Evidence map›Paper›PMID 15199392›Full record

ArticleBritish journal of cancer2004

DNA replication licensing and cell cycle kinetics of oligodendroglial tumours.

S B Wharton, S Hibberd, K L Eward, D Crimmins, D A Jellinek, D Levy, K Stoeber, G H Williams

Open access · hybridAbstract readComparative Study
In one paragraph

Article in British journal of cancer, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

19 citing papers in PubMed, 65 citations in OpenAlex.

  1. Trial
  2. Article
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  4. Expression Profile and Prognostic Values of Mini-Chromosome Maintenance Families (MCMs) in Breast Cancer.Medical science monitor : international medical journal of experimental and clinical research · 2020
    Article
  5. Article
  6. MCM2: An alternative to Ki-67 for measuring breast cancer cell proliferation.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2017
    Article
  7. Article
  8. Article
  9. DNA replication licensing factors and aneuploidy are linked to tumor cell cycle state and clinical outcome in penile carcinoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2009
    Article
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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

8 authors at 5 institutions in 1 country.

S B Wharton1Academic Unit of Pathology, University of Sheffield, UK.
S Hibberd
K L Eward
D Crimmins
D A Jellinek
D Levy
K Stoeber
G H Williams
Royal Hallamshire Hospital · GBWolfson Foundation · GBUniversity College London · GBUniversity of Sheffield · GBWeston Park Cancer Centre · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The convergence point of growth-signalling pathways that control cell proliferation is the initiation of genome replication, the core of which is the assembly of pre-replicative complexes (pre-RCs), resulting in chromatin being 'licensed' for DNA replication in the subsequent S phase. The Mcm2-7 complex is a core constituent of the pre-RC, whose recruitment to replication origins is dependent on the Cdt1 loading factor. Geminin is a potent inhibitor of the initiation of DNA replication by preventing Mcm2-7 assembly at origins via its interaction with Cdt1, ensuring genomic integrity through suppression of re-initiation events in S phase. Here we investigate the regulation of Ki67, Mcm2, p21, caspase 3 and Geminin in a series of 55 oligodendrogliomas to provide an integrated picture of how cellular proliferation and programmed cell death are dysregulated in these tumours. Geminin does not behave as an inhibitor of cell proliferation, its labelling index rising with increasing growth fraction as defined by Ki67 or Mcm2 expression. Geminin is expressed in a higher proportion of cells in higher grade tumours (P<0.001) and shows a strong correlation to proliferation and replication licensing (P<0.01), but not apoptosis. Increasing tumour anaplasia is not associated with loss of Geminin. Importantly, the G1 phase of the proliferative cell cycle, as assessed by the Geminin/Ki67 ratio, shortens with increasing anaplasia, providing new potential algorithms for prognostic assessment. Origin licensing proteins thus provide powerful novel tools for assessment of tumour cell cycle kinetics in routinely processed surgical biopsy material.

Indexed as

DNA ReplicationAdultAnimalsBrain NeoplasmsCaspase 3CaspasesCell CycleCell Cycle ProteinsCyclin-Dependent Kinase Inhibitor p21CyclinsFemaleGemininHumansImmunoglobulin GKi-67 AntigenKineticsCASP3 protein, humanCaspase 3CaspasesCDKN1A protein, humanCell Cycle ProteinsCyclin-Dependent Kinase Inhibitor p21CyclinsGemininGMNN protein, humanImmunoglobulin GKi-67 AntigenMCM2 protein, humanMinichromosome Maintenance Complex Component 2Nuclear Proteins

Identifiers

PMID15199392
PMCPMC2409817
OpenAlexW2014694169

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.