Evidence map›Paper›PMID 17940619›Full record

ReviewThe Yale journal of biology and medicine2006

Mechanisms of oncogenic cooperation in cancer initiation and metastasis.

Laura G Pedraza-Fariña

Open access · greenAbstract readReview
In one paragraph

Review in The Yale journal of biology and medicine, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
0.6field-weighted citation impact, top 36% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.

  1. The Effects of Hysterectomy on Urinary and Sexual Functions of Women with Cervical Cancer: A Systematic Review.Revista brasileira de ginecologia e obstetricia : revista da Federacao Brasileira das Sociedades de Ginecologia e Obstetricia · 2022
    Pooled it
  2. Review
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  6. The Supression of Migration and Metastasis via Inhibition of Vascular Endothelial Growth Factor in Pancreatic Adenocarcinoma Cells Applied Danusertib.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2024
    Article
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  10. Frontiers in immunology · 2022
    Article
  11. Review
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  14. HCMDB: the human cancer metastasis database.Nucleic acids research · 2018
    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

1 author at 1 institution in 1 country.

Laura G Pedraza-FariñaDepartment of Genetics, Yale University School of Medicine, New Haven, Connecticut 06536, USA. lpedraza@law.harvard.edu
Yale University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer is a disease of extreme heterogeneity. Microarray analysis has identified thousands of genes that are transcriptionally up- or down-regulated in tumor samples; molecularly characterized lesions that play a causative role in tumorigenesis constitute more than 1 percent of the human genome. Such a large number of "cancer genes" stirs the debate of whether it is relevant to continue classifying cancer as a single condition. Yet, a discrete set of cellular processes has been found to underlie such complexity. Their deregulation has been proposed to act as a common denominator that enables tumors to evade cellular barriers to proliferation and metastasis. Efforts have been made to identify and model the mechanistic origins of cancer. Two such models are discussed here: the multistage model of cancer and the cancer platform model. The former suggests cancer arises by the sequential acquisition of mutations leading to the progressive erosion of normal cellular control mechanisms. In contrast, the latter reduces cancer initiation to two interdependent conditions: sustained proliferation with the concomitant inhibition of cell death. This review proposes that a third condition - cellular differentiation - should be added to the cancer platform model. Differentiation can act as a fail-safe mechanism against unrestrained cellular growth - much like cell death. Clinical implications of the different models are also analyzed.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsApoptosisCell CycleCell DifferentiationCell LineageCell ProliferationCell Transformation, NeoplasticCellular SenescenceDisease ProgressionGenomeHumansMutationNeoplasm InvasivenessNeoplasm MetastasisNeoplasms

Identifiers

PMID17940619
PMCPMC1994802
OpenAlexW1716180479

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.