Evidence map›Paper›PMID 30071644›Full record

ReviewInternational journal of molecular sciences2018

Typical and Atypical Inducers of Lysosomal Cell Death: A Promising Anticancer Strategy.

Antoni Domagala, Klaudyna Fidyt, Malgorzata Bobrowicz, Joanna Stachura, Kacper Szczygiel, Malgorzata Firczuk

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed, 1 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

57 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  17. Phenazine Cations as Anticancer TheranosticsJournal of the American Chemical Society · 2024
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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

6 authors.

Antoni DomagalaDepartment of Immunology, Medical University of Warsaw, 02-097 Warsaw, Poland. antoni.domagala@wum.edu.pl.
Klaudyna FidytDepartment of Immunology, Medical University of Warsaw, 02-097 Warsaw, Poland. klaudyna.fidyt@wum.edu.pl.
Malgorzata BobrowiczDepartment of Immunology, Medical University of Warsaw, 02-097 Warsaw, Poland. malgorzata.bobrowicz@wum.edu.pl.
Joanna StachuraDepartment of Immunology, Medical University of Warsaw, 02-097 Warsaw, Poland. joanna.stachura@wum.edu.pl.
Kacper SzczygielDepartment of Immunology, Medical University of Warsaw, 02-097 Warsaw, Poland. kacper.jan.szczygiel@gmail.com.
Malgorzata FirczukDepartment of Immunology, Medical University of Warsaw, 02-097 Warsaw, Poland. mfirczuk@wum.edu.pl.ORCID 0000-0002-1719-5233

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lysosomes are conservative organelles with an indispensable role in cellular degradation and the recycling of macromolecules. However, in light of recent findings, it has emerged that the role of lysosomes in cancer cells extends far beyond cellular catabolism and includes a variety of cellular pathways, such as proliferation, metastatic potential, and drug resistance. It has been well described that malignant transformation leads to alterations in lysosomal structure and function, which, paradoxically, renders cancer cells more sensitive to lysosomal destabilization. Furthermore, lysosomes are implicated in the regulation and execution of cell death in response to diverse stimuli and it has been shown that lysosome-dependent cell death can be utilized to overcome apoptosis and drug resistance. Thus, the purpose of this review is to characterize the role of lysosome in cancer therapy and to describe how these organelles impact treatment resistance. We summarized the characteristics of typical inducers of lysosomal cell death, which exert its function primarily via alterations in the lysosomal compartment. The review also presents other anticancer agents with the predominant mechanism of action different from lysosomal destabilization, the activity of which is influenced by lysosomal signaling, including classical chemotherapeutics, kinase inhibitors, monoclonal antibodies, as well as photodynamic therapy.

Indexed as

AnimalsAntineoplastic AgentsCell DeathHumansLysosomesNeoplasmsPhotochemotherapyAntineoplastic Agentsapoptosisautophagydrug resistancelysosomal membrane permeabilizationlysosomeslysosomotropic agents

Identifiers

PMID30071644
PMCPMC6121368

What OpenQuestion holds

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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.