Evidence map›Paper›PMID 38275386›Full record

ReviewBiomedicines2023

Cellular Senescence in Liver Cancer: How Dying Cells Become "Zombie" Enemies.

Aurora Gazzillo, Camilla Volponi, Cristiana Soldani, Michela Anna Polidoro, Barbara Franceschini, Ana Lleo, Eduardo Bonavita, Matteo Donadon

Open access · goldAbstract readReview
In one paragraph

Review in Biomedicines, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

11 citing papers in PubMed, 10 citations in OpenAlex.

  1. The dark side of apoptosis: how dying cells fuel tumor angiogenesis.Apoptosis : an international journal on programmed cell death · 2026
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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

8 authors at 3 institutions in 1 country.

Aurora GazzilloCellular and Molecular Oncoimmunology Laboratory, IRCCS Humanitas Research Hospital, 20089 Rozzano, Italy.
Camilla VolponiCellular and Molecular Oncoimmunology Laboratory, IRCCS Humanitas Research Hospital, 20089 Rozzano, Italy.
Cristiana SoldaniHepatobiliary Immunopathology Laboratory, IRCCS Humanitas Research Hospital, 20089 Rozzano, Italy.ORCID 0000-0001-5041-9588
Michela Anna PolidoroHepatobiliary Immunopathology Laboratory, IRCCS Humanitas Research Hospital, 20089 Rozzano, Italy.ORCID 0000-0002-9162-6855
Barbara FranceschiniHepatobiliary Immunopathology Laboratory, IRCCS Humanitas Research Hospital, 20089 Rozzano, Italy.ORCID 0000-0001-6348-248X
Ana LleoDepartment of Biomedical Sciences, Humanitas University, 20072 Pieve Emanuele, Italy.ORCID 0000-0002-0561-7902
Eduardo BonavitaCellular and Molecular Oncoimmunology Laboratory, IRCCS Humanitas Research Hospital, 20089 Rozzano, Italy.ORCID 0000-0003-2335-5827
Matteo DonadonHepatobiliary Immunopathology Laboratory, IRCCS Humanitas Research Hospital, 20089 Rozzano, Italy.ORCID 0000-0003-0296-7648
Humanitas University · ITIRCCS Humanitas Research Hospital · ITUniversità degli Studi del Piemonte Orientale “Amedeo Avogadro” · IT

Funding

AIRC AIRC start-up grant 25828Ricerca Finalizzata 2018 of the Italian Ministry of Health RF-2018-12367150
6 · The paper itself

Abstract

Liver cancer represents the fourth leading cause of cancer-associated death worldwide. The heterogeneity of its tumor microenvironment (TME) is a major contributing factor of metastasis, relapse, and drug resistance. Regrettably, late diagnosis makes most liver cancer patients ineligible for surgery, and the frequent failure of non-surgical therapeutic options orientates clinical research to the investigation of new drugs. In this context, cellular senescence has been recently shown to play a pivotal role in the progression of chronic inflammatory liver diseases, ultimately leading to cancer. Moreover, the stem-like state triggered by senescence has been associated with the emergence of drug-resistant, aggressive tumor clones. In recent years, an increasing number of studies have emerged to investigate senescence-associated hepatocarcinogenesis and its derived therapies, leading to promising results. In this review, we intend to provide an overview of the recent evidence that unveils the role of cellular senescence in the most frequent forms of primary and metastatic liver cancer, focusing on the involvement of this mechanism in therapy resistance.

Indexed as

cellular senescencecholangiocarcinoma (CCA)colorectal liver mestastases (CLM)hepatocellular carcinoma (HCC)liver cancersenescence-associated secretory phenotypetherapy resistance

Identifiers

PMID38275386
PMCPMC10813254
OpenAlexW4390058534

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.