Evidence map›Paper›PMID 25932044›Full record

ReviewEcancermedicalscience2015

Biology of colorectal cancer.

Francisco Arvelo, Felipe Sojo, Carlos Cotte

Open access · goldAbstract readReview
In one paragraph

Review in Ecancermedicalscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed, 2 pooled it
6.8field-weighted citation impact, top 2% 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

72 citing papers in PubMed, 2 syntheses or guidelines pooled it, 149 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Article
  6. Article
  7. Clinical implications of Alu-based cell-free DNA and serum onco-piRNA monitoring in colorectal cancer management.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Recent Insights into Nanotechnology in Colorectal Cancer.Applied biochemistry and biotechnology · 2024
    Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. Article
  20. Article

12 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

3 authors at 1 institution in 1 country.

Francisco ArveloCentre for Biosciences, Institute for Advanced Studies Foundation-IDEA, Caracas 1015-A, Apartado 17606, Venezuela ; Laboratory for Tissue Culture and Tumour Biology, Institute of Experimental Biology, Central University of Venezuela, Apartado 47114, Caracas, Venezuela.
Felipe SojoCentre for Biosciences, Institute for Advanced Studies Foundation-IDEA, Caracas 1015-A, Apartado 17606, Venezuela ; Laboratory for Tissue Culture and Tumour Biology, Institute of Experimental Biology, Central University of Venezuela, Apartado 47114, Caracas, Venezuela.
Carlos CotteLaboratory for Tissue Culture and Tumour Biology, Institute of Experimental Biology, Central University of Venezuela, Apartado 47114, Caracas, Venezuela.
Central University of Venezuela · VE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Colorectal cancer is a serious health problem, a challenge for research, and a model for studying the molecular mechanisms involved in its development. According to its incidence, this pathology manifests itself in three forms: family, hereditary, and most commonly sporadic, apparently not associated with any hereditary or familial factor. For the types having inheritance patterns and a family predisposition, the tumours develop through defined stages ranging from adenomatous lesions to the manifestation of a malignant tumour. It has been established that environmental and hereditary factors contribute to the development of colorectal cancer, as indicated by the accumulation of mutations in oncogenes, genes which suppress and repair DNA, signaling the existence of various pathways through which the appearance of tumours may occur. In the case of the suppressive and mutating tracks, these are characterised by genetic disorders related to the phenotypical changes of the morphological progression sequence in the adenoma/carcinoma. Moreover, alternate pathways through mutation in BRAF and KRAS genes are associated with the progression of polyps to cancer. This review surveys the research done at the cellular and molecular level aimed at finding specific alternative therapeutic targets for fighting colorectal cancer.

Indexed as

adenomacolorectal cancerfamilial adenomatous polyposishereditary non-polyposis colorectal cancermetastasismicrosatellite instabilityproto-oncogenestumour suppressor genes

Identifiers

PMID25932044
PMCPMC4404039
OpenAlexW2321477918

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.