Evidence map›Paper›PMID 36471481›Full record

ArticleClinical and translational medicine2022

The dual role of CD70 in B-cell lymphomagenesis.

Man Nie, Weicheng Ren, Xiaofei Ye, Mattias Berglund, Xianhuo Wang, Karin Fjordén, Likun Du, Yvonne Giannoula, Dexin Lei, Wenjia Su and 16 more

Abstract read
In one paragraph

Article in Clinical and translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed.

  1. Article
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  4. Development and Preclinical Evaluation of [Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2025
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  15. The dual role of CD70 in B-cell lymphomagenesis.Clinical and translational medicine · 2022
    Article
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

26 authors.

Man NieDepartment of Medical Oncology, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, China.ORCID 0000-0001-6109-9268
Weicheng RenDepartment of Biosciences and Nutrition, Karolinska Institutet, Stockholm, Sweden.
Xiaofei YeDepartment of Biosciences and Nutrition, Karolinska Institutet, Stockholm, Sweden.
Mattias BerglundDepartment of Biosciences and Nutrition, Karolinska Institutet, Stockholm, Sweden.
Xianhuo WangDepartment of Lymphoma, National Clinical Research Center of Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin Medical University Cancer Institute and Hospital, Tianjin, China.ORCID 0000-0002-7663-2923
Karin FjordénDepartment of Oncology, Skåne University Hospital, Lund, Sweden.
Likun DuDepartment of Biosciences and Nutrition, Karolinska Institutet, Stockholm, Sweden.
Yvonne GiannoulaDepartment of Biosciences and Nutrition, Karolinska Institutet, Stockholm, Sweden.
Dexin LeiDepartment of Medical Oncology, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, China.
Wenjia SuDepartment of Biosciences and Nutrition, Karolinska Institutet, Stockholm, Sweden.
Wei LiDepartment of Lymphoma, National Clinical Research Center of Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin Medical University Cancer Institute and Hospital, Tianjin, China.
Dongbing LiuBGI-Shenzhen, Shenzhen, China.
Johan LinderothDepartment of Oncology, Skåne University Hospital, Lund, Sweden.
Chengyi JiangDepartment of Hematology, Jilin Cancer Hospital, Changchun, China.
Huijing BaoDepartment of Hematology, Jilin Cancer Hospital, Changchun, China.
Wenqi JiangDepartment of Medical Oncology, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, China.
Huiqiang HuangDepartment of Medical Oncology, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, China.
Yong HouBGI-Shenzhen, Shenzhen, China.
Shida ZhuBGI-Shenzhen, Shenzhen, China.
Gunilla EnbladDepartment of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden.
Mats JerkemanDepartment of Oncology, Skåne University Hospital, Lund, Sweden.
Kui WuBGI-Shenzhen, Shenzhen, China.
Huilai ZhangDepartment of Lymphoma, National Clinical Research Center of Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin Medical University Cancer Institute and Hospital, Tianjin, China.
Rose-Marie AminiDepartment of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden.
Zhi-Ming LiDepartment of Medical Oncology, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, China.
Qiang Pan-HammarströmDepartment of Biosciences and Nutrition, Karolinska Institutet, Stockholm, Sweden.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCD70 is a costimulatory molecule that is transiently expressed on a small set of activated lymphocytes and is involved in T-cell-mediated immunity. However, the role of CD70 in B-cell malignancies remains controversial.

methodsWe investigated the clinical relevance of CD70 genetic alterations and its protein expression in two diffuse large B-cell lymphoma (DLBCL) cohorts with different ethnic backgrounds. We also performed transcriptomic analysis to explore the role of CD70 alterations in tumour microenvironment. We further tested the blockade of CD70 in combination with PD-L1 inhibitor in a murine lymphoma model.

resultsWe showed that CD70 genetic aberrations occurred more frequently in the Chinese DLBCL cohort (56/233, 24.0%) than in the Swedish cohort (9/84, 10.8%), especially in those with concomitant hepatitis B virus (HBV) infection. The CD70 genetic changes in DLBCL resulted in a reduction/loss of protein expression and/or CD27 binding, which might impair T cell priming and were independently associated with poor overall survival. Paradoxically, we observed that over-expression of CD70 protein was also associated with a poor treatment response, as well as an advanced disease stage and EBV infection. More exhausted CD8

conclusionsOur findings suggest that CD70 can play a role in either tumour suppression or oncogenesis in DLBCL, likely via distinct immune evasion mechanisms, that is, impairing T cell priming or inducing T cell exhaustion. Characterisation of specific dysfunction of CD70 in DLBCL may thus provide opportunities for the development of novel targeted immuno-therapeutic strategies.

Indexed as

CD27 LigandEpstein-Barr Virus InfectionsLymphoma, Large B-Cell, DiffuseAnimalsB-LymphocytesCD8-Positive T-LymphocytesHumansMiceTumor MicroenvironmentCD27 LigandCD70 protein, humanCD70diffuse large B-cell lymphomagenetic aberrationHBV infectionimmune evasion

Identifiers

PMID36471481
PMCPMC9722974

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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.