Evidence map›Paper›PMID 19842938›Full record

ReviewPharmacogenomics2009

Genetic factors influencing cytarabine therapy.

Jatinder K Lamba

Open access · greenAbstract readReview
In one paragraph

Review in Pharmacogenomics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 16% 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

72 citing papers in PubMed, 1 synthesis or guideline pooled it, 135 citations in OpenAlex.

  1. Pooled it
  2. Pharmacogenomic Score Effectively Personalizes Treatment of Acute Myeloid Leukemia.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024
    Trial
  3. Trial
  4. Trial
  5. Pharmacokinetics and Model-Based Dosing to Optimize Fludarabine Therapy in Pediatric Hematopoietic Cell Transplant Recipients.Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation · 2017
    Trial
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Cytidine and dCMP Deaminases-Current Methods of Activity Analysis.International journal of molecular sciences · 2025
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

12 more citing papers are in PubMed but not listed here.

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

1 author at 1 institution in 1 country.

Jatinder K LambaDepartment of Experimental and Clinical Pharmacology, University of Minnesota, Minneapolis, MN 55455, USA. lamba004@umn.edu
University of Minnesota · US

Funding

Pharmacogenomics of Ara-C in AMLR01CA132946 · NCI · UNIVERSITY OF MINNESOTA · PI LAMBA, JATINDER K., POUNDS, STANLEY BARRETT · 2008 to 2025
$5.3M
NCI NIH HHS R01 CA132946NCI NIH HHS R01CA132946
6 · The paper itself

Abstract

The mainstay of acute myeloid leukemia chemotherapy is the nucleoside analog cytarabine (ara-C). Numerous studies suggest that the intracellular concentrations of the ara-C active metabolite, ara-CTP, vary widely among patients and, in turn, are associated with variability in clinical response to acute myeloid leukemia treatment. Thus, genetic variation in key genes in the ara-C metabolic pathway--specifically, deoxycytidine kinase (a rate-limiting activating enzyme), 5 nucleotidase, cytidine deaminase and deoxycytidylate deaminase (all three are inactivating enzymes), human equilibrative nucleoside transporter (ara-C uptake transporter) and ribonucleotide reductase (RRM1 and RRM2--enzymes regulating intracellular deoxycytidine triphosphate pools)--form the molecular basis of the interpatient variability observed in intracellular ara-CTP concentrations and response to ara-C. Understanding genetic variants in the key candidate genes involved in the metabolic activation of ara-C, as well as the pharmacodynamic targets of ara-C, will provide an opportunity to identify patients at an increased risk of adverse reactions or decreased likelihood of response, based upon their genetic profile, which in future could help in dose optimization to reduce drug toxicity without compromising efficacy. The pharmacogenetic studies on ara-C would also be equally applicable to other nucleoside analogs, such as gemcitabine, decitabine, clofarabine and so on, which are metabolized by the same pathway.

Indexed as

5'-NucleotidaseAntimetabolites, AntineoplasticArabinofuranosylcytosine TriphosphateCytarabineCytidine DeaminaseDeoxycytidine KinaseEquilibrative Nucleoside Transporter 1ForecastingGenetic VariationHumansLeukemia, Myeloid, AcuteNucleoside DeaminasesPharmacogeneticsRibonucleotide Reductases5'-NucleotidaseAntimetabolites, AntineoplasticArabinofuranosylcytosine TriphosphateCytarabineCytidine Deaminasedeoxycytidine deaminaseDeoxycytidine KinaseEquilibrative Nucleoside Transporter 1Nucleoside DeaminasesRibonucleotide Reductases

Identifiers

PMID19842938
PMCPMC2828057
OpenAlexW2074129070

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

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.