Evidence map›Paper›PMID 29641911›Full record

ReviewAnnual review of genomics and human genetics2018

Sickle Cell Anemia and Its Phenotypes.

Thomas N Williams, Swee Lay Thein

Registry-linked trialOpen access · bronzeAbstract readReview
In one paragraph

Review in Annual review of genomics and human genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06158945 (The Role of Endothelin 1 as a Marker of Renal Impairment in Sickle Cell Disease), which is not on this map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
5.8field-weighted citation impact, top 3% of its field
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.

NCT06158945 unknown statusnot on this mapstarted 2023, after this paper: background citation

The Role of Endothelin 1 as a Marker of Renal Impairment in Sickle Cell Disease

TypeobservationalSponsorSohag UniversityRan2023 to 2024Enrolled30ConditionsSickle Cell DiseaseArmsurinary endothelin 1
3 · Its place in the literature

Who cites it

70 citing papers in PubMed, 136 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Observational
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Updated Review of Current Therapeutic Approaches for the Management of Sickle Cell Disease.Cardiovascular & hematological disorders drug targets · 2026
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article

10 more citing papers are in PubMed but not listed here.

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

2 authors at 2 institutions in 3 countries.

Thomas N WilliamsDepartment of Epidemiology and Demography, KEMRI/Wellcome Trust Research Programme, Kilifi, Kenya.
Swee Lay TheinSickle Cell Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892-1589, USA; email: sweelay.thein@nih.gov.
Kenya Medical Research Institute · KENational Heart Lung and Blood Institute · US

Funding

Wellcome Trust 202800Wellcome Trust 202800/Z/16/ZWellcome Trust 203077
6 · The paper itself

Abstract

In the 100 years since sickle cell anemia (SCA) was first described in the medical literature, studies of its molecular and pathophysiological basis have been at the vanguard of scientific discovery. By contrast, the translation of such knowledge into treatments that improve the lives of those affected has been much too slow. Recent years, however, have seen major advances on several fronts. A more detailed understanding of the switch from fetal to adult hemoglobin and the identification of regulators such as BCL11A provide hope that these findings will be translated into genomic-based approaches to the therapeutic reactivation of hemoglobin F production in patients with SCA. Meanwhile, an unprecedented number of new drugs aimed at both the treatment and prevention of end-organ damage are now in the pipeline, outcomes from potentially curative treatments such as allogeneic hematopoietic stem cell transplantation are improving, and great strides are being made in gene therapy, where methods employing both antisickling β-globin lentiviral vectors and gene editing are now entering clinical trials. Encouragingly, after a century of neglect, the profile of the vast majority of those with SCA in Africa and India is also finally improving.

Indexed as

PhenotypeAnemia, Sickle CellCarrier ProteinsGenetic TherapyHemoglobinsHumansNuclear ProteinsRepressor ProteinsTreatment OutcomeBCL11A protein, humanCarrier ProteinsHemoglobinsNuclear ProteinsRepressor ProteinsAfricagenetic modifiersgeneticsgenomicssickle cell anemia

Identifiers

PMID29641911
PMCPMC7613509
OpenAlexW2797498165

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

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.