Evidence map›Paper›PMID 35761387›Full record

ArticleGenome biology2022

Widespread redundancy in -omics profiles of cancer mutation states.

Jake Crawford, Brock C Christensen, Maria Chikina, Casey S Greene

Abstract read
In one paragraph

Article in Genome biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
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

6 citing papers in PubMed.

  1. Article
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  3. Article
  4. Article
  5. wenda_gpu: fast domain adaptation for genomic data.Bioinformatics (Oxford, England) · 2022
    Article
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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

4 authors.

Jake CrawfordGenomics and Computational Biology Graduate Group, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.ORCID 0000-0001-6207-0782
Brock C ChristensenDepartment of Epidemiology, Geisel School of Medicine, Dartmouth College, Lebanon, NH, USA.ORCID 0000-0003-3022-426X
Maria ChikinaDepartment of Computational and Systems Biology, School of Medicine, University of Pittsburgh, Pittsburgh, PA, USA.ORCID 0000-0003-2550-5403
Casey S GreeneDepartment of Biochemistry and Molecular Genetics, University of Colorado School of Medicine, Aurora, CO, USA. casey.s.greene@cuanschutz.edu.ORCID 0000-0001-8713-9213

Funding

DNA-based Immune Phenotyping in HNSCC for Biomarkers of Response to ImmunotherapyR01CA253976 · NCI · BROWN UNIVERSITY · PI CHRISTENSEN, BROCK C, KELSEY, KARL TIMOTHY · 2021 to 2025
$3.3M
Network-based algorithms for target identification and drug repositioning from genetic associationsR01HG010067 · NHGRI · UNIVERSITY OF PENNSYLVANIA · PI GREENE, CASEY S · 2018 to 2022
$3.2M
Characterization of high-grade serous ovarian cancer subtypes via single-cell profilingR01CA237170 · NCI · UNIVERSITY OF PENNSYLVANIA · PI DOHERTY, JENNIFER A., GREENE, CASEY S · 2019 to 2024
$3.0M
(PQ3) Immune epigenetic biomarkers of bladder cancer outcomesR01CA216265 · NCI · DARTMOUTH COLLEGE · PI CHRISTENSEN, BROCK CLARKE · 2017 to 2021
$2.9M
Functional Proteomics by Reverse Phase Protein Array in CancerR50CA221675 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LU, YILING · 2017 to 2021
$726k
NCI NIH HHS R01 CA216265NCI NIH HHS R01 CA237170NCI NIH HHS R01 CA253976NCI NIH HHS R50 CA221675NHGRI NIH HHS R01 HG010067
6 · The paper itself

Abstract

backgroundIn studies of cellular function in cancer, researchers are increasingly able to choose from many -omics assays as functional readouts. Choosing the correct readout for a given study can be difficult, and which layer of cellular function is most suitable to capture the relevant signal remains unclear.

resultsWe consider prediction of cancer mutation status (presence or absence) from functional -omics data as a representative problem that presents an opportunity to quantify and compare the ability of different -omics readouts to capture signals of dysregulation in cancer. From the TCGA Pan-Cancer Atlas that contains genetic alteration data, we focus on RNA sequencing, DNA methylation arrays, reverse phase protein arrays (RPPA), microRNA, and somatic mutational signatures as -omics readouts. Across a collection of genes recurrently mutated in cancer, RNA sequencing tends to be the most effective predictor of mutation state. We find that one or more other data types for many of the genes are approximately equally effective predictors. Performance is more variable between mutations than that between data types for the same mutation, and there is little difference between the top data types. We also find that combining data types into a single multi-omics model provides little or no improvement in predictive ability over the best individual data type.

conclusionsBased on our results, for the design of studies focused on the functional outcomes of cancer mutations, there are often multiple -omics types that can serve as effective readouts, although gene expression seems to be a reasonable default option.

Indexed as

MicroRNAsNeoplasmsHumansMutationMicroRNAs

Identifiers

PMID35761387
PMCPMC9238138

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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.