Evidence map›Paper›PMID 35365585›Full record

ArticleJournal for immunotherapy of cancer2022

Genetic characteristics involving the PD-1/PD-L1/L2 and CD73/A2aR axes and the immunosuppressive microenvironment in DLBCL.

Tingting Zhang, Hengqi Liu, Lei Jiao, Zhenzhen Zhang, Jin He, Lanfang Li, Lihua Qiu, Zhengzi Qian, Shiyong Zhou, Wenchen Gong and 4 more

Open access · goldAbstract read
In one paragraph

Article in Journal for immunotherapy of cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 2 pooled it
5.8field-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

42 citing papers in PubMed, 2 syntheses or guidelines pooled it, 59 citations in OpenAlex.

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  14. Topological importance of CD8Annals of hematology · 2025
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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

14 authors at 1 institution in 1 country.

Tingting Zhang *Department of Lymphoma, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center of Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin's Clinical Research Center for Cancer, the Sino-US Center for Lymphoma and Leukemia Research, Tianjin, China.
Hengqi Liu *Department of Lymphoma, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center of Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin's Clinical Research Center for Cancer, the Sino-US Center for Lymphoma and Leukemia Research, Tianjin, China.
Lei JiaoPanovue Biological Technology Co., Ltd, Beijing, China.
Zhenzhen ZhangMarvel Medical Laboratory, Tianjin Marvelbio Technology Co., Ltd, Tianjin, China.
Jin HeDepartment of Lymphoma, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center of Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin's Clinical Research Center for Cancer, the Sino-US Center for Lymphoma and Leukemia Research, Tianjin, China.
Lanfang LiDepartment of Lymphoma, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center of Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin's Clinical Research Center for Cancer, the Sino-US Center for Lymphoma and Leukemia Research, Tianjin, China.
Lihua QiuDepartment of Lymphoma, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center of Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin's Clinical Research Center for Cancer, the Sino-US Center for Lymphoma and Leukemia Research, Tianjin, China.
Zhengzi QianDepartment of Lymphoma, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center of Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin's Clinical Research Center for Cancer, the Sino-US Center for Lymphoma and Leukemia Research, Tianjin, China.
Shiyong ZhouDepartment of Lymphoma, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center of Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin's Clinical Research Center for Cancer, the Sino-US Center for Lymphoma and Leukemia Research, Tianjin, China.
Wenchen GongDepartment of Pathology, Tianjin Medical University Cancer Institute and Hospital, Tianjin, China.
Bin MengDepartment of Pathology, Tianjin Medical University Cancer Institute and Hospital, Tianjin, China.
Xiubao RenDepartment of Immunology/Biotherapy, Tianjin Medical University Cancer Institute and Hospital, Tianjin, China.
Huilai ZhangDepartment of Lymphoma, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center of Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin's Clinical Research Center for Cancer, the Sino-US Center for Lymphoma and Leukemia Research, Tianjin, China tjzlyy_xianhuow@163.com zhlwgq@126.com.
Xianhuo WangDepartment of Lymphoma, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center of Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin's Clinical Research Center for Cancer, the Sino-US Center for Lymphoma and Leukemia Research, Tianjin, China tjzlyy_xianhuow@163.com zhlwgq@126.com.ORCID 0000-0002-7663-2923
Tianjin Medical University Cancer Institute and Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTargeting the PD-1/PD-L1/L2 (programmed cell death protein 1/programmed cell death ligand 1/ligand 2) pathway combined with other immunosuppressive signalings, such as CD73/A2aR (A2a adenosine receptor) adenosine signaling, has emerged as a promising strategy for cancer treatment. The genetic characteristics of these immune checkpoints need to be further investigated in diffuse large B-cell lymphoma (DLBCL).

methodsWe performed whole-exome sequencing/targeted deep sequencing to investigate the genetic characteristics of PD-1/PD-L1/L2 and CD73/A2aR. The immunosuppressive effect of these two pathways on the tumor microenvironment was evaluated via RNA sequencing. Single-cell RNA sequencing was further applied to investigate the dysfunctional CD8+ T cells. In addition, multiplex immunofluorescence staining was used to quantitatively assess the expression of dysfunctional CD8

resultsSP140 was identified as a novel translocation partner for PD-L1, and a new inversion was detected between PD-L1 and PD-L2, both leading to the upregulation of PD-L1 expression. CD73 genetic mutations did not increase mRNA and protein expression. Patients with genetically altered CD73 tended to have a better overall survival than patients with wild-type CD73. Both PD-1/PD-L1 and CD73/A2aR signaling mediated the immunosuppressive microenvironment in DLBCL. The numbers of CD8

conclusionsThis study describes the additional genetic basis of PD-L1 overexpression and characterizes certain genetic alterations of CD73/A2aR in DLBCL. The degree of T-cell dysfunction is correlated with clinical outcomes. Strategies that reverse T-cell dysfunction by inhibiting PD-1/PD-L1/L2, particularly in combination with CD73/A2aR, may show potential as effective therapeutic options for DLBCL.

Indexed as

Lymphoma, Large B-Cell, DiffuseProgrammed Cell Death 1 ReceptorB7-H1 AntigenCD8-Positive T-LymphocytesHumansTumor MicroenvironmentB7-H1 AntigenProgrammed Cell Death 1 ReceptorHematologic NeoplasmsProgrammed Cell Death 1 ReceptorTumor Microenvironment

Identifiers

PMID35365585
PMCPMC8977791
OpenAlexW4220821267

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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.