Evidence map›Paper›PMID 12920061›Full record

ReviewJournal of medical genetics2003

New approaches to investigating heterogeneity in complex traits.

R Bomprezzi, P E Kovanen, R Martin

Abstract readReview
In one paragraph

Review in Journal of medical genetics, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Review
  6. Replication study of GWAS risk loci in Greek multiple sclerosis patients.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2019
    Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
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

3 authors.

R BomprezziCancer Genetics Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland 20892, USA. rbomprez@nhgri.nih.gov
P E Kovanen
R Martin

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Great advances in the field of genetics have been made in the last few years. However, resolving the complexity that underlies the susceptibility to many polygenic human diseases remains a major challenge to researchers. The fast increase in availability of genetic data and the better understanding of the clinical and pathological heterogeneity of many autoimmune diseases such as multiple sclerosis, but also Parkinson's disease, Alzheimer's disease, and many more, have changed our views on their pathogenesis and diagnosis, and begins to influence clinical management. At the same time, more powerful methods that allow the analysis of large numbers of genes and proteins simultaneously open opportunities to examine their complex interactions. Using multiple sclerosis as a prototype, we review here how new methodologies such as gene expression profiling can be exploited to gain insight into complex trait diseases.

Indexed as

Gene Expression ProfilingGenetic HeterogeneityOligonucleotide Array Sequence AnalysisQuantitative Trait, HeritableBase SequenceFemaleHumansMaleMolecular Sequence DataPedigree

Identifiers

PMID12920061
PMCPMC1735544

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.