Evidence map›Paper›PMID 25725369›Full record

ReviewSeminars in cell & developmental biology2015

Cell death in genome evolution.

Xinchen Teng, J Marie Hardwick

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Seminars in cell & developmental biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 35% 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

4 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Noncoding RNAs in apoptosis: identification and function.Turkish journal of biology = Turk biyoloji dergisi · 2022
    Review
  3. Review
  4. Filamentation protectsMicrobial cell (Graz, Austria) · 2016
    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

2 authors at 1 institution in 2 countries.

Xinchen TengCollege of Pharmaceutical Sciences, Soochow University, Suzhou, Jiangsu Province 215123, PR China; W. Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD 21205, USA. Electronic address: xcteng@suda.edu.cn.
J Marie HardwickW. Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD 21205, USA. Electronic address: hardwick@jhu.edu.
Johns Hopkins University · US

Funding

REGULATION OF BCL XL BY CASPASESR01NS037402 · NINDS · JOHNS HOPKINS UNIVERSITY · PI HARDWICK, J. MARIE · 1999 to 2014
$4.5M
REGULATION OF VIRAL INFECTIONS BY CELLULAR GENESR01NS034175 · NINDS · JOHNS HOPKINS UNIVERSITY · PI HARDWICK, J. MARIE · 1995 to 2009
$2.5M
Mechanisms of NeurodegenerationR01NS083373 · NINDS · JOHNS HOPKINS UNIVERSITY · PI HARDWICK, J. MARIE · 2013 to 2017
$1.8M
Conserved Cell Death Pathways in Mammals and YeastR01GM077875 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI HARDWICK, J. MARIE · 2006 to 2010
$1.4M
NIGMS NIH HHS GM077875NIGMS NIH HHS R01 GM077875NINDS NIH HHS NS037402NINDS NIH HHS NS083373NINDS NIH HHS R01 NS034175NINDS NIH HHS R01 NS037402NINDS NIH HHS R01 NS083373
6 · The paper itself

Abstract

Inappropriate survival of abnormal cells underlies tumorigenesis. Most discoveries about programmed cell death have come from studying model organisms. Revisiting the experimental contexts that inspired these discoveries helps explain confounding biases that inevitably accompany such discoveries. Amending early biases has added a newcomer to the collection of cell death models. Analysis of gene-dependent death in yeast revealed the surprising influence of single gene mutations on subsequent eukaryotic genome evolution. Similar events may influence the selection for mutations during early tumorigenesis. The possibility that any early random mutation might drive the selection for a cancer driver mutation is conceivable but difficult to demonstrate. This was tested in yeast, revealing that mutation of almost any gene appears to specify the selection for a new second mutation. Some human tumors contain pairs of mutant genes homologous to co-occurring mutant genes in yeast. Here we consider how yeast again provide novel insights into tumorigenesis.

Indexed as

Biological EvolutionCell DeathAnimalsHumansMetamorphosis, BiologicalMutationNeoplasmsSaccharomyces cerevisiaeTumor MicroenvironmentApoptosisCancer progressionEvolutionProgrammed cell deathTumorigenesisYeast

Identifiers

PMID25725369
PMCPMC4410082
OpenAlexW1970288720

What OpenQuestion holds

Textmetadata
LicenceTDM
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.