetal hemoglobin (HbF) expression is an effective treatment strategy for sickle cell disease (SCD) and β-thalassemia. Pomalidomide is a potent structural analog of thalidomide and member of a new class of immunomodulatory drugs. Recent reports demonstrated that pomalidomide reduced or eliminated transfusion requirements in certain hematologic malignancies and induced HbF ex vivo in CD34(+) progenitor cells from healthy and SCD donors. We investigated the effects of pomalidomide on erythropoiesis and hemoglobin synthesis in a transgenic mouse model of SCD. We found that 8 weeks of treatment with pomalidomide induced modest increases of HbF with similar efficacy as hydroxyurea. However, in stark contrast to hydroxyurea's myelosuppressive effects, pomalidomide augmented erythropoiesis and preserved bone marrow function. Surprisingly, combinatory therapy with both drugs failed to mitigate hydroxyurea's myelotoxic effects and caused loss of HbF induction. These findings support further evaluation of pomalidomide as a novel therapy for SCD.
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Registered trials
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 OpenQuestion graph.