Evidence map›Paper›PMID 30678090›Full record

ReviewGenes2019

From Genotype to Phenotype: Through Chromatin.

Julia Romanowska, Anagha Joshi

Open access · goldAbstract readReview
In one paragraph

Review in Genes, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

17 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Frontiers in pharmacology · 2024
    Article
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  11. Review
  12. Review
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  14. Review
  15. International journal of molecular sciences · 2020
    Article
  16. Article
  17. 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

2 authors at 1 institution in 1 country.

Julia RomanowskaDepartment of Global Public Health and Primary Care, University of Bergen, 5018, Bergen, Norway. Julia.Romanowska@uib.no.ORCID 0000-0001-6733-1953
Anagha JoshiComputational Biology Unit, Department of Clinical Science, University of Bergen, 5021, Bergen, Norway. Anagha.Joshi@uib.no.
University of Bergen · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Advances in sequencing technologies have enabled the exploration of the genetic basis for several clinical disorders by allowing identification of causal mutations in rare genetic diseases. Sequencing technology has also facilitated genome-wide association studies to gather single nucleotide polymorphisms in common diseases including cancer and diabetes. Sequencing has therefore become common in the clinic for both prognostics and diagnostics. The success in follow-up steps, i.e., mapping mutations to causal genes and therapeutic targets to further the development of novel therapies, has nevertheless been very limited. This is because most mutations associated with diseases lie in inter-genic regions including the so-called regulatory genome. Additionally, no genetic causes are apparent for many diseases including neurodegenerative disorders. A complementary approach is therefore gaining interest, namely to focus on

Indexed as

Chromatin Assembly and DisassemblyEpigenesis, GeneticAnimalsGene-Environment InteractionGenetic Predisposition to DiseaseGenomicsHumanschromatin modificationdisease variantsepigeneticsregulatory genomicssequencing

Identifiers

PMID30678090
PMCPMC6410296
OpenAlexW2911658010

What OpenQuestion holds

Textmetadata
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.