Evidence map›Paper›PMID 27608016›Full record

ReviewInternational journal of molecular sciences2016

Escaping Antiangiogenic Therapy: Strategies Employed by Cancer Cells.

Mauricio P Pinto, Paula Sotomayor, Gonzalo Carrasco-Avino, Alejandro H Corvalan, Gareth I Owen

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

49 citing papers in PubMed, 66 citations in OpenAlex.

  1. Review
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  10. Review
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  13. Article
  14. Promising Nanomedicines of Shikonin for Cancer Therapy.International journal of nanomedicine · 2023
    Review
  15. Review
  16. Article
  17. Mechanisms of chemotherapy resistance in ovarian cancer.Cancer drug resistance (Alhambra, Calif.) · 2022
    Review
  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

5 authors at 3 institutions in 1 country.

Mauricio P PintoDepartment of Physiology, Faculty of Biological Sciences, Pontificia Universidad Católica de Chile, Santiago 8331150, Chile. mauricio_pinto@outlook.com.
Paula SotomayorCenter for Integrative Medicine and Innovative Science, Facultad de Medicina, Universidad Andrés Bello, Santiago 8370071, Chile. paulacsf@yahoo.com.
Gonzalo Carrasco-AvinoDepartment of Pathology, Faculty of Medicine, Universidad de Chile, Santiago 8380456, Chile. gcarrasa@me.com.
Alejandro H CorvalanDepartment of Hematology-Oncology, Faculty of Medicine, Pontificia Universidad Católica de Chile, Santiago 8330032, Chile. corvalan@med.puc.cl.
Gareth I OwenDepartment of Physiology, Faculty of Biological Sciences, Pontificia Universidad Católica de Chile, Santiago 8331150, Chile. gowen@bio.puc.cl.
Pontificia Universidad Católica de Chile · CLUniversidad Andrés Bello · CLUniversity of Chile · CL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor angiogenesis is widely recognized as one of the "hallmarks of cancer". Consequently, during the last decades the development and testing of commercial angiogenic inhibitors has been a central focus for both basic and clinical cancer research. While antiangiogenic drugs are now incorporated into standard clinical practice, as with all cancer therapies, tumors can eventually become resistant by employing a variety of strategies to receive nutrients and oxygen in the event of therapeutic assault. Herein, we concentrate and review in detail three of the principal mechanisms of antiangiogenic therapy escape: (1) upregulation of compensatory/alternative pathways for angiogenesis; (2) vasculogenic mimicry; and (3) vessel co-option. We suggest that an understanding of how a cancer cell adapts to antiangiogenic therapy may also parallel the mechanisms employed in the bourgeoning tumor and isolated metastatic cells delivering responsible for residual disease. Finally, we speculate on strategies to adapt antiangiogenic therapy for future clinical uses.

Indexed as

Drug Resistance, NeoplasmAngiogenesis InhibitorsAnimalsGene Expression Regulation, NeoplasticHumansNeovascularization, PathologicAngiogenesis Inhibitorscancer dormancyresidual diseasevascular co-optionvasculogenic mimicry

Identifiers

PMID27608016
PMCPMC5037767
OpenAlexW2508752584

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.