Evidence map›Paper›PMID 26913068›Full record

ReviewEcancermedicalscience2016

Tumour progression and metastasis.

Francisco Arvelo, Felipe Sojo, Carlos Cotte

Open access · goldAbstract readReview
In one paragraph

Review in Ecancermedicalscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
6.0field-weighted citation impact, top 3% 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

39 citing papers in PubMed, 90 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Factors Determining Epithelial-Mesenchymal Transition in Cancer Progression.International journal of molecular sciences · 2024
    Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Basic concepts of cancer genetics and receptor tyrosine kinase inhibition for pharmacists. A narrative review.Journal of oncology pharmacy practice : official publication of the International Society of Oncology Pharmacy Practitioners · 2023
    Review
  14. Observational
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review
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 2 institutions in 1 country.

Francisco ArveloCentro de Biociencias, Fundación Instituto de Estudios Avanzado [IDEA], Caracas 1015-A, Venezuela, Apartado 17606, Caracas 1015-A, Venezuela; Laboratorio de Cultivo de Tejidos y Biología de Tumores, Instituto de Biología Experimental, Universidad Central de Venezuela, Apartado 47114, Caracas, 1041-A, Venezuela.
Felipe SojoCentro de Biociencias, Fundación Instituto de Estudios Avanzado [IDEA], Caracas 1015-A, Venezuela, Apartado 17606, Caracas 1015-A, Venezuela; Laboratorio de Cultivo de Tejidos y Biología de Tumores, Instituto de Biología Experimental, Universidad Central de Venezuela, Apartado 47114, Caracas, 1041-A, Venezuela.
Carlos CotteLaboratorio de Cultivo de Tejidos y Biología de Tumores, Instituto de Biología Experimental, Universidad Central de Venezuela, Apartado 47114, Caracas, 1041-A, Venezuela.
Central University of Venezuela · VEInstituto de Estudios Avanzados · VE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The two biological mechanisms that determine types of malignancy are infiltration and metastasis, for which tumour microenvironment plays a key role in developing and establishing the morphology, growth and invasiveness of a malignancy. The microenvironment is formed by complex tissue containing the extracellular matrix, tumour and non-tumour cells, a signalling network of cytokines, chemokines, growth factors, and proteases that control autocrine and paracrine communication among individual cells, facilitating tumour progression. During the development of the primary tumour, the tumour stroma and continuous genetic changes within the cells makes it possible for them to migrate, having to count on a pre-metastatic niche receptor that allows the tumour's survival and distant growth. These niches are induced by factors produced by the primary tumour; if it is eradicated, the active niches become responsible for activating the latent disseminated cells. Due to the importance of these mechanisms, the strategies that develop tumour cells during tumour progression and the way in which the microenvironment influences the formation of metastasis are reviewed. It also suggests that the metastatic niche can be an ideal target for new treatments that make controlling metastasis possible.

Indexed as

cancerepithelial–mesenchymal transitioninfiltrationlatencymetastasismetastatic nichemicroenvironment

Identifiers

PMID26913068
PMCPMC4754119
OpenAlexW2403348132

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.