Evidence map›Paper›PMID 31472232›Full record

ReviewSeminars in cancer biology2020

Autophagy as a mechanism for anti-angiogenic therapy resistance.

Ankush Chandra, Jonathan Rick, Garima Yagnik, Manish K Aghi

Open access · greenAbstract readReview
In one paragraph

Review in Seminars in cancer biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

38 citing papers in PubMed, 48 citations in OpenAlex.

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  6. Dual regulation of autophagy: paradoxical effects on tumor angiogenesis.Frontiers in cell and developmental biology · 2026
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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

4 authors at 1 institution in 1 country.

Ankush ChandraDepartment of Neurological Surgery, University of California at San Francisco, San Francisco, CA, United States of America (USA); School of Medicine, Wayne State University, Detroit, MI, United States of America (USA). Electronic address: ankush.chandra@ucsf.edu.
Jonathan RickDepartment of Neurological Surgery, University of California at San Francisco, San Francisco, CA, United States of America (USA). Electronic address: jonathan.rick@ucsf.edu.
Garima YagnikDepartment of Neurological Surgery, University of California at San Francisco, San Francisco, CA, United States of America (USA). Electronic address: garima.yagnik@ucsf.edu.
Manish K AghiDepartment of Neurological Surgery, University of California at San Francisco, San Francisco, CA, United States of America (USA). Electronic address: manish.aghi@ucsf.edu.
Neurological Surgery · US

Funding

Training Program in Translational Brain Tumor ResearchT32CA151022 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Joseph F Costello · 2010 to 2026
$6.6M
Tumor cell and microenvironment changes causing antiangiogenic therapy resistanceR01NS079697 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI AGHI, MANISH · 2013 to 2021
$3.2M
Modeling and druggable-genome screening of glioblastoma invasion using regional biopsy-guided biomaterials systemsR01CA227136 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI AGHI, MANISH · 2018 to 2022
$2.2M
NCI NIH HHS R01 CA227136NCI NIH HHS T32 CA151022NINDS NIH HHS R01 NS079697
6 · The paper itself

Abstract

Autophagy is a lysosomal-dependent degradation process that is highly conserved and maintains cellular homeostasis by sequestering cytosolic material for degradation either non-specifically by non-selective autophagy, or targeting specific proteins aggregates by selective autophagy. Autophagy serves as a protective mechanism defending the cell from stressors and also plays an important role in enabling tumor cells to overcome harsh conditions arising in their microenvironment during growth as well as oxidative and non-oxidative injuries secondary to therapeutic stressors. Recently, autophagy has been implicated to cause tumor resistance to anti-angiogenic therapy, joining an existing literature implicating autophagy in cancer resistance to conventional DNA damaging chemotherapy and ionizing radiation. In this review, we discuss the role of angiogenesis in malignancy, mechanisms of resistance to anti-angiogenic therapy in general, the role of autophagy in driving malignancy, and the current literature in autophagy-mediated anti-angiogenic therapy resistance. Finally, we provide future insight into the current challenges of using autophagy inhibitors in the clinic and provides tips for future studies to focus on to effectively target autophagy in overcoming resistance to anti-angiogenic therapy.

Indexed as

Angiogenesis InhibitorsAnimalsAutophagyDrug Resistance, NeoplasmHumansNeoplasmsNeovascularization, PathologicTumor MicroenvironmentAngiogenesis InhibitorsAngiogenesisAnti-angiogenesisAutophagyCancerDrug resistanceVEGF

Identifiers

PMID31472232
PMCPMC7047534
OpenAlexW2970012340

What OpenQuestion holds

Textmetadata
LicenceTDM
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.