Evidence map›Paper›PMID 31548659›Full record

ReviewNature reviews. Genetics2020

Context is everything: aneuploidy in cancer.

Uri Ben-David, Angelika Amon

Open access · greenAbstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Genetics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 427 papers.

0numbers the graph read from it
0cells of the map it votes in
427citing papers in PubMed
27.3field-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

427 citing papers in PubMed, 721 citations in OpenAlex.

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 2 countries.

Uri Ben-DavidDepartment of Human Molecular Genetics and Biochemistry, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel. ubendavid@tauex.tau.ac.il.
Angelika AmonKoch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA, USA. angelika@mit.edu.ORCID http://orcid.org/0000-0001-9837-0314
Howard Hughes Medical Institute · USTel Aviv University · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer is driven by multiple types of genetic alterations, which range in size from point mutations to whole-chromosome gains and losses, known as aneuploidy. Chromosome instability, the process that gives rise to aneuploidy, can promote tumorigenesis by increasing genetic heterogeneity and promoting tumour evolution. However, much less is known about how aneuploidy itself contributes to tumour formation and progression. Unlike some pan-cancer oncogenes and tumour suppressor genes that drive transformation in virtually all cell types and cellular contexts, aneuploidy is not a universal promoter of tumorigenesis. Instead, recent studies suggest that aneuploidy is a context-dependent, cancer-type-specific oncogenic event that may have clinical relevance as a prognostic marker and as a potential therapeutic target.

Indexed as

AneuploidyChromosomal InstabilityAnimalsCell Transformation, NeoplasticHumansNeoplasmsPhenotype

Identifiers

PMID31548659
OpenAlexW2973350525

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.