Evidence map›Paper›PMID 39415848›Full record

ReviewMedComm2024

Inducing disulfidptosis in tumors:potential pathways and significance.

Tao Mi, Xiangpan Kong, Meiling Chen, Peng Guo, Dawei He

Abstract readReview
In one paragraph

Review in MedComm, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
–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

27 citing papers in PubMed.

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  17. Metabolic Regulation of Ferroptosis in Breast Cancer.International journal of molecular sciences · 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

5 authors.

Tao MiDepartment of Urology Children's Hospital of Chongqing Medical University National Clinical Research Center for Child Health and Disorders Ministry of Education Key Laboratory of Child Development and Disorders Chongqing P.R. China.
Xiangpan KongDepartment of Urology Children's Hospital of Chongqing Medical University National Clinical Research Center for Child Health and Disorders Ministry of Education Key Laboratory of Child Development and Disorders Chongqing P.R. China.
Meiling ChenDepartment of Urology Children's Hospital of Chongqing Medical University National Clinical Research Center for Child Health and Disorders Ministry of Education Key Laboratory of Child Development and Disorders Chongqing P.R. China.
Peng GuoDepartment of Urology Children's Hospital of Chongqing Medical University National Clinical Research Center for Child Health and Disorders Ministry of Education Key Laboratory of Child Development and Disorders Chongqing P.R. China.
Dawei HeDepartment of Urology Children's Hospital of Chongqing Medical University National Clinical Research Center for Child Health and Disorders Ministry of Education Key Laboratory of Child Development and Disorders Chongqing P.R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Regulated cell death (RCD) is crucial for the elimination of abnormal cells. In recent years, strategies aimed at inducing RCD, particularly apoptosis, have become increasingly important in cancer therapy. However, the ability of tumor cells to evade apoptosis has led to treatment resistance and relapse, prompting extensive research into alternative death processes in cancer cells. A recent study identified a novel form of RCD known as disulfidptosis, which is linked to disulfide stress. Cancer cells import cystine from the extracellular environment via solute carrier family 7 member 11 (SLC7A11) and convert it to cysteine using nicotinamide adenine dinucleotide phosphate (NADPH). When NADPH is deficient or its utilization is impaired, cystine accumulates, leading to the formation of disulfide bonds in the actin cytoskeleton, triggering disulfidptosis. Disulfidptosis reveals a metabolic vulnerability in tumors, offering new insights into cancer therapy strategies. This review provides a detailed overview of the mechanisms underlying disulfidptosis, the current research progress, and limitations. It also highlights innovative strategies for inducing disulfidptosis and explores the potential of combining these approaches with traditional cancer therapies, particularly immunotherapy, to expedite clinical translation.

Indexed as

cystinedisulfidptosisNADPHSLC7A11tumor immunity

Identifiers

PMID39415848
PMCPMC11480524

What OpenQuestion holds

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Registered trials

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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.