Evidence map›Paper›PMID 36100320›Full record

ArticleJournal of advanced research2022

Cisplatin and gemcitabine exert opposite effects on immunotherapy with PD-1 antibody in K-ras-driven cancer.

Christophe Glorieux, Xiaojun Xia, Xin You, Zining Wang, Yi Han, Jing Yang, Gauthier Noppe, Christophe de Meester, Jianhua Ling, Annie Robert and 7 more

Open access · goldAbstract read
In one paragraph

Article in Journal of advanced research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.2field-weighted citation impact, top 9% 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

36 citing papers in PubMed, 45 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

17 authors at 6 institutions in 3 countries.

Christophe GlorieuxSun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou 510060, China.
Xiaojun XiaSun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou 510060, China.
Xin YouSun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou 510060, China.
Zining WangSun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou 510060, China.
Yi HanSun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou 510060, China.
Jing YangSun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou 510060, China.
Gauthier NoppeDepartment of Quality Control, MaSTherCell, Gosselies 6041, Belgium.
Christophe de MeesterPôle de Recherche Cardiovasculaire, Institut de Recherche Expérimentale et Clinique, Université catholique de Louvain, Brussels 1200, Belgium.
Jianhua LingDepartment of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston 77030, TX, USA.
Annie RobertPôle Epidémiologie et Biostatistique, Institut de Recherche Expérimentale et Clinique, Université catholique de Louvain, Brussels 1200, Belgium.
Hui ZhangSun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou 510060, China; Metabolic Innovation Center, Sun Yat-Sen University, Guangzhou 510060, China.
Sheng-Ping LiDepartment of Hepatobiliary and Pancreatic Surgery, Sun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou 510060, China.
Huamin WangDepartment of Pathology, The University of Texas MD Anderson Cancer Center, Houston 77030, TX, USA.
Paul J ChiaoDepartment of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston 77030, TX, USA.
Li ZhangDepartment of Medical Oncology, Sun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou 510060, China.
Xiaobing LiThe First Department of Thoracic Oncology, Hubei Cancer Hospital Affiliated to Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430079, China. Electronic address: lixiaobing0629@126.com.
Peng HuangSun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou 510060, China; Metabolic Innovation Center, Sun Yat-Sen University, Guangzhou 510060, China. Electronic address: huangpeng@sysucc.org.cn.
Sun Yat-sen University · CNSun Yat-sen University Cancer Center · CNThe University of Texas MD Anderson Cancer Center · USState Key Laboratory of Oncology in South ChinaUCLouvain · BEHuazhong University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionImmunochemotherapy using PD-1/PD-L1 antibodies in combination with chemotherapeutic agents has become a mainstream treatment for cancer patients, but it remains unclear which drug combinations would produce best therapeutic outcome.

objectivesThe purpose of this study was to investigate two common chemotherapeutic drugs, gemcitabine and cisplatin, for their impacts on the therapeutic efficacy of PD-1 antibody in K-ras-driven cancers known to overexpress PD-L1.

methodsBoth in vitro assays and syngeneic mouse tumor models were used in this study. Biochemical and molecular assays were used to determine the effects of drugs on T cell functions in cell culture models and in mouse/human tumor tissues. Allograft tumor models with K-ras mutation were used to investigate the combination effect of gemcitabine or cisplatin with immunotherapy. Data of lung cancer patients with K-ras mutation treated with cisplatin and toripalimab were analyzed to evaluate the clinical relevance of the lab findings.

resultsCisplatin and gemcitabine unexpectedly exert opposite effect on the therapeutic activity of PD-1 antibody in vivo. Gemcitabine antagonizes the therapeutic effect of PD-1 antibody due to its significant inhibition on CD8

conclusionsOur study shows that a key factor in selecting chemotherapeutic agents for immunochemotherapy is the drug's impact on T cell functions, and that cisplatin-based chemotherapy is an excellent choice for combination with immune checkpoint antibody to achieve favorable clinical outcome.

Indexed as

Antineoplastic AgentsLung NeoplasmsAnimalsB7-H1 AntigenCD8-Positive T-LymphocytesCell Line, TumorCisplatinDeoxycytidineGemcitabineHumansImmunologic FactorsImmunotherapyMiceProgrammed Cell Death 1 ReceptorProto-Oncogene Proteins p21(ras)Antineoplastic AgentsB7-H1 AntigenCisplatinDeoxycytidineGemcitabineHras protein, mouseImmunologic FactorsKRAS protein, humanProgrammed Cell Death 1 ReceptorProto-Oncogene Proteins p21(ras)CisplatinGemcitabineImmunochemotherapyK-rasPD-1/PD-L1

Identifiers

PMID36100320
PMCPMC9481954
OpenAlexW4200530769

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.