Evidence map›Paper›PMID 25646566›Full record

ArticleeLife2015

The evolution of drug resistance in clinical isolates of Candida albicans.

Christopher B Ford, Jason M Funt, Darren Abbey, Luca Issi, Candace Guiducci, Diego A Martinez, Toni Delorey, Bi Yu Li, Theodore C White, Christina Cuomo and 4 more

Open access · goldAbstract read
In one paragraph

Article in eLife, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 200 papers.

0numbers the graph read from it
0cells of the map it votes in
200citing papers in PubMed
21.4field-weighted citation impact, top 1% 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

200 citing papers in PubMed, 364 citations in OpenAlex.

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 4 institutions in 2 countries.

Christopher B FordDepartment of Biology, Broad Institute of MIT and Harvard, Cambridge, United States.
Jason M FuntDepartment of Biology, Broad Institute of MIT and Harvard, Cambridge, United States.
Darren AbbeyDepartment of Genetics, Cell Biology and Development, University of Minnesota, Minneapolis, United States.
Luca IssiDepartment of Biology and Biotechnology, Worcester Polytechnic Institute, Worcester, United States.
Candace GuiducciBroad Institute of MIT and Harvard, Cambridge, United States.
Diego A MartinezBroad Institute of MIT and Harvard, Cambridge, United States.
Toni DeloreyBroad Institute of MIT and Harvard, Cambridge, United States.
Bi Yu LiBroad Institute of MIT and Harvard, Cambridge, United States.
Theodore C WhiteSchool of Biological Sciences, University of Missouri at Kansas City, Kansas City, United States.
Christina CuomoBroad Institute of MIT and Harvard, Cambridge, United States.
Reeta P RaoDepartment of Biology and Biotechnology, Worcester Polytechnic Institute, Worcester, United States.
Judith BermanDepartment of Genetics, Cell Biology and Development, University of Minnesota, Minneapolis, United States.
Dawn A ThompsonBroad Institute of MIT and Harvard, Cambridge, United States.
Aviv RegevDepartment of Biology, Broad Institute of MIT and Harvard, Cambridge, United States.
Broad Institute · USUniversity of Minnesota · USWorcester Polytechnic Institute · USUniversity of Missouri–Kansas City · US

Funding

Genome-wide analysis of regulated chromosomal domains: From mechanisms to cancerR01CA119176 · NCI · WEIZMANN INSTITUTE OF SCIENCE · PI REGEV, AVIV, SEGAL, ERAN · 2006 to 2015
$3.7M
The temporal reconfiguration of regulatory networks: From yeast to cancerDP1CA174427 · NCI · BROAD INSTITUTE, INC. · PI REGEV, AVIV · 2012 to 2012
$839k
Howard Hughes Medical InstituteNCI NIH HHS 2R01CA119176-01NCI NIH HHS 8DP1CA174427NCI NIH HHS DP1 CA174427NCI NIH HHS R01 CA119176
6 · The paper itself

Abstract

Candida albicans is both a member of the healthy human microbiome and a major pathogen in immunocompromised individuals. Infections are typically treated with azole inhibitors of ergosterol biosynthesis often leading to drug resistance. Studies in clinical isolates have implicated multiple mechanisms in resistance, but have focused on large-scale aberrations or candidate genes, and do not comprehensively chart the genetic basis of adaptation. Here, we leveraged next-generation sequencing to analyze 43 isolates from 11 oral candidiasis patients. We detected newly selected mutations, including single-nucleotide polymorphisms (SNPs), copy-number variations and loss-of-heterozygosity (LOH) events. LOH events were commonly associated with acquired resistance, and SNPs in 240 genes may be related to host adaptation. Conversely, most aneuploidies were transient and did not correlate with drug resistance. Our analysis also shows that isolates also varied in adherence, filamentation, and virulence. Our work reveals new molecular mechanisms underlying the evolution of drug resistance and host adaptation.

Indexed as

Evolution, MolecularAdhesivenessAneuploidyCandida albicansCandidiasisDrug Resistance, FungalFluconazoleGenetic FitnessGenome, HumanHost-Pathogen InteractionsHumansLoss of HeterozygosityMicrobial Sensitivity TestsMutationPhenotypePolymorphism, Single NucleotideFluconazoleCandida albicansdrug resistanceevolutionevolutionary biologygenomicsinfectious diseasemicrobiologyvirulence

Identifiers

PMID25646566
PMCPMC4383195
OpenAlexW2089758228

What OpenQuestion 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 OpenQuestion graph.