Evidence map›Paper›PMID 38261338›Full record

ReviewBriefings in bioinformatics2024

Prediction of cancer driver genes and mutations: the potential of integrative computational frameworks.

Mona Nourbakhsh, Kristine Degn, Astrid Saksager, Matteo Tiberti, Elena Papaleo

Abstract readReview
In one paragraph

Review in Briefings in bioinformatics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 citing papers in PubMed.

  1. The Mutational Landscape of Acute Myeloid Leukemia and Its Impact.International journal of molecular sciences · 2026
    Review
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
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.

Mona NourbakhshCancer Systems Biology, Section for Bioinformatics, Department of Health Technology, Technical University of Denmark, 2800 Lyngby, Denmark.
Kristine DegnCancer Systems Biology, Section for Bioinformatics, Department of Health Technology, Technical University of Denmark, 2800 Lyngby, Denmark.
Astrid SaksagerCancer Systems Biology, Section for Bioinformatics, Department of Health Technology, Technical University of Denmark, 2800 Lyngby, Denmark.
Matteo TibertiCancer Structural Biology, Danish Cancer Institute, 2100 Copenhagen, Denmark.
Elena PapaleoCancer Systems Biology, Section for Bioinformatics, Department of Health Technology, Technical University of Denmark, 2800 Lyngby, Denmark.

Funding

Carlsberg Foundation Distinguished Fellowship CF18-0314Center of Excellence in Autophagy, Recycling and DiseaseDanish National Research Foundation DNRF-125Hartmanns Fond R241-A33877LEO Fondet LF17006NovoNordisk Fonden Bioscience and Basic Biomedicine NNF20OC0065262
6 · The paper itself

Abstract

The vast amount of available sequencing data allows the scientific community to explore different genetic alterations that may drive cancer or favor cancer progression. Software developers have proposed a myriad of predictive tools, allowing researchers and clinicians to compare and prioritize driver genes and mutations and their relative pathogenicity. However, there is little consensus on the computational approach or a golden standard for comparison. Hence, benchmarking the different tools depends highly on the input data, indicating that overfitting is still a massive problem. One of the solutions is to limit the scope and usage of specific tools. However, such limitations force researchers to walk on a tightrope between creating and using high-quality tools for a specific purpose and describing the complex alterations driving cancer. While the knowledge of cancer development increases daily, many bioinformatic pipelines rely on single nucleotide variants or alterations in a vacuum without accounting for cellular compartments, mutational burden or disease progression. Even within bioinformatics and computational cancer biology, the research fields work in silos, risking overlooking potential synergies or breakthroughs. Here, we provide an overview of databases and datasets for building or testing predictive cancer driver tools. Furthermore, we introduce predictive tools for driver genes, driver mutations, and the impact of these based on structural analysis. Additionally, we suggest and recommend directions in the field to avoid silo-research, moving towards integrative frameworks.

Indexed as

NeoplasmsOncogenesBenchmarkingComputational BiologyConsensusMutationcancercomputational researchdriver genesdriver mutationspathogenicitypredictive toolsprotein structural analysis

Identifiers

PMID38261338
PMCPMC10805075

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.