Evidence map›Paper›PMID 33718382›Full record

ReviewFrontiers in cell and developmental biology2021

Lysosomes and Cancer Progression: A Malignant Liaison.

Eda R Machado, Ida Annunziata, Diantha van de Vlekkert, Gerard C Grosveld, Alessandra d'Azzo

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cell and developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
11.6field-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

56 citing papers in PubMed, 100 citations in OpenAlex.

  1. The role of lysosome-dependent cell death in cancer.Apoptosis : an international journal on programmed cell death · 2026
    Review
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  12. Possible Roles for Purinergic Receptor P2RX4 in Breast and Prostate Cancers.International journal of molecular sciences · 2025
    Review
  13. Article
  14. Article
  15. Article
  16. Activation of lysophagy by a TBK1-SCFNature communications · 2025
    Article
  17. Review
  18. Article
  19. Article
  20. The IPBiochimica et biophysica acta. Molecular basis of disease · 2025
    Article
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

5 authors at 2 institutions in 1 country.

Eda R MachadoDepartment of Genetics, St. Jude Children's Research Hospital, Memphis, TN, United States.
Ida AnnunziataDepartment of Genetics, St. Jude Children's Research Hospital, Memphis, TN, United States.
Diantha van de VlekkertDepartment of Genetics, St. Jude Children's Research Hospital, Memphis, TN, United States.
Gerard C GrosveldDepartment of Genetics, St. Jude Children's Research Hospital, Memphis, TN, United States.
Alessandra d'AzzoDepartment of Genetics, St. Jude Children's Research Hospital, Memphis, TN, United States.
St. Jude Children's Research Hospital · USUniversity of Tennessee Health Science Center · US

Funding

Viral Vector Technology (VVTSR)P30CA021765 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI CHARLES ROBERTS · 1985 to 2026
$166.9M
Excessive Lysosomal Exocytosis Triggers Pathogenic Mechanisms in Sialidosis MiceR01GM104981 · NIGMS · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI D'AZZO, ALESSANDRA · 2013 to 2017
$1.4M
NCI NIH HHS P30 CA021765NIGMS NIH HHS R01 GM104981
6 · The paper itself

Abstract

During primary tumorigenesis isolated cancer cells may undergo genetic or epigenetic changes that render them responsive to additional intrinsic or extrinsic cues, so that they enter a transitional state and eventually acquire an aggressive, metastatic phenotype. Among these changes is the alteration of the cell metabolic/catabolic machinery that creates the most permissive conditions for invasion, dissemination, and survival. The lysosomal system has emerged as a crucial player in this malignant transformation, making this system a potential therapeutic target in cancer. By virtue of their ubiquitous distribution in mammalian cells, their multifaced activities that control catabolic and anabolic processes, and their interplay with other organelles and the plasma membrane (PM), lysosomes function as platforms for inter- and intracellular communication. This is due to their capacity to adapt and sense nutrient availability, to spatially segregate specific functions depending on their position, to fuse with other compartments and with the PM, and to engage in membrane contact sites (MCS) with other organelles. Here we review the latest advances in our understanding of the role of the lysosomal system in cancer progression. We focus on how changes in lysosomal nutrient sensing, as well as lysosomal positioning, exocytosis, and fusion perturb the communication between tumor cells themselves and between tumor cells and their microenvironment. Finally, we describe the potential impact of MCS between lysosomes and other organelles in propelling cancer growth and spread.

Indexed as

cancer progressionlysosomal exocytosislysosomal membrane contact siteslysosome movementlysosome positioning

Identifiers

PMID33718382
PMCPMC7952443
OpenAlexW3134915483

What OpenQuestion 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 OpenQuestion graph.