Evidence map›Paper›PMID 26691424›Full record

Trial reportBone marrow transplantation2016

Influence of glutathione S-transferase gene polymorphisms on busulfan pharmacokinetics and outcome of hematopoietic stem-cell transplantation in thalassemia pediatric patients.

M Ansari, P Huezo-Diaz, M A Rezgui, S Marktel, M Duval, H Bittencourt, B Cappelli, M Krajinovic

Open access · hybridAbstract readClinical Trial
In one paragraph

Trial report in Bone marrow transplantation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

19 citing papers in PubMed, 45 citations in OpenAlex.

  1. Trial
  2. Frontiers in pharmacology · 2026
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  7. Review
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  12. Review
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  15. Busulfan Pharmacokinetics in Adenosine Deaminase-Deficient Severe Combined Immunodeficiency Gene Therapy.Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation · 2020
    Article
  16. Article
  17. Article
  18. Article
  19. Article
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

8 authors at 4 institutions in 3 countries.

M AnsariDepartment of Pediatrics, Onco-Haematology unit, Geneva University Hospital, Faculty of Medicine, Geneva, Switzerland.
P Huezo-DiazDepartment of Pediatrics, Onco-Haematology unit, Geneva University Hospital, Faculty of Medicine, Geneva, Switzerland.
M A RezguiCharles-Bruneau Cancer Center, CHU Sainte-Justine Research Center, Montreal, Quebec, Canada.
S MarktelStem Cell Programme, IRCCS, San Raffaele Scientific Institute, Milano, Italy.
M DuvalCharles-Bruneau Cancer Center, CHU Sainte-Justine Research Center, Montreal, Quebec, Canada.
H BittencourtCharles-Bruneau Cancer Center, CHU Sainte-Justine Research Center, Montreal, Quebec, Canada.
B CappelliPediatric Immuno-Hematology and BMT unit, IRCCS San Raffaele Hospital, Milano, Italy.
M KrajinovicCharles-Bruneau Cancer Center, CHU Sainte-Justine Research Center, Montreal, Quebec, Canada.
Centre Hospitalier Universitaire Sainte-Justine · CAIstituti di Ricovero e Cura a Carattere Scientifico · ITUniversité de Montréal · CAUniversity of Geneva · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hematopoietic stem-cell transplantation (HSCT) is currently the only curative therapeutic option for the treatment of thalassemia. In spite of the high cure rate, HSCT can lead to life-threatening adverse events in some patients. Busulfan (Bu) is a key component of the conditioning regimen prior to HSCT. Inter-individual differences in Bu pharmacokinetics (PK) are hypothesized to influence Bu efficacy and toxicity. Since Bu is mainly metabolized by glutathione S-transferase (GST), we investigated the relationship of GSTA1 and GSTM1 genotypes with first-dose PK and HSCT outcomes in 44 children with thalassemia intermedia and thalassemia major. All children received a myeloablative conditioning regimen with IV Bu. Association analysis revealed a relationship between GSTA169C>T (or haplotype *A/*B) and first Bu dose PK that was dependent on sex and Pesaro risk classification (PRC). Among female patients and patients with PRC I-II, homozygous individuals for the GSTA1T-69 allele defining haplotype *B, had higher Bu exposure and lower clearance (P⩽0.01). Association with HSCT outcomes showed that patients with the GSTM1 null genotypes had higher occurrence of regimen-related toxicity (P=0.01). These results suggest that GST genotypes could be useful to tailor the first Bu dose accordingly to improve HSCT outcome.

Indexed as

beta-ThalassemiaBusulfanHematopoietic Stem Cell TransplantationPolymorphism, GeneticTransplantation ConditioningAllelesAllograftsChildFemaleGenotypeGlutathione TransferaseHaplotypesHumansMaleBusulfanGlutathione TransferaseGSTA1 protein, human

Identifiers

PMID26691424
PMCPMC4777888
OpenAlexW2206010137

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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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 OpenQuestion graph.