Evidence map›Paper›PMID 32495519›Full record

Observational studyCancer science2020

Expression of classical human leukocyte antigen class I antigens, HLA-E and HLA-G, is adversely prognostic in pancreatic cancer patients.

Nobuyoshi Hiraoka, Yoshinori Ino, Shutaro Hori, Rie Yamazaki-Itoh, Chie Naito, Mari Shimasaki, Minoru Esaki, Satoshi Nara, Yoji Kishi, Kazuaki Shimada and 3 more

Open access · goldAbstract readObservational Study
In one paragraph

Observational study in Cancer science, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 4 pooled it
3.6field-weighted citation impact, top 6% 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

43 citing papers in PubMed, 4 syntheses or guidelines pooled it, 55 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

13 authors at 5 institutions in 1 country.

Nobuyoshi HiraokaDivision of Molecular Pathology, National Cancer Center Research Institute, Tokyo, Japan.ORCID https://orcid.org/0000-0003-4215-4385
Yoshinori InoDivision of Molecular Pathology, National Cancer Center Research Institute, Tokyo, Japan.
Shutaro HoriDivision of Molecular Pathology, National Cancer Center Research Institute, Tokyo, Japan.
Rie Yamazaki-ItohDivision of Molecular Pathology, National Cancer Center Research Institute, Tokyo, Japan.
Chie NaitoDivision of Molecular Pathology, National Cancer Center Research Institute, Tokyo, Japan.
Mari ShimasakiDivision of Molecular Pathology, National Cancer Center Research Institute, Tokyo, Japan.
Minoru EsakiHepato-Biliary and Pancreatic Surgery Division, National Cancer Center Hospital, Tokyo, Japan.
Satoshi NaraHepato-Biliary and Pancreatic Surgery Division, National Cancer Center Hospital, Tokyo, Japan.
Yoji KishiHepato-Biliary and Pancreatic Surgery Division, National Cancer Center Hospital, Tokyo, Japan.
Kazuaki ShimadaHepato-Biliary and Pancreatic Surgery Division, National Cancer Center Hospital, Tokyo, Japan.
Naoya NakamuraDepartment of Pathology, Tokai University School of Medicine, Isehara, Japan.
Toshihiko TorigoeDepartment of Pathology, Sapporo Medical University, Sapporo, Japan.
Yuji HeikeDivision of Biomedical Sciences, St. Luke's International University Graduate School of Public Health, Tokyo, Japan.
National Cancer Centre Japan · JPTokai University · JPSapporo Medical University · JPSt. Luke's International University · JPTokyo National Hospital · JP

Funding

a Grant-in-Aid for Scientific Research from the Ministry of Education, Culture, Sports, Science and Technology of Japan (NH)the Japan Agency for Medical Research and Development (NH)the National Cancer Center Research and Development Fund (NH and YH)
6 · The paper itself

Abstract

The expression of classical human leukocyte antigen class I antigens (HLA-I) on the surfaces of cancer cells allows cytotoxic T cells to recognize and eliminate these cells. Reduction or loss of HLA-I is a mechanism of escape from antitumor immunity. The present study aimed to investigate the clinicopathological impacts of HLA-I and non-classical HLA-I antigens expressed on pancreatic ductal adenocarcinoma (PDAC) cells. We performed immunohistochemistry to detect expression of HLA-I antigens in PDAC using 243 PDAC cases and examined their clinicopathological influences. We also investigated the expression of immune-related genes to characterize PDAC tumor microenvironments. Lower expression of HLA-I, found in 33% of PDAC cases, was significantly associated with longer overall survival. Higher expression of both HLA-E and HLA-G was significantly associated with shorter survival. Multivariate analyses revealed that higher expression of these three HLA-I antigens was significantly correlated with shorter survival. Higher HLA-I expression on PDAC cells was significantly correlated with higher expression of IFNG, which also correlated with PD1, PD-L1 and PD-L2 expression. In vitro assay revealed that interferon gamma (IFNγ) stimulation increased surface expression of HLA-I in three PDAC cell lines. It also upregulated surface expression of HLA-E, HLA-G and immune checkpoint molecules, including PD-L1 and PD-L2. These results suggest that the higher expression of HLA-I, HLA-E and HLA-G on PDAC cells is an unfavorable prognosticator. It is possible that IFNγ promotes a tolerant microenvironment by inducing immune checkpoint molecules in PDAC tissues with higher HLA-I expression on PDAC cells.

Indexed as

Tumor EscapeAgedB7-H1 AntigenCarcinoma, Pancreatic DuctalDisease-Free SurvivalFemaleGene Expression Regulation, NeoplasticHistocompatibility Antigens Class IHLA-E AntigensHLA-G AntigensHumansImmunohistochemistryInterferon-gammaKaplan-Meier EstimateMaleMiddle AgedB7-H1 AntigenCD274 protein, humanHistocompatibility Antigens Class IHLA-E AntigensHLA-G AntigensIFNG protein, humanInterferon-gammaPDCD1LG2 protein, humanPDCD1 protein, humanProgrammed Cell Death 1 Ligand 2 ProteinProgrammed Cell Death 1 ReceptorHLA class I antigensHLA-EHLA-GIFNγpancreatic cancer

Identifiers

PMID32495519
PMCPMC7419048
OpenAlexW3028991244

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.