Evidence map›Paper›PMID 26178236›Full record

ReviewAmerican journal of hematology2015

2015 Clinical trials update in sickle cell anemia.

Natasha Archer, Frédéric Galacteros, Carlo Brugnara

Open access · bronzeAbstract readReview
In one paragraph

Review in American journal of hematology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 7% 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.

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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

  1. Pooled it
  2. Hemoglobin Variants as Targets for Stabilizing Drugs.Molecules (Basel, Switzerland) · 2025
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. New Therapeutic Options for the Treatment of Sickle Cell Disease.Mediterranean journal of hematology and infectious diseases · 2019
    Review
  8. Review
  9. Sickle Cell Disease Clinical Trials and Phenotypes.Journal of tropical diseases & public health · 2018
    Article
  10. Review
  11. Review
  12. Review
  13. Emerging cellular and gene therapies for congenital anemias.American journal of medical genetics. Part C, Seminars in medical genetics · 2016
    Review
  14. Article
  15. World Sickle Cell Day 2016 : A time for appraisal.The Indian journal of medical research · 2016
    Article
  16. 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

3 authors at 3 institutions in 2 countries.

Natasha ArcherPediatric Hematology/Oncology Dana-Farber/Children's Hospital Blood Disorders and Cancer Center, Boston, Massachusetts.
Frédéric GalacterosCentre De Référence Des Syndromes Drépanocytaires Majeurs, Hôpital Henri-Mondor, APHP, UPEC, Creteil, France.
Carlo BrugnaraDepartment of Laboratory Medicine, Boston Children's Hospital, Harvard Medical School Boston, Massachusetts.
Dana-Farber/Boston Children's Cancer and Blood Disorders Center · USHarvard University · USUniversité Paris-Est Créteil · FR

Funding

PATHOPHYSIOLOGY OF HUMAN BLOOD CELLST32HL007574 · NHLBI · CHILDREN'S HOSPITAL BOSTON · PI Daniel Evan Bauer · 1985 to 2026
$18.4M
Clinical Hematology Research Career Development Program (K12)K12HL087164 · NHLBI · BOSTON CHILDREN'S HOSPITAL · PI CANTOR, ALAN B. · 2006 to 2016
$3.9M
NHLBI NIH HHS 5K12HL087164-09NHLBI NIH HHS 5T32HL007574NHLBI NIH HHS K12 HL087164NHLBI NIH HHS T32 HL007574
6 · The paper itself

Abstract

Polymerization of HbS and cell sickling are the prime pathophysiological events in sickle cell disease (SCD). Over the last 30 years, a substantial understanding at the molecular level has been acquired on how a single amino acid change in the structure of the beta chain of hemoglobin leads to the explosive growth of the HbS polymer and the associated changes in red cell morphology. O2 tension and intracellular HbS concentration are the primary molecular drivers of this process, and are obvious targets for developing new therapies. However, polymerization and sickling are driving a complex network of associated cellular changes inside and outside of the erythrocyte, which become essential components of the inflammatory vasculopathy and result in a large range of potential acute and chronic organ damages. In these areas, a multitude of new targets for therapeutic developments have emerged, with several ongoing or planned new therapeutic interventions. This review outlines the key points of SCD pathophysiology as they relate to the development of new therapies, both at the pre-clinical and clinical levels.

Indexed as

Anemia, Sickle CellClinical Trials as TopicErythrocytes, AbnormalHemoglobin, SickleHumansOxygenVascular DiseasesHemoglobin, SickleOxygen

Identifiers

PMID26178236
PMCPMC5752136
OpenAlexW2100922847

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

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 OpenQuestion graph.