Evidence map›Paper›PMID 32707662›Full record

ReviewPharmaceuticals (Basel, Switzerland)2020

Autophagy as a Potential Therapy for Malignant Glioma.

Angel Escamilla-Ramírez, Rosa A Castillo-Rodríguez, Sergio Zavala-Vega, Dolores Jimenez-Farfan, Isabel Anaya-Rubio, Eduardo Briseño, Guadalupe Palencia, Patricia Guevara, Arturo Cruz-Salgado, Julio Sotelo and 1 more

Open access · goldAbstract readReview
In one paragraph

Review in Pharmaceuticals (Basel, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
8.6field-weighted citation impact, top 1% 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

58 citing papers in PubMed, 88 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. A bibliometric analysis of global research trends in autophagy and glioblastomas.Naunyn-Schmiedeberg's archives of pharmacology · 2026
    Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Regulation of autophagy by non-coding RNAs in human glioblastoma.Medical oncology (Northwood, London, England) · 2024
    Review
  16. Article
  17. Review
  18. A Synopsis of Biomarkers in Glioblastoma: Past and Present.Current issues in molecular biology · 2024
    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

11 authors at 3 institutions in 1 country.

Angel Escamilla-RamírezDepartamento de Neuroinmunología, Instituto Nacional de Neurología y Neurocirugía, Ciudad de México 14269, Mexico.ORCID 0000-0002-7240-3437
Rosa A Castillo-RodríguezLaboratorio de Oncología Experimental, CONACYT-Instituto Nacional de Pediatría, Ciudad de México 04530, Mexico.ORCID 0000-0003-4117-6689
Sergio Zavala-VegaDepartamento de Patología, Instituto Nacional de Neurología y Neurocirugía, Ciudad de México 14269, Mexico.
Dolores Jimenez-FarfanLaboratorio de Inmunología, División de Estudios de Posgrado e Investigación, Facultad de Odontología, Universidad Nacional Autónoma de México, Ciudad de México 04510, Mexico.ORCID 0000-0002-0152-5429
Isabel Anaya-RubioDepartamento de Neuroinmunología, Instituto Nacional de Neurología y Neurocirugía, Ciudad de México 14269, Mexico.
Eduardo BriseñoClínica de Neurooncología, Instituto Nacional de Neurología y Neurocirugía, Ciudad de México 14269, Mexico.
Guadalupe PalenciaDepartamento de Neuroinmunología, Instituto Nacional de Neurología y Neurocirugía, Ciudad de México 14269, Mexico.
Patricia GuevaraDepartamento de Neuroinmunología, Instituto Nacional de Neurología y Neurocirugía, Ciudad de México 14269, Mexico.
Arturo Cruz-SalgadoDepartamento de Neuroinmunología, Instituto Nacional de Neurología y Neurocirugía, Ciudad de México 14269, Mexico.
Julio SoteloDepartamento de Neuroinmunología, Instituto Nacional de Neurología y Neurocirugía, Ciudad de México 14269, Mexico.
Cristina Trejo-SolísDepartamento de Neuroinmunología, Instituto Nacional de Neurología y Neurocirugía, Ciudad de México 14269, Mexico.
Instituto Nacional de Neurología y Neurocirugía · MXInstituto Nacional de Pediatria · MXUniversidad Nacional Autónoma de México · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioma is the most frequent and aggressive type of brain neoplasm, being anaplastic astrocytoma (AA) and glioblastoma multiforme (GBM), its most malignant forms. The survival rate in patients with these neoplasms is 15 months after diagnosis, despite a diversity of treatments, including surgery, radiation, chemotherapy, and immunotherapy. The resistance of GBM to various therapies is due to a highly mutated genome; these genetic changes induce a de-regulation of several signaling pathways and result in higher cell proliferation rates, angiogenesis, invasion, and a marked resistance to apoptosis; this latter trait is a hallmark of highly invasive tumor cells, such as glioma cells. Due to a defective apoptosis in gliomas, induced autophagic death can be an alternative to remove tumor cells. Paradoxically, however, autophagy in cancer can promote either a cell death or survival. Modulating the autophagic pathway as a death mechanism for cancer cells has prompted the use of both inhibitors and autophagy inducers. The autophagic process, either as a cancer suppressing or inducing mechanism in high-grade gliomas is discussed in this review, along with therapeutic approaches to inhibit or induce autophagy in pre-clinical and clinical studies, aiming to increase the efficiency of conventional treatments to remove glioma neoplastic cells.

Indexed as

autophagychemotherapyglioma

Identifiers

PMID32707662
PMCPMC7407942
OpenAlexW3042397662

What Socratic 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 Socratic graph.