Evidence map›Paper›PMID 36261830›Full record

ArticleBMC medical genomics2022

Turning up the heat on non-immunoreactive tumors: autophagy influences the immune microenvironment in pancreatic cancer.

Si-Yuan Lu, Jie Hua, Jiang Liu, Miao-Yan Wei, Chen Liang, Qing-Cai Meng, Bo Zhang, Xian Jun Yu, Wei Wang, Jin Xu

Open access · goldAbstract read
In one paragraph

Article in BMC medical genomics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.1field-weighted citation impact, top 52% 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

0 citing papers in PubMed, 1 citations in OpenAlex.

No citing paper in PubMed yet.

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

10 authors at 2 institutions in 1 country.

Si-Yuan Lu *Department of Pancreatic Surgery, Fudan University Shanghai Cancer Center, No. 270 Dong'An Road, 200032, Shanghai, China.
Jie Hua *Department of Pancreatic Surgery, Fudan University Shanghai Cancer Center, No. 270 Dong'An Road, 200032, Shanghai, China.
Jiang Liu *Department of Pancreatic Surgery, Fudan University Shanghai Cancer Center, No. 270 Dong'An Road, 200032, Shanghai, China.
Miao-Yan WeiDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, No. 270 Dong'An Road, 200032, Shanghai, China.
Chen LiangDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, No. 270 Dong'An Road, 200032, Shanghai, China.
Qing-Cai MengDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, No. 270 Dong'An Road, 200032, Shanghai, China.
Bo ZhangDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, No. 270 Dong'An Road, 200032, Shanghai, China.
Xian Jun YuDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, No. 270 Dong'An Road, 200032, Shanghai, China.
Wei WangDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, No. 270 Dong'An Road, 200032, Shanghai, China. wangwei@fudanpci.org.
Jin XuDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, No. 270 Dong'An Road, 200032, Shanghai, China. xujin@fudanpci.org.
Fudan University Shanghai Cancer Center · CNShanghai Medical College of Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAutophagy regulators play important roles in the occurrence and development of a variety of tumors and are involved in immune regulation and drug resistance. However, the modulatory roles and prognostic value of autophagy regulators in pancreatic cancer have not been identified.

methodsTranscriptomic data and survival information from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases were used to construct a risk score model. Important clinical features were analyzed to generate a nomogram. In addition, we used various algorithms, including ssGSEA, CIBERSORT, XCELL, EPIC, TIMER, and QUANTISEQ, to evaluate the roles of autophagy regulators in the pancreatic cancer immune microenvironment. Furthermore, the mutation landscape was compared between different risk groups.

resultsPan cancer analysis indicated that most of the autophagy regulators were upregulated in pancreatic cancer and were correlated with methylation and CNV level. MET, TSC1, and ITGA6 were identified as the prognostic autophagy regulators and used to construct a risk score model. Some critical clinical indicators, such as age, American Joint Committee on Cancer (AJCC) T stage, AJCC N stage, alcohol and sex, were combined with the risk model to establish the nomogram, which may offer clinical guidance. In addition, our study demonstrated that the low score groups exhibited high immune activity and high abundances of various immune cells, including T cells, B cells, and NK cells. Patients with high risk scores exhibited lower half inhibitory concentration (IC50) values for paclitaxel and had downregulated expression profiles of PD1, CTLA4, and LAG3. Mutation investigation indicated that the high risk groups exhibited a higher mutation burden and higher mutation number compared to the low risk groups. additionally, we verified our risk stratification method using cytology and histology data from our center, and the results are satisfactory.

conclusionWe speculated that autophagy regulators have large effects on the prognosis, immune landscape and drug sensitivity of pancreatic cancer. Our model, which combines critical autophagy regulators and clinical indicators, will provide guidance for clinical treatment.

Indexed as

Pancreatic NeoplasmsAutophagyCTLA-4 AntigenHumansPaclitaxelPrognosisTumor MicroenvironmentCTLA-4 AntigenPaclitaxelAutophagyBioinformatics analysisImmune microenvironmentPancreatic cancer

Identifiers

PMID36261830
PMCPMC9580150
OpenAlexW4306770016

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LicenceCC BY
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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.