Evidence map›Paper›PMID 38565900›Full record

ArticleExperimental & molecular medicine2024

Entosis: the core mechanism and crosstalk with other cell death programs.

Sunghoon Kim, Donghyuk Lee, Sung Eun Kim, Michael Overholtzer

Abstract read
In one paragraph

Article in Experimental & molecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

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

  1. Pooled it
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  9. Role of oxeiptosis in disease mechanisms and therapeutic opportunities.Apoptosis : an international journal on programmed cell death · 2025
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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

4 authors.

Sunghoon Kim *Department of Biosystems and Biomedical Sciences, College of Health Sciences, Korea University, Seoul, Republic of Korea.
Donghyuk Lee *Department of Pharmacology and Brain Korea 21 Project for Medical Science, Yonsei University College of Medicine, Seoul, Republic of Korea.
Sung Eun KimDepartment of Biosystems and Biomedical Sciences, College of Health Sciences, Korea University, Seoul, Republic of Korea. sek19@korea.ac.kr.ORCID http://orcid.org/0000-0002-4281-5625
Michael OverholtzerCell Biology Program, Sloan Kettering Institute for Cancer Research, New York, NY, USA. overhom1@mskcc.org.

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI SELWYN M VICKERS · 1985 to 2026
$347.4M
Regulated cell death and responses to starvation in cancerR35CA263846 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI Michael H. Overholtzer · 2022 to 2026
$4.5M
NCI NIH HHS P30 CA008748NCI NIH HHS R35 CA263846
6 · The paper itself

Abstract

Cell death pathways play critical roles in organism development and homeostasis as well as in the pathogenesis of various diseases. While studies over the last decade have elucidated numerous different forms of cell death that can eliminate cells in various contexts, how certain mechanisms impact physiology is still not well understood. Moreover, recent studies have shown that multiple forms cell death can occur in a cell population, with different forms of death eliminating individual cells. Here, we aim to describe the known molecular mechanisms of entosis, a non-apoptotic cell engulfment process, and discuss signaling mechanisms that control its induction as well as its possible crosstalk with other cell death mechanisms.

Indexed as

Cell DeathEntosisSignal TransductionAnimalsApoptosisHumans

Identifiers

PMID38565900
PMCPMC11059358

What Socratic 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 Socratic graph.