Evidence map›Paper›PMID 29255248›Full record

ReviewOncogene2018

Dual role of autophagy in hallmarks of cancer.

Shikha Satendra Singh, Somya Vats, Amelia Yi-Qian Chia, Tuan Zea Tan, Shuo Deng, Mei Shan Ong, Frank Arfuso, Celestial T Yap, Boon Cher Goh, Gautam Sethi and 4 more

Abstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 330 papers.

0numbers the graph read from it
0cells of the map it votes in
330citing papers in PubMed
34.5field-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

330 citing papers in PubMed, 543 citations in OpenAlex.

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270 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

14 authors at 3 institutions in 3 countries.

Shikha Satendra SinghCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.
Somya VatsMolecular Biology and Genetics Unit, Jawaharlal Nehru Centre for Advanced Scientific Research, Bengaluru, Karnataka, India.
Amelia Yi-Qian ChiaDepartment of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
Tuan Zea TanCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.ORCID 0000-0001-6624-1593
Shuo DengDepartment of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
Mei Shan OngDepartment of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
Frank ArfusoStem Cell and Cancer Biology Laboratory, School of Biomedical Sciences, Curtin Health Innovation Research Institute, Curtin University, Perth, WA, Australia.
Celestial T YapDepartment of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
Boon Cher GohCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.
Gautam SethiDepartment of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
Ruby Yun-Ju HuangCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.
Han Ming ShenDepartment of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
Ravi ManjithayaMolecular Biology and Genetics Unit, Jawaharlal Nehru Centre for Advanced Scientific Research, Bengaluru, Karnataka, India. ravim@jncasr.ac.in.
Alan Prem KumarCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore. csiapk@nus.edu.sg.
National University of Singapore · SGJawaharlal Nehru Centre for Advanced Scientific Research · INCurtin University · AU

Funding

DBT-Wellcome Trust India Alliance 500159-Z-09-Z
6 · The paper itself

Abstract

Evolutionarily conserved across eukaryotic cells, macroautophagy (herein autophagy) is an intracellular catabolic degradative process targeting damaged and superfluous cellular proteins, organelles, and other cytoplasmic components. Mechanistically, it involves formation of double-membrane vesicles called autophagosomes that capture cytosolic cargo and deliver it to lysosomes, wherein the breakdown products are eventually recycled back to the cytoplasm. Dysregulation of autophagy often results in various disease manifestations, including neurodegeneration, microbial infections, and cancer. In the case of cancer, extensive attention has been devoted to understanding the paradoxical roles of autophagy in tumor suppression and tumor promotion. In this review, while we summarize how this self-eating process is implicated at various stages of tumorigenesis, most importantly, we address the link between autophagy and hallmarks of cancer. This would eventually provide a better understanding of tumor dependence on autophagy. We also discuss how therapeutics targeting autophagy can counter various transformations involved in tumorigenesis. Finally, this review will provide a novel insight into the mutational landscapes of autophagy-related genes in several human cancers, using genetic information collected from an array of cancers.

Indexed as

AutophagyAnimalsCell Transformation, NeoplasticHumansNeoplasms

Identifiers

PMID29255248
OpenAlexW2772927056

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.