Evidence map›Paper›PMID 18271928›Full record

ArticleCancer science2008

Expression of CCL17 and CCL22 by latent membrane protein 1-positive tumor cells in age-related Epstein-Barr virus-associated B-cell lymphoproliferative disorder.

Sumio Takegawa, Zhe Jin, Takashi Nakayama, Takashi Oyama, Kunio Hieshima, Daisuke Nagakubo, Aiko-Konno Shirakawa, Toyonori Tsuzuki, Shigeo Nakamura, Osamu Yoshie

Abstract read
In one paragraph

Article in Cancer science, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing 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

28 citing papers in PubMed.

  1. Article
  2. Review
  3. Aflatoxin B1 and Epstein-Barr virus-induced CCL22 expression stimulates B cell infection.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  4. Article
  5. Article
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  9. Article
  10. Review
  11. Review
  12. Article
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  17. Review
  18. Article
  19. Higher circulating levels of chemokine CCL22 in patients with breast cancer: evaluation of the influences of tumor stage and chemokine gene polymorphism.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Article
  20. 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

10 authors.

Sumio TakegawaDepartment of Microbiology, Kinki University School of Medicine, Osaka-Sayama, 589-8511, Japan.
Zhe Jin
Takashi Nakayama
Takashi Oyama
Kunio Hieshima
Daisuke Nagakubo
Aiko-Konno Shirakawa
Toyonori Tsuzuki
Shigeo Nakamura
Osamu Yoshie

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Age-related Epstein-Barr virus-positive (EBV(+)) B-cell lymphoproliferative disorder (ALPD) is a disease entity identified from a large-scale re-survey of cases diagnosed as diffuse large B-cell lymphoma. ALPD is a group of EBV(+) polymorphic B-cell lymphoma typically seen in elderly patients. An age-associated decline in host immunity against EBV might be partly responsible for the pathogenesis of ALPD. Histologically, ALPD is often characterized by a minor proportion of EBV-encoded RNA-positive tumor cells in a background of extensive cellular infiltration, similar to that of classical Hodgkin's lymphoma. In contrast to Hodgkin and Reed-Sternberg cells, ALPD tumor cells are clearly positive for B cell markers CD20 and/or CD79a. Hodgkin and Reed-Sternberg cells produce various chemokines, including CCL17 and CCL22, that attract chemokine receptor CCR4-expressing Th2 cells and regulatory T cells. Previously, we have shown that EBV-immortalized B cells also produce CCL17 and CCL22 through latent membrane protein 1 (LMP1)-mediated activation of nuclear factor kappaB. Here we examined expression of CCL17 and CCL22 in ALPD. ALPD tumor cells were often heterogeneous in size in accordance with the differential expression of EBV latent genes at the single cell level. LMP1-expressing tumor cells were typically large in size and selectively positive for CCL17 and CCL22. CCR4(+) cells and forkhead box protein 3(+) regulatory T cells were abundantly present, and the majority of forkhead box protein 3(+) cells were CCR4(+). Collectively, our data show production of CCL17 and CCL22 by LMP1(+) large-sized tumor cells and accumulation of CCR4-expressing cells including regulatory T cells in ALPD.

Indexed as

Herpesvirus 4, HumanB-LymphocytesChemokine CCL17Chemokine CCL22Forkhead Transcription FactorsHumansImmunohistochemistryLymphoproliferative DisordersTumor Cells, CulturedViral Matrix ProteinsChemokine CCL17Chemokine CCL22EBV-associated membrane antigen, Epstein-Barr virusForkhead Transcription FactorsViral Matrix Proteins

Identifiers

PMID18271928
PMCPMC11158311

What OpenQuestion holds

Textmetadata
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.