Evidence map›Paper›PMID 27416373›Full record

ReviewSmall GTPases2017

What makes oncogenes mutually exclusive?

Jaroslaw Cisowski, Martin O Bergo

Abstract readReview
In one paragraph

Review in Small GTPases, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing 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

27 citing papers in PubMed.

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  14. Routine Clinically Detected IncreasedJTO clinical and research reports · 2023
    Article
  15. Oncogene-like addiction to aneuploidy in human cancers.bioRxiv : the preprint server for biology · 2023
    Article
  16. Article
  17. Identifying cancer driver genes in individual tumours.Computational and structural biotechnology journal · 2023
    Review
  18. Article
  19. 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

2 authors.

Jaroslaw Cisowskia Sahlgrenska Cancer Center, Department of Molecular and Clinical Medicine, Institute of Medicine , University of Gothenburg , Gothenburg , Sweden.
Martin O Bergoa Sahlgrenska Cancer Center, Department of Molecular and Clinical Medicine, Institute of Medicine , University of Gothenburg , Gothenburg , Sweden.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer is driven by mutations in genes whose products participate in major signaling pathways that fuel cell proliferation and survival. It is easy to assume that the more of these so-called driver mutations a tumor accumulates, the faster it progresses. However, this does not appear to be the case: Data from large-scale genome sequencing studies indicate that mutations in driver oncogenes often are mutually exclusive. The mechanisms underlying the mutual exclusivity of oncogenes are not completely understood, but recent reports suggest that the mechanisms may depend on the tumor type, and the nature of interacting oncogenes. Here we discuss our recent findings that the oncogenes KRAS

Indexed as

AnimalsCell DeathCellular SenescenceGene Expression Regulation, NeoplasticHumansMutationNeoplasmsOncogenesmutual exclusivityoncogeneRAFRASsenescence

Identifiers

PMID27416373
PMCPMC5584735

What OpenQuestion holds

Textmetadata
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.