Evidence map›Paper›PMID 30723315›Full record

ArticleThe pharmacogenomics journal2019

Variants in vincristine pharmacodynamic genes involved in neurotoxicity at induction phase in the therapy of pediatric acute lymphoblastic leukemia.

Idoia Martin-Guerrero, Angela Gutierrez-Camino, Aizpea Echebarria-Barona, Itziar Astigarraga, Nagore Garcia de Andoin, Aurora Navajas, Africa Garcia-Orad

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In one paragraph

Article in The pharmacogenomics journal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 12% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.

  1. Pooled it
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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

7 authors at 3 institutions in 1 country.

Idoia Martin-GuerreroDepartment of Genetics, Physical Anthropology and Animal Physiology, Faculty of Medicine and Nursery, University of the Basque Country (UPV/EHU), Leioa, Spain.
Angela Gutierrez-CaminoDepartment of Genetics, Physical Anthropology and Animal Physiology, Faculty of Medicine and Nursery, University of the Basque Country (UPV/EHU), Leioa, Spain.
Aizpea Echebarria-BaronaUnit of Pediatric Hematology/Oncology, University Hospital Cruces, Bilbao, Spain.
Itziar AstigarragaUnit of Pediatric Hematology/Oncology, University Hospital Cruces, Bilbao, Spain.
Nagore Garcia de AndoinUnit of Pediatric Oncohematology, University Hospital Donostia, San Sebastian, Spain.
Aurora NavajasBioCruces Health Research Institute, Barakaldo, Spain.
Africa Garcia-OradDepartment of Genetics, Physical Anthropology and Animal Physiology, Faculty of Medicine and Nursery, University of the Basque Country (UPV/EHU), Leioa, Spain. africa.garciaorad@ehu.eus.ORCID http://orcid.org/0000-0002-5575-3080
University of the Basque Country · ESBioCruces Health research Institute · ESBiogipuzkoa Health Research Institute · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vincristine is an important drug of acute lymphoblastic leukemia (ALL) treatment protocols that can cause neurotoxicity. Patients treated with LAL/SHOP protocols often suffer from vincristine-related neurotoxicity in early phases of treatment. A genetic variant in CEP72, a gene involved in vincristine pharmacodynamics, was recently associated with neurotoxicity after prolonged vincristine treatment. This association was not replicated in our Spanish population during induction phase. To test the possibility that other variants in genes involved in vincristine pharmacodynamics were associated with vincristine neuropathy in early phases of the treatment, we evaluated the correlation with toxicity of 24 polymorphisms in 9 key genes in a large cohort of 152 Spanish children with B-ALL homogeneously treated. Results showed no association between any genetic variant in the TUBB1, TUBB2A, TUBB2B, TUBB3, TUBB4, MAPT, MIR146a, MIR202, and MIR411 genes and vincristine-related neurotoxicity. These results are in line with the hypothesis that there are different mechanisms causing pheripheral neurotoxicity after prolonged and short-term vincristine treatments.

Indexed as

Antineoplastic Agents, PhytogenicChild, PreschoolFemaleGenotypeHumansMaleMicrotubule-Associated ProteinsNeurotoxicity SyndromesPolymorphism, Single NucleotidePrecursor Cell Lymphoblastic Leukemia-LymphomaVincristineAntineoplastic Agents, PhytogenicMicrotubule-Associated ProteinsVincristine

Identifiers

PMID30723315
OpenAlexW2913132570

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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.