Evidence map›Paper›PMID 21857118›Full record

ReviewJournal of biosciences2011

Genome-based versus gene-based theory of cancer: possible implications for clinical practice.

Natasa Todorovic-Rakovic

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of biosciences, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Full Karyotype Interphase Cell Analysis.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2018
    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.

Natasa Todorovic-RakovicDepartment of Experimental Oncology, Institute for Oncology and Radiology of Serbia, Pasterova 14, 11000 Belgrade, Serbia. todorovicn@ncrc.ac.rs

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The current state in oncology research indicates that the attempts to explain such complex process as cancerogenesis by a single or several genetic mutations were not successful enough. On the other hand, chromosomal/genomic instability--almost universal features of malignant tumours which influence a global pattern of gene expression and, subsequently, many oncogenic pathways--were often disregarded and considered nonessential to clinical application. However, a new arising field of system biology including 'new forms' of genome diversity such as copy number variations (CNV) and high-throughput oncogene mutation profiling now reveal all the complexity of cancer and provide the final explanation of the oncogenic pathways, based on stochastic (onco)genomic variation rather than on (onco)genic concepts.

Indexed as

EpigenomicsNeoplasmsAneuploidyComparative Genomic HybridizationDNA Copy Number VariationsGene DosageGene Expression Regulation, NeoplasticGenome, HumanGenomic InstabilityHumansMutationSystems Biology

Identifiers

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.