Evidence map›Paper›PMID 32030650›Full record

ReviewAdvances in experimental medicine and biology2020

The Multifaceted Effects of Autophagy on the Tumor Microenvironment.

Rui Kang, Herbert Zeh, Michael Lotze, Daolin Tang

Abstract readReview
PubMed Publisher
In one paragraph

Review in Advances in experimental medicine and biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
13.8field-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

17 citing papers in PubMed, 21 citations in OpenAlex.

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  15. Autophagy and Exosomes Relationship in Cancer: Friends or Foes?Frontiers in cell and developmental biology · 2020
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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 2 institutions in 1 country.

Rui KangDepartment of Surgery, UT Southwestern Medical Center, Dallas, TX, USA. rui.kang@utsouthwestern.edu.
Herbert ZehDepartment of Surgery, UT Southwestern Medical Center, Dallas, TX, USA.
Michael LotzeDepartment of Surgery, University of Pittsburgh, Pittsburgh, PA, USA.
Daolin TangDepartment of Surgery, UT Southwestern Medical Center, Dallas, TX, USA. daolin.tang@utsouthwestern.edu.
Southwestern Medical Center · USUniversity of Pittsburgh · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The tumor microenvironment is composed of cancer cells, noncancer cells (e.g., immune cells, stromal cells, endothelial cells, and adipocytes), and various mediators (e.g., cytokines, chemokines, growth factors, and humoral factors) that work together to support cancer growth, progression, and resistance to therapies. Autophagy is an evolutionarily conserved degradation mechanism by which various cytosolic cargos (e.g., damaged organelles, unused molecules, or invaded pathogens) are engulfed by double-membrane autophagosomes, and then delivered into the lysosome for degradation and recycling. The level of autophagy is a crucial threshold to either promote cell survival or induce cell death in response to environmental stresses. Autophagy plays a context-dependent role in tumorigenesis and anticancer therapy via shaping the inflammatory, hypoxic, immunosuppressive, and metabolic tumor microenvironment. In particular, impaired autophagy flux is associated with chronic inflammation, immunosuppression, stromal formation, cancer stemness, angiogenesis, metastasis, and metabolic reprogramming in the tumor microenvironment. Understanding the molecular machinery of autophagy and its communication with hallmarks of cancer could lead to potential new anticancer strategies or drugs.

Indexed as

AutophagyTumor MicroenvironmentHumansNeoplasmsAngiogenesisAutophagyCancer stem cellsCell deathCytokineFerroptosisFibroblastHypoxiaImmune cellsImmunosuppressionInflammationMetabolic reprogrammingMetastasisTumor microenvironment

Identifiers

PMID32030650
OpenAlexW3004920676

What OpenQuestion holds

Textmetadata
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.