Evidence map›Paper›PMID 34230614›Full record

ArticleOncogene2021

Integration of genome-level data to allow identification of subtype-specific vulnerability genes as novel therapeutic targets.

Edward C Schwalbe, Lalchungnunga H, Fadhel Lafta, Timothy M Barrow, Gordon Strathdee

Abstract read
In one paragraph

Article in Oncogene, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. Identification ofInternational journal of molecular sciences · 2023
    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

5 authors.

Edward C Schwalbe *Biosciences Institute, Newcastle University Centre for Cancer, Newcastle University, Newcastle, UK.ORCID http://orcid.org/0000-0002-1190-9469
Lalchungnunga H *Biosciences Institute, Newcastle University Centre for Cancer, Newcastle University, Newcastle, UK.ORCID http://orcid.org/0000-0003-2718-6223
Fadhel Lafta *Biosciences Institute, Newcastle University Centre for Cancer, Newcastle University, Newcastle, UK.
Timothy M BarrowBiosciences Institute, Newcastle University Centre for Cancer, Newcastle University, Newcastle, UK.
Gordon StrathdeeBiosciences Institute, Newcastle University Centre for Cancer, Newcastle University, Newcastle, UK. Gordon.Strathdee@ncl.ac.uk.ORCID http://orcid.org/0000-0001-9681-8429

Funding

Bloodwise 14024
6 · The paper itself

Abstract

The identification of cancer-specific vulnerability genes is one of the most promising approaches for developing more effective and less toxic cancer treatments. Cancer genomes exhibit thousands of changes in DNA methylation and gene expression, with the vast majority likely to be passenger changes. We hypothesised that, through integration of genome-wide DNA methylation/expression data, we could exploit this inherent variability to identify cancer subtype-specific vulnerability genes that would represent novel therapeutic targets that could allow cancer-specific cell killing. We developed a bioinformatics pipeline integrating genome-wide DNA methylation/gene expression data to identify candidate subtype-specific vulnerability partner genes for the genetic drivers of individual genetic/molecular subtypes. Using acute lymphoblastic leukaemia as an initial model, 21 candidate subtype-specific vulnerability genes were identified across the five common genetic subtypes, with at least one per subtype. To confirm the approach was applicable across cancer types, we also assessed medulloblastoma, identifying 15 candidate subtype-specific vulnerability genes across three of four established subtypes. Almost all identified genes had not previously been implicated in these diseases. Functional analysis of seven candidate subtype-specific vulnerability genes across the two tumour types confirmed that siRNA-mediated knockdown induced significant inhibition of proliferation/induction of apoptosis, which was specific to the cancer subtype in which the gene was predicted to be specifically lethal. Thus, we present a novel approach that integrates genome-wide DNA methylation/expression data to identify cancer subtype-specific vulnerability genes as novel therapeutic targets. We demonstrate this approach is applicable to multiple cancer types and identifies true functional subtype-specific vulnerability genes with high efficiency.

Indexed as

DNA MethylationPrecursor Cell Lymphoblastic Leukemia-LymphomaApoptosisCell Line, TumorComputational BiologyGene Expression Regulation, NeoplasticGenome, HumanHumansMedulloblastomaMolecular Targeted Therapy

Identifiers

PMID34230614
PMCPMC8376645

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Registered trials

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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.