Evidence map›Paper›PMID 15824438›Full record

ReviewJournal of biosciences2005

Stochasticity or the fatal 'imperfection' of cloning.

Reiner A Veitia

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of biosciences, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. 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

1 author.

Reiner A VeitiaUniversité Denis Diderot/Paris VII, INSERM U361 Reproduction et Physiopathologie Obstetricale, Hospital Cochin, Pavillon Baudelocque, 123 Bd de Port Royal, 75014 Paris, France. veitia@cochin.inserm.fr

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The concept of clone is analysed with the aim of exploring the limits to which a phenotype can be said to be determined geneticaly. First of all, mutations that result from the replication, topological manipulation or lesion of DNA introduce a source of heritable variation in an otherwise identical genetic background. But more important, stochastic effects in many biological processes may superimpose a phenotypic variation which is not encoded in the genome. The source of stochasticity ranges from the random selection of alleles or whole chromosomes to be expressed in small cell populations, to fluctuations in processes such as gene expression, due to limiting amounts of the players involved. The picture emerging is that the term clone is a statistical over-simplification representing a series of individuals having essentially the same genome but capable of exhibiting wide phenotypic variation. Finally, to what extent fluctuations in biological processes, usually thought of as noise, are in fact signal is also discussed.

Indexed as

Cloning, OrganismPhenotypeStochastic ProcessesAnimalsGene Expression Regulation, DevelopmentalGenetic VariationHumans

Identifiers

PMID15824438

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.