Trial reportLeukemia2008
Prognostic role of glutathione S-transferase polymorphisms in acute myeloid leukemia.
Trial report in Leukemia, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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.
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.
Who cites it
14 citing papers in PubMed, 37 citations in OpenAlex.
- The added value of multi-state modelling in a randomized controlled trial: The HOVON 102 study re-analyzed.Cancer medicine · 2022Trial
- Article
- Deciphering the role of Wnt signaling in acute myeloid leukemia prognosis: how alterations in DNA methylation come into play in patients' prognosis.Journal of cancer research and clinical oncology · 2020Review
- Genetic variants of glutathione S-transferase and the risk of acute myeloid leukemia in a Saudi population.Saudi journal of biological sciences · 2019Article
- Review
- Article
- Significance of Polymorphisms and Expression of Enzyme-Encoding Genes Related to Glutathione in Hematopoietic Cancers and Solid Tumors.BioMed research international · 2015Review
- Investigation of DNA repair gene variants on myelodysplastic syndromes in a Turkish population.Medical oncology (Northwood, London, England) · 2014Article
- Impact of polymorphisms in drug pathway genes on disease-free survival in adults with acute myeloid leukemia.Journal of human genetics · 2013Article
- The clinically relevant pharmacogenomic changes in acute myelogenous leukemia.Pharmacogenomics · 2012Review
- Regulatory functions of glutathione S-transferase P1-1 unrelated to detoxification.Drug metabolism reviews · 2011Review
- The impact of redox and thiol status on the bone marrow: Pharmacological intervention strategies.Pharmacology & therapeutics · 2011Review
- Involvement of oxidative stress in the relapse of acute myeloid leukemia.The Journal of biological chemistry · 2010Article
- Influence of GSTP1 I105V polymorphism on cumulative neuropathy and outcome of FOLFOX-4 treatment in Asian patients with colorectal carcinoma.Cancer science · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glutathione S-transferases (GSTs) are phase II detoxification enzymes involved in the metabolism of carcinogens and anticancer drugs, known also to interact with kinase complexes during oxidative or chemical stress-induced apoptosis. We were interested whether their polymorphic variants may account for differences in outcome of patients with acute myeloid leukemia (AML) following chemotherapy. We studied the prognostic role of polymorphisms in three GST genes (GSTP1/M1/T1) in a large patient cohort of the German Austrian Acute Myeloid Leukemia Study Group, treated according to prospective multicenter clinical trials (AML HD98A: 254 patients; AML HD98-B: 100 patients), with a median follow-up of 46 months. Looking at short-term adverse drug reactions, homozygous carriers of the GSTP1*105 Val allele had a faster neutrophil and platelet recovery (P=0.002 and 0.02, respectively) and a reduced need of red cell and platelet transfusions (P=0.01 and 0.03, respectively). Response to induction chemotherapy did not vary according to GST polymorphisms. Multivariable Cox regression models revealed a significant better relapse-free (RFS) and overall survival for the GSTP1(*)105 Val (P=0.003 and 0.03, respectively), whereas GSTT1 and GSTM1 genotypes had no significant impact. The favorable impact of GSTP1(*)105 Val on RFS seems to be restricted to the subgroup of patients exhibiting a normal karyotype.
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Registered trials
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