Evidence map›Paper›PMID 37797616›Full record

ArticleCell reports. Medicine2023

Glutathione dynamics is a potential predictive and therapeutic trait for neoadjuvant chemotherapy response in bladder cancer.

YongHwan Kim, Hyein Ju, Seung-Yeon Yoo, Jinahn Jeong, Jinbeom Heo, Seungun Lee, Ja-Min Park, Sun Young Yoon, Se Un Jeong, Jinyoung Lee and 16 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports. Medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
6.4field-weighted citation impact, top 3% 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

12 citing papers in PubMed, 20 citations in OpenAlex.

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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

26 authors at 4 institutions in 1 country.

YongHwan KimDepartment of Cell and Genetic Engineering, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Korea.
Hyein JuDepartment of Cell and Genetic Engineering, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Korea.
Seung-Yeon YooPathology Center, Seegene Medical Foundation, Seoul 04805, Korea.
Jinahn JeongDepartment of Pathology, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Korea.
Jinbeom HeoDepartment of Cell and Genetic Engineering, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Korea.
Seungun LeeDepartment of Cell and Genetic Engineering, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Korea.
Ja-Min ParkDepartment of Pathology, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Korea.
Sun Young YoonDepartment of Pathology, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Korea.
Se Un JeongDepartment of Pathology, Ewha Womans University College of Medicine, Ewha Womans University Mokdong Hospital, Seoul 07985, Korea.
Jinyoung LeeDepartment of Biochemistry and Molecular Biology, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Korea.
HongDuck YunDepartment of Cell and Genetic Engineering, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Korea.
Chae-Min RyuCenter for Cell Therapy, Asan Medical Center, Seoul 05505, Korea.
Jinah LeeDepartment of Cell and Genetic Engineering, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Korea.
Yun Ji NamDepartment of Cell and Genetic Engineering, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Korea.
Hyungu KwonDepartment of Cell and Genetic Engineering, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Korea.
Jaekyoung SonDepartment of Biochemistry and Molecular Biology, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Korea.
Gowun JeongAI Recommendation, T3K, SK Telecom, Seoul 04539, Korea.
Ji-Hye OhDepartment of Pathology, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Korea.
Chang Ohk SungDepartment of Pathology, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Korea.
Eui Man JeongCollege of Pharmacy, Jeju National University, Jeju 63243, Korea.
Jaehoon AnDepartment of Public Health Sciences, Seoul National University, Seoul 08826, Korea; RexSoft, Inc., Seoul 08826, Korea.
Sungho WonDepartment of Public Health Sciences, Seoul National University, Seoul 08826, Korea; RexSoft, Inc., Seoul 08826, Korea.
Bumsik HongDepartment of Urology, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Korea.
Jae Lyun LeeDepartment of Oncology, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Korea. Electronic address: jaelyun@amc.seoul.kr.
Yong Mee ChoDepartment of Pathology, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Korea. Electronic address: yongcho@amc.seoul.kr.
Dong-Myung ShinDepartment of Cell and Genetic Engineering, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Korea. Electronic address: d0shin03@amc.seoul.kr.
Ulsan College · KRAsan Medical Center · KREwha Womans University · KRSeoul National University · KR

Funding

NCIRD CDC HHS U01 IP000035NCIRD CDC HHS U38 IP000870
6 · The paper itself

Abstract

Radical cystectomy with preoperative cisplatin-based neoadjuvant chemotherapy (NAC) is the standard care for muscle-invasive bladder cancers (MIBCs). However, the complete response rate to this modality remains relatively low, and current clinicopathologic and molecular classifications are inadequate to predict NAC response in patients with MIBC. Here, we demonstrate that dysregulation of the glutathione (GSH) pathway is fundamental for MIBC NAC resistance. Comprehensive analysis of the multicohort transcriptomes reveals that GSH metabolism and immune-response genes are enriched in NAC-resistant and NAC-sensitive MIBCs, respectively. A machine-learning-based tumor/stroma classifier is applied for high-throughput digitalized immunohistochemistry analysis, finding that GSH dynamics proteins, including glutaminase-1, are associated with NAC resistance. GSH dynamics is activated in cisplatin-resistant MIBC cells, and combination treatment with a GSH dynamics modulator and cisplatin significantly suppresses tumor growth in an orthotopic xenograft animal model. Collectively, these findings demonstrate the predictive and therapeutic values of GSH dynamics in determining the NAC response in MIBCs.

Indexed as

CisplatinUrinary Bladder NeoplasmsAnimalsGlutathioneHumansNeoadjuvant TherapyPhenotypeCisplatinGlutathionebladder cancercombination therapydigital pathologyglutaminase-1glutathioneneoadjuvant chemotherapy

Identifiers

PMID37797616
PMCPMC10591055
OpenAlexW4387343417

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.