KRAS-driven protein disulfide isomerase family A member 6 expression suppresses PRKR-like endoplasmic reticulum kinase-mediated immunogenic cell death to desensitise pancreatic ductal adenocarcinoma to immune checkpoint blockers.
Article in Gut, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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0cells of the map it votes in
1citing 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.
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
19 authors.
Ronglin Wang *Department of Oncology Tangdu Hospital, the State Key Laboratory of Holistic Integrative Management of Gastrointestinal Cancers, Fourth Military Medical University, Xi'an, Shaanxi, China.ORCID http://orcid.org/0009-0006-4475-5749
Junqiang Li *Department of Oncology Tangdu Hospital, the State Key Laboratory of Holistic Integrative Management of Gastrointestinal Cancers, Fourth Military Medical University, Xi'an, Shaanxi, China.ORCID http://orcid.org/0000-0002-2786-1252
Danjie Su *Department of Obstetrics and Gynecology, Tangdu Hospital, Fourth Military Medical University, Xi'an, Shaanxi, China.ORCID http://orcid.org/0000-0003-0439-7722
Jing Yang *Department of Oncology Tangdu Hospital, the State Key Laboratory of Holistic Integrative Management of Gastrointestinal Cancers, Fourth Military Medical University, Xi'an, Shaanxi, China.ORCID http://orcid.org/0009-0005-0174-4372
Peixiang MaDepartment of Oncology, Second Medical Center, Chinese People's Liberation Army (PLA) General Hospital, Beijing, China.ORCID http://orcid.org/0009-0006-9644-7262
Jing LuoDepartment of Oncology Tangdu Hospital, the State Key Laboratory of Holistic Integrative Management of Gastrointestinal Cancers, Fourth Military Medical University, Xi'an, Shaanxi, China.ORCID http://orcid.org/0000-0003-4509-1770
Jingyi LiuDepartment of Oncology Tangdu Hospital, the State Key Laboratory of Holistic Integrative Management of Gastrointestinal Cancers, Fourth Military Medical University, Xi'an, Shaanxi, China.ORCID http://orcid.org/0009-0000-8018-9808
Rui YangDepartment of Oncology Tangdu Hospital, the State Key Laboratory of Holistic Integrative Management of Gastrointestinal Cancers, Fourth Military Medical University, Xi'an, Shaanxi, China.ORCID http://orcid.org/0009-0009-7944-0335
Liang ZhangDepartment of Oncology Tangdu Hospital, the State Key Laboratory of Holistic Integrative Management of Gastrointestinal Cancers, Fourth Military Medical University, Xi'an, Shaanxi, China.ORCID http://orcid.org/0009-0002-1023-3724
Xiangjing ShenDepartment of Oncology Tangdu Hospital, the State Key Laboratory of Holistic Integrative Management of Gastrointestinal Cancers, Fourth Military Medical University, Xi'an, Shaanxi, China.ORCID http://orcid.org/0009-0008-5235-4114
Hongrui WangDepartment of Oncology Tangdu Hospital, the State Key Laboratory of Holistic Integrative Management of Gastrointestinal Cancers, Fourth Military Medical University, Xi'an, Shaanxi, China.ORCID http://orcid.org/0009-0005-1604-8302
Hong LiDepartment of Oncology Tangdu Hospital, the State Key Laboratory of Holistic Integrative Management of Gastrointestinal Cancers, Fourth Military Medical University, Xi'an, Shaanxi, China.ORCID http://orcid.org/0000-0003-3606-2070
Ting ZhaoDepartment of Oncology Tangdu Hospital, the State Key Laboratory of Holistic Integrative Management of Gastrointestinal Cancers, Fourth Military Medical University, Xi'an, Shaanxi, China.ORCID http://orcid.org/0009-0007-7192-1121
Jie MinDepartment of Oncology Tangdu Hospital, the State Key Laboratory of Holistic Integrative Management of Gastrointestinal Cancers, Fourth Military Medical University, Xi'an, Shaanxi, China.ORCID http://orcid.org/0009-0000-9169-5466
Lili LiuDepartment of Oncology Tangdu Hospital, the State Key Laboratory of Holistic Integrative Management of Gastrointestinal Cancers, Fourth Military Medical University, Xi'an, Shaanxi, China.ORCID http://orcid.org/0000-0002-6035-3583
Chenggong LiaoDepartment of Oncology Tangdu Hospital, the State Key Laboratory of Holistic Integrative Management of Gastrointestinal Cancers, Fourth Military Medical University, Xi'an, Shaanxi, China.ORCID http://orcid.org/0000-0002-7624-0196
Yang SongDepartment of Oncology Tangdu Hospital, the State Key Laboratory of Holistic Integrative Management of Gastrointestinal Cancers, Fourth Military Medical University, Xi'an, Shaanxi, China suhc@fmmu.edu.cn songyang212212@163.com.ORCID http://orcid.org/0000-0002-9673-5399
Haichuan SuDepartment of Oncology Tangdu Hospital, the State Key Laboratory of Holistic Integrative Management of Gastrointestinal Cancers, Fourth Military Medical University, Xi'an, Shaanxi, China suhc@fmmu.edu.cn songyang212212@163.com.ORCID http://orcid.org/0000-0002-3316-9959
Funding
No grant is acknowledged in the PubMed record.
6 · The paper itself
Abstract
backgroundPancreatic ductal adenocarcinoma (PDAC) is characterised by a dismal prognosis and insensitivity to immune checkpoint blockers (ICBs); however, the underlying mechanism remains elusive.
objectiveThis study aimed to identify tumour cell-intrinsic regulators that promote immune evasion and ICB resistance in PDAC.
designMulti-omics analysis and clinical cohort studies identified protein disulfide isomerase family A member 6 (PDIA6) as a regulator of the immune microenvironment. Flow cytometry, multiplex immunohistochemistry, electron microscopy and Glutathione S-Transferase (GST) pulldown assays confirmed that PDIA6 repressed PRKR-like endoplasmic reticulum kinase (PERK) activation and immunogenic cell death (ICD). Chromatin immunoprecipitation confirmed that KRAS
resultsMulti-omics screening identified PDIA6 as a biomarker of CD8
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.
KRAS-driven protein disulfide isomerase family A member 6 expression suppresses PRKR-like endoplasmic reticulum kinase-mediated immunogenic cell death to desensitise pancreatic ductal adenocarcinoma to immune checkpoint blockers. · full record | Socratic