Evidence map›Paper›PMID 25316146›Full record

ArticleGenome biology2014

The multitude of molecular analyses in cancer: the opening of Pandora’s box.

Hege G Russnes, Per E Lønning, Anne-Lise Børresen-Dale, Ole C Lingjærde

Abstract read
In one paragraph

Article in Genome biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 2 pooled it
–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

8 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
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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.

Hege G Russnes
Per E Lønning
Anne-Lise Børresen-Dale
Ole C Lingjærde

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The availability of large amounts of molecular data of unprecedented depth and width has instigated new paths of interdisciplinary activity in cancer research. Translation of such information to allow its optimal use in cancer therapy will require molecular biologists to embrace statistical and computational concepts and models. Progress in science has been and should be driven by our innate curiosity. This is the human quality that led Pandora to open the forbidden box, and like her, we do not know the nature or consequences of the output resulting from our actions. Throughout history, ground-breaking scientific achievements have been closely linked to advances in technology. The microscope and the telescope are examples of inventions that profoundly increased the amount of observable features that further led to paradigmatic shifts in our understanding of life and the Universe. In cell biology, the microscope revealed details of different types of tissue and their cellular composition; it revealed cells, their structures and their ability to divide, develop and die. Further, the molecular compositions of individual cell types were revealed gradually by generations of scientists. For each level of insight gained, new mathematical and statistical descriptive and analytical tools were needed (Figure 1a). The integration of knowledge of ever-increasing depth and width in order to develop useful therapies that can prevent and cure diseases such as cancer will continue to require the joint effort of scientists in biology, medicine, statistics, mathematics and computation. Here, we discuss some major challenges that lie ahead of us and why we believe that a deeper integration of biology and medicine with mathematics and statistics is required to gain the most from the diverse and extensive body of data now being generated. We also argue that to take full advantage of current technological opportunities, we must explore biomarkers using clinical studies that are optimally designed for this purpose. The need for a tight interdisciplinary collaboration has never been stronger.

Indexed as

AnimalsBiomarkers, TumorBiomedical ResearchDatabases, GeneticGenotypeHumansMutationNeoplasmsBiomarkers, Tumor

Identifiers

PMID25316146
PMCPMC4709983

What OpenQuestion holds

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LicenceCC BY
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.