Evidence map›Paper›PMID 22200846›Full record

ArticleInternational journal of oncology2012

Diethyldithiocarbamate induces apoptosis in HHV-8-infected primary effusion lymphoma cells via inhibition of the NF-κB pathway.

Takashi Matsuno, Ryusho Kariya, Shuichiro Yano, Saori Morino-Koga, Manabu Taura, Mary Ann Suico, Yuichiro Shimauchi, Shingo Matsuyama, Yuka Okamoto, Tsuyoshi Shuto and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in International journal of oncology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.7field-weighted citation impact, top 29% 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

14 citing papers in PubMed, 23 citations in OpenAlex.

  1. Diethyldithiocarbamate-CuNanomedicine (London, England) · 2025
    Article
  2. Article
  3. How can we establish animal models of HIV-associated lymphoma?Animal models and experimental medicine · 2024
    Review
  4. Cytotoxicity of bismuth(III) dithiocarbamate derivatives by promoting a mitochondrial-dependent apoptotic pathway and suppressing MCF-7 breast adenocarcinoma cell invasion.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2024
    Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Viral Oncology: Molecular Biology and Pathogenesis.Journal of clinical medicine · 2017
    Review
  10. Article
  11. Article
  12. Current status of treatment for primary effusion lymphoma.Intractable & rare diseases research · 2014
    Review
  13. Article
  14. Review
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

12 authors at 1 institution in 1 country.

Takashi MatsunoDepartment of Molecular Medicine, Graduate School of Pharmaceutical Sciences, Global COE 'Cell Fate Regulation Research and Education Unit', Kumamoto University, 5-1 Oe-honmachi, Kumamoto 862-0973, Japan.
Ryusho Kariya
Shuichiro Yano
Saori Morino-Koga
Manabu Taura
Mary Ann Suico
Yuichiro Shimauchi
Shingo Matsuyama
Yuka Okamoto
Tsuyoshi Shuto
Hirofumi Kai
Seiji Okada
Kumamoto University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Primary effusion lymphoma (PEL) is a subtype of B-cell lymphoma caused by human herpes virus 8/Kaposi sarcoma-associated herpes virus (HHV-8/KSHV), which is mostly found in patients with AIDS and has poor prognosis. Nuclear factor (NF)-κB pathway is constitutively activated in HHV-8-infected PEL cells and plays a crucial role in tumorigenesis. Recently, it has been shown that diethyldithiocarbamate (DDTC), an active metabolite of disulfiram, has apoptotic activity in cancer cells. Here, we investigated the effect of DDTC on PEL using a PEL mouse model generated by intraperitoneal injection of BC-3 cells, a PEL cell line. DDTC ameliorated the symptoms of PEL in these mice, such as development of ascites, splenomegaly and increase of body weight, in comparison with PBS-treated controls. Moreover, we determined in vitro that DDTC suppressed the constitutively activated NF-κB pathway in BC-3 cells. Methylthiotetrazole assay revealed that the cell proliferation of various PEL cell lines was significantly suppressed by the treatment of DDTC. DDTC also induced the expression of cleaved caspase-3, an apoptosis marker, whereas the addition of Q-VD-OPh, a pan-caspase inhibitor, inhibited cell apoptosis induced by DDTC treatment. Together, our results indicated that DDTC induces apoptosis via inhibition of the NF-κB signaling pathway in HHV-8-infected PEL cells. This study suggests the potential use of DDTC as a therapeutic approach for PEL.

Indexed as

AnimalsApoptosisCaspase 3Cell Growth ProcessesCell Line, TumorDitiocarbFemaleHerpesviridae InfectionsHerpesvirus 8, HumanHumansLymphoma, Primary EffusionMaleMiceMice, Inbred BALB CMice, TransgenicNF-kappa BCaspase 3DitiocarbNF-kappa B

Identifiers

PMID22200846
PMCPMC3584624
OpenAlexW2149884691

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.