Evidence map›Paper›PMID 22408433›Full record

ReviewInternational journal of molecular sciences2012

Tumor heterogeneity: mechanisms and bases for a reliable application of molecular marker design.

Salvador J Diaz-Cano

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed, 2 pooled it
–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

81 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Mucoepidermoid carcinoma (MEC) and adenosquamous carcinoma (ASC), the same or different entities?Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2022
    Pooled it
  2. Association of APE1 Gene Asp148Glu Variant with Digestive Cancer: A Meta-Analysis.Medical science monitor : international medical journal of experimental and clinical research · 2015
    Pooled it
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  11. Antibody-conjugated polymer nanoparticles for brain cancer.Drug delivery and translational research · 2025
    Review
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21 more citing papers are in PubMed but not listed here.

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.

Salvador J Diaz-CanoDepartment Histopathology, King's College Hospital and King's Health Partners, Denmark Hill, London SE5 9RS, UK.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor heterogeneity is a confusing finding in the assessment of neoplasms, potentially resulting in inaccurate diagnostic, prognostic and predictive tests. This tumor heterogeneity is not always a random and unpredictable phenomenon, whose knowledge helps designing better tests. The biologic reasons for this intratumoral heterogeneity would then be important to understand both the natural history of neoplasms and the selection of test samples for reliable analysis. The main factors contributing to intratumoral heterogeneity inducing gene abnormalities or modifying its expression include: the gradient ischemic level within neoplasms, the action of tumor microenvironment (bidirectional interaction between tumor cells and stroma), mechanisms of intercellular transference of genetic information (exosomes), and differential mechanisms of sequence-independent modifications of genetic material and proteins. The intratumoral heterogeneity is at the origin of tumor progression and it is also the byproduct of the selection process during progression. Any analysis of heterogeneity mechanisms must be integrated within the process of segregation of genetic changes in tumor cells during the clonal expansion and progression of neoplasms. The evaluation of these mechanisms must also consider the redundancy and pleiotropism of molecular pathways, for which appropriate surrogate markers would support the presence or not of heterogeneous genetics and the main mechanisms responsible. This knowledge would constitute a solid scientific background for future therapeutic planning.

Indexed as

Genetic Association StudiesGenetic HeterogeneityAnimalsBiomarkers, TumorClonal EvolutionDisease ProgressionGenetic MarkersHumansNeoplasmsTumor MicroenvironmentBiomarkers, TumorGenetic Markerscell segregationclonal expansionexosomemetastasisneoplasmtopographic compartmentstumor heterogeneitytumor hypoxiatumor microenvironmenttumor progression

Identifiers

PMID22408433
PMCPMC3292002

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Registered trials

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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.