Evidence map›Paper›PMID 31575041›Full record

ArticleGenes2019

A Humanized Yeast Phenomic Model of Deoxycytidine Kinase to Predict Genetic Buffering of Nucleoside Analog Cytotoxicity.

Sean M Santos, Mert Icyuz, Ilya Pound, Doreen William, Jingyu Guo, Brett A McKinney, Michael Niederweis, John Rodgers, John L Hartman

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Genes, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.3field-weighted citation impact, top 43% 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

1 citing paper in PubMed, 6 citations in OpenAlex.

  1. 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

9 authors at 2 institutions in 1 country.

Sean M SantosDepartment of Genetics, University of Alabama at Birmingham, Birmingham, AL 35294, USA . seansantos18@gmail.com.
Mert IcyuzDepartment of Genetics, University of Alabama at Birmingham, Birmingham, AL 35294, USA . icyuz@uab.edu.
Ilya PoundDepartment of Genetics, University of Alabama at Birmingham, Birmingham, AL 35294, USA . poundilya@yahoo.com.
Doreen WilliamDepartment of Microbiology, University of Alabama at Birmingham, Birmingham, AL 35294, USA. doreen.william@nct-dresden.de.
Jingyu GuoDepartment of Genetics, University of Alabama at Birmingham, Birmingham, AL 35294, USA . guo.jingyu@gmail.com.
Brett A McKinneyTandy School of Computer Science and Department of Mathematics, The University of Tulsa, Tulsa, OK 74104, USA. jwrodger@uab.edu.
Michael NiederweisDepartment of Microbiology, University of Alabama at Birmingham, Birmingham, AL 35294, USA. mnieder@uab.edu.
John RodgersDepartment of Genetics, University of Alabama at Birmingham, Birmingham, AL 35294, USA . brett.mckinney@gmail.com.
John L HartmanDepartment of Genetics, University of Alabama at Birmingham, Birmingham, AL 35294, USA . jhartman@uab.edu.
University of Alabama at Birmingham · USUniversity of Tulsa · US

Funding

XRAY CRYSTALLOGRAPHYP30CA013148 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Omer Jamy · 1985 to 2026
$165.9M
Ribosomal perturbation as a mechanism to prevent misfolding of CFTRR01HL136414 · NHLBI · EMORY UNIVERSITY · PI HARTMAN, JOHN L, SORSCHER, ERIC J · 2018 to 2025
$4.5M
Constructing gene-regulatory networks to reveal the metabolic basis of lifespan in yeastR01AG043076 · NIA · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI HARTMAN, JOHN L · 2012 to 2016
$1.9M
Howard Hughes Medical Institute P/S ECA 57005927NCI NIH HHS P30 CA013148NHLBI NIH HHS R01 HL136414NIA NIH HHS R01 AG043076
6 · The paper itself

Abstract

Knowledge about synthetic lethality can be applied to enhance the efficacy of anticancer therapies in individual patients harboring genetic alterations in their cancer that specifically render it vulnerable. We investigated the potential for high-resolution phenomic analysis in yeast to predict such genetic vulnerabilities by systematic, comprehensive, and quantitative assessment of drug-gene interaction for gemcitabine and cytarabine, substrates of deoxycytidine kinase that have similar molecular structures yet distinct antitumor efficacy. Human deoxycytidine kinase (dCK) was conditionally expressed in the

Indexed as

Antimetabolites, AntineoplasticCytarabineDeoxycytidineDeoxycytidine KinaseEpistasis, GeneticGemcitabineGene OntologyGene Regulatory NetworksHigh-Throughput Screening AssaysHumansNucleosidesPharmacogeneticsPhenomicsSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsAntimetabolites, AntineoplasticCytarabineDeoxycytidineDeoxycytidine KinaseGemcitabineNucleosidesSaccharomyces cerevisiae Proteinscytarabinegene–drug interactiongenetic bufferingquantitative high throughput cell array phenotyping (Q-HTCP), cell proliferation parameters (CPPs), gemcitabinerecursive expectation-maximization clustering (REMc), pharmacogenomicsyeast phenomics

Identifiers

PMID31575041
PMCPMC6826991
OpenAlexW2975673364

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.