Evidence map›Paper›PMID 35527244›Full record

ArticleBMC cancer2022

Influence of cytochrome P450 and glutathione S transferase polymorphisms on response to nilotinib therapy among chronic myeloidleukemia patients from Pakistan.

Samina Naz Mukry, Aneeta Shahni, Uzma Zaidi, Tahir Sultan Shamsi

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed, 1 pooled it
0.6field-weighted citation impact, top 30% 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

3 citing papers in PubMed, 1 synthesis or guideline pooled it, 5 citations in OpenAlex.

  1. Pooled it
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  3. 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

4 authors at 1 institution in 1 country.

Samina Naz MukryDepartment of Molecular Biology, National Institute of Blood Diseases & Bone Marrow Transplantation, Karachi, Pakistan. smukry.nibd@gmail.com.ORCID http://orcid.org/0000-0002-6876-0802
Aneeta ShahniDepartment of Molecular Biology, National Institute of Blood Diseases & Bone Marrow Transplantation, Karachi, Pakistan.
Uzma ZaidiDepartment of Clinical Hematology, National Institute of Blood Diseases & Bone Marrow Transplantation, Karachi, Pakistan.
Tahir Sultan ShamsiDepartment of Post Graduate Studies & Research, National Institute of Blood Diseases & Bone Marrow Transplantation, Karachi, Pakistan.
National Institute Of Blood Disease and Bone Marrow Transplantation · PK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCytochrome P450 (CYP) and glutathione S transferases (GSTs) are important biotransforming enzymes responsible for detoxification of anticancer drugs and carcinogens. Polymorphisms in these enzymes may greatly influence the susceptibility to CML and overall efficacy of tyrosine kinase inhibitors. This study was aimed to estimate the possible influence of the polymorphisms of GSTs and CYP in the occurrence of CML as well as in predicting therapeutic outcome of nilotinib therapy in Pakistani CML patients.

methodsThe polymorphic variability in CYP 1A1*2C, GSTP1 (A3131G), GSTT1 and GSTM1 was assessed either by RFLP or multiplex PCR. The BCR ABL1 transcripts were quantified by qPCR to monitor response to nilotinib.

resultsThe CYP1A1*2C heterozygous and GSTP1 homozygous polymorphisms seemed to be a contributing factor in developing CML. Altogether, there were 12 non-responders, 66 responders and 21 partial responders. The most frequent genotype was null GSTM1 in responders followed by CYP 1A1 and GSTP1 -wild type (p =  < 0.05). Whereas, homozygous GSTP1 and GSTT1 null genotype is significantly higher only among nilotinib non-responders.

conclusionHence, it can be concluded that wild type CYP1A1, GSTP1 and null GSTM1 may be frequently linked to favorable outcome in patients treated with nilotinib as depicted by sustained deep molecular response in most CML patients.

Indexed as

Cytochrome P-450 CYP1A1Glutathione TransferaseLeukemia, Myelogenous, Chronic, BCR-ABL PositivePyrimidinesCase-Control StudiesGenetic Predisposition to DiseaseGenotypeGlutathione S-Transferase piHumansPakistanPolymorphism, GeneticRisk FactorsCytochrome P-450 CYP1A1Glutathione S-Transferase piglutathione S-transferase T1Glutathione TransferaseGSTP1 protein, humannilotinibPyrimidinesChronic myeloid leukemiaDrug metabolizing enzymesNilotinibResponseTreatment

Identifiers

PMID35527244
PMCPMC9080200
OpenAlexW4229336469

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LicenceCC BY
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Registered trials

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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.