Evidence map›Paper›PMID 27664235›Full record

ReviewGenes & development2016

Recent insights into the function of autophagy in cancer.

Ravi Amaravadi, Alec C Kimmelman, Eileen White

Open access · diamondAbstract readReview
In one paragraph

Review in Genes & development, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 499 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
499citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

499 citing papers in PubMed, 2 syntheses or guidelines pooled it, 810 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Targeting MYC-Driven Cancers: From Oncogenic Addiction to Therapeutic Vulnerability.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2026
    Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Autophagy · 2026
    Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review

439 more citing papers are in PubMed but not listed here.

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 3 institutions in 1 country.

Ravi AmaravadiAbramson Cancer Center, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA; Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA;
Alec C KimmelmanPerlmutter Cancer Center, New York University Langone Medical Center, New York, New York 10016, USA; Department of Radiation Oncology, New York University Langone Medical Center, New York, New York 10016, USA;
Eileen WhiteRutgers Cancer Institute of New Jersey, New Brunswick, New Jersey 08903, USA; Department of Molecular Biology and Biochemistry, Rutgers University, Piscataway, New Jersey 08854, USA.
NYU Langone Health · USRutgers, The State University of New Jersey · USUniversity of Pennsylvania · US

Funding

UNIVERSITY OF PENNSYLVANIA CAN CTR SUPPORT GRANTP30CA016520 · NCI · UNIVERSITY OF PENNSYLVANIA · PI SHELLEY L BERGER · 1985 to 2026
$222.3M
TRANSCRIPTIONAL PROFILINGP30CA072720 · NCI · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI Chang S Chan · 1997 to 2026
$94.5M
Targeting the MAP and PI3 Kinase Pathways in MelanomaP01CA114046 · NCI · WISTAR INSTITUTE · PI MURPHY, MAUREEN E. · 2008 to 2023
$37.1M
Targeted Combination Therapy for MelanomaP50CA174523 · NCI · WISTAR INSTITUTE · PI HERLYN, MEENHARD F · 2014 to 2018
$11.1M
Tumor cell metabolism in actionR01CA163591 · NCI · RUTGERS, THE STATE UNIV OF N.J. · PI JOSHUA D RABINOWITZ, Eileen P. White · 2012 to 2026
$7.0M
Role of Autophagy in CancerR01CA130893 · NCI · RUTGERS, THE STATE UNIV OF N.J. · PI WHITE, EILEEN P. · 2008 to 2017
$3.4M
Network organization of the human autophagy systemR01GM095567 · NIGMS · HARVARD MEDICAL SCHOOL · PI HARPER, JEFFREY W, KIMMELMAN, ALEC · 2011 to 2018
$3.0M
Investigating the Role of Autophagy in Pancreatic Cancer Radiation ResistanceR01CA157490 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI KIMMELMAN, ALEC · 2011 to 2018
$2.5M
Targeting Autophagy in Hereditary Breast CancerR01CA188096 · NCI · RBHS -CANCER INSTITUTE OF NEW JERSEY · PI WHITE, EILEEN P., XIA, BING · 2015 to 2019
$2.4M
Promoting Bim-driven apoptosis through MAPK inhibition: A therapeutic strategy in advanced melanomaR01CA193970 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI MEHNERT, JANICE M., SULLIVAN, RYAN J · 2016 to 2020
$2.3M
Molecular mechanisms of BRAF inhibitor induced UPR and autophagyR01CA198015 · NCI · UNIVERSITY OF PENNSYLVANIA · PI AMARAVADI, RAVI K · 2015 to 2019
$1.8M
HLTF gene silencing: a novel determinant of sensitivity to autophagy inhibitionR01CA169134 · NCI · UNIVERSITY OF PENNSYLVANIA · PI AMARAVADI, RAVI K · 2013 to 2017
$1.7M
NCI NIH HHS P01 CA114046NCI NIH HHS P30 CA016520NCI NIH HHS P30 CA072720NCI NIH HHS P50 CA174523NCI NIH HHS R01 CA130893NCI NIH HHS R01 CA157490NCI NIH HHS R01 CA163591NCI NIH HHS R01 CA169134NCI NIH HHS R01 CA188048NCI NIH HHS R01 CA188096NCI NIH HHS R01 CA193970NCI NIH HHS R01 CA198015NIGMS NIH HHS R01 GM095567
6 · The paper itself

Abstract

Macroautophagy (referred to here as autophagy) is induced by starvation to capture and degrade intracellular proteins and organelles in lysosomes, which recycles intracellular components to sustain metabolism and survival. Autophagy also plays a major homeostatic role in controlling protein and organelle quality and quantity. Dysfunctional autophagy contributes to many diseases. In cancer, autophagy can be neutral, tumor-suppressive, or tumor-promoting in different contexts. Large-scale genomic analysis of human cancers indicates that the loss or mutation of core autophagy genes is uncommon, whereas oncogenic events that activate autophagy and lysosomal biogenesis have been identified. Autophagic flux, however, is difficult to measure in human tumor samples, making functional assessment of autophagy problematic in a clinical setting. Autophagy impacts cellular metabolism, the proteome, and organelle numbers and quality, which alter cell functions in diverse ways. Moreover, autophagy influences the interaction between the tumor and the host by promoting stress adaptation and suppressing activation of innate and adaptive immune responses. Additionally, autophagy can promote a cross-talk between the tumor and the stroma, which can support tumor growth, particularly in a nutrient-limited microenvironment. Thus, the role of autophagy in cancer is determined by nutrient availability, microenvironment stress, and the presence of an immune system. Here we discuss recent developments in the role of autophagy in cancer, in particular how autophagy can promote cancer through suppressing p53 and preventing energy crisis, cell death, senescence, and an anti-tumor immune response.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsAutophagyDisease Models, AnimalDrug Delivery SystemsHumansNeoplasmsATGautophagycancerchloroquinemouse models

Identifiers

PMID27664235
PMCPMC5066235
OpenAlexW2524192596

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.