Evidence map›Paper›PMID 26090398›Full record

ArticleBioMed research international2015

Role of Genetic Polymorphisms of Deoxycytidine Kinase and Cytidine Deaminase to Predict Risk of Death in Children with Acute Myeloid Leukemia.

Aurora Medina-Sanson, Arturo Ramírez-Pacheco, Silvia Selene Moreno-Guerrero, Elisa María Dorantes-Acosta, Metzeri Sánchez-Preza, Alfonso Reyes-López

Open access · hybridAbstract read
In one paragraph

Article in BioMed research international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

9 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Review
  6. Deciphering the Therapeutic Resistance in Acute Myeloid Leukemia.International journal of molecular sciences · 2020
    Review
  7. Article
  8. Review
  9. Predicting Chemotherapy Resistance in AML.Current hematologic malignancy reports · 2017
    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

6 authors at 1 institution in 1 country.

Aurora Medina-SansonHospital Infantil de México Federico Gómez, Department of Hematology and Oncology, Calle Doctor Márquez 162, Colonia Doctores, Delegación Cuauhtémoc, 06720 Mexico City, DF, Mexico.
Arturo Ramírez-PachecoHospital Infantil de México Federico Gómez, Department of Hematology and Oncology, Calle Doctor Márquez 162, Colonia Doctores, Delegación Cuauhtémoc, 06720 Mexico City, DF, Mexico.
Silvia Selene Moreno-GuerreroHospital Infantil de México Federico Gómez, Department of Hematology and Oncology, Calle Doctor Márquez 162, Colonia Doctores, Delegación Cuauhtémoc, 06720 Mexico City, DF, Mexico.
Elisa María Dorantes-AcostaHospital Infantil de México Federico Gómez, Department of Hematology and Oncology, Calle Doctor Márquez 162, Colonia Doctores, Delegación Cuauhtémoc, 06720 Mexico City, DF, Mexico.
Metzeri Sánchez-PrezaHospital Infantil de México Federico Gómez, Department of Hematology and Oncology, Calle Doctor Márquez 162, Colonia Doctores, Delegación Cuauhtémoc, 06720 Mexico City, DF, Mexico.
Alfonso Reyes-LópezHospital Infantil de México Federico Gómez, Research Division, Calle Doctor Márquez 162, Colonia Doctores, Delegación Cuauhtémoc, 06720 Mexico City, DF, Mexico.
Hospital Infantil de México Federico Gómez · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cytarabine is one of the most effective antineoplastic agents among those used for the treatment of acute myeloid leukemia. However, some patients develop resistance and/or severe side effects to the drug, which may interfere with the efficacy of the treatment. The polymorphisms of some Ara-C metabolizing enzymes seem to affect outcome and toxicity in AML patients receiving cytarabine. We conducted this study in a cohort of Mexican pediatric patients with AML to investigate whether the polymorphisms of the deoxycytidine kinase and cytidine deaminase enzymes are implicated in clinical response and toxicity. Bone marrow and/or peripheral blood samples obtained at diagnosis from 27 previously untreated pediatric patients with de novo AML were processed for genotyping and in vitro chemosensitivity assay, and we analyzed the impact of genotypes and in vitro sensitivity on disease outcome and toxicity. In the multivariate Cox regression analysis, we found that age at diagnosis, wild-type genotype of the CDA A79C polymorphism, and wild-type genotype of the dCK C360G polymorphism were the most significant prognostic factors for predicting the risk of death.

Indexed as

AdolescentChildChild, PreschoolCytidine DeaminaseDeathDeoxycytidine KinaseDrug Resistance, NeoplasmFemaleGenotypeHumansInfantLeukemia, Myeloid, AcuteMalePolymorphism, Single NucleotideRisk FactorsCytidine DeaminaseDeoxycytidine Kinase

Identifiers

PMID26090398
PMCPMC4450239
OpenAlexW1542695502

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.