Evidence map›Paper›PMID 39321027›Full record

ArticleCancer science2024

Decreased PU.1 expression in mature B cells induces lymphomagenesis.

Shinya Endo, Nao Nishimura, Kosuke Toyoda, Yoshihiro Komohara, Joaquim Carreras, Hiromichi Yuki, Takafumi Shichijo, Shikiko Ueno, Niina Ueno, Shinya Hirata and 13 more

Abstract read
In one paragraph

Article in Cancer science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. Article
  3. 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

23 authors.

Shinya EndoDepartment of Hematology, Rheumatology, and Infectious Disease, Kumamoto University Graduate School of Medicine, Kumamoto, Japan.
Nao NishimuraDepartment of Hematology, Rheumatology, and Infectious Disease, Kumamoto University Graduate School of Medicine, Kumamoto, Japan.
Kosuke ToyodaDepartment of Hematology, Rheumatology, and Infectious Disease, Kumamoto University Graduate School of Medicine, Kumamoto, Japan.ORCID https://orcid.org/0000-0001-8125-4528
Yoshihiro KomoharaDepartment of Cell Pathology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.ORCID https://orcid.org/0000-0001-9723-0846
Joaquim CarrerasDepartment of Pathology, Tokai University School of Medicine, Isehara, Japan.ORCID https://orcid.org/0000-0002-6129-8299
Hiromichi YukiDepartment of Hematology, Rheumatology, and Infectious Disease, Kumamoto University Graduate School of Medicine, Kumamoto, Japan.
Takafumi ShichijoDepartment of Hematology, Rheumatology, and Infectious Disease, Kumamoto University Graduate School of Medicine, Kumamoto, Japan.ORCID https://orcid.org/0000-0002-1272-3738
Shikiko UenoDepartment of Hematology, Rheumatology, and Infectious Disease, Kumamoto University Graduate School of Medicine, Kumamoto, Japan.
Niina UenoDepartment of Hematology, Rheumatology, and Infectious Disease, Kumamoto University Graduate School of Medicine, Kumamoto, Japan.
Shinya HirataDepartment of Hematology, Rheumatology, and Infectious Disease, Kumamoto University Graduate School of Medicine, Kumamoto, Japan.
Yawara KawanoDepartment of Hematology, Rheumatology, and Infectious Disease, Kumamoto University Graduate School of Medicine, Kumamoto, Japan.ORCID https://orcid.org/0000-0002-8269-440X
Kisato NosakaDepartment of Hematology, Rheumatology, and Infectious Disease, Kumamoto University Graduate School of Medicine, Kumamoto, Japan.ORCID https://orcid.org/0000-0001-6682-2451
Masashi MiyaokaDepartment of Pathology, Tokai University School of Medicine, Isehara, Japan.
Naoya NakamuraDepartment of Pathology, Tokai University School of Medicine, Isehara, Japan.
Ai SatoDepartment of Hematology-Oncology, Tokai University School of Medicine, Isehara, Japan.
Kiyoshi AndoDepartment of Hematology-Oncology, Tokai University School of Medicine, Isehara, Japan.
Hiroaki MitsuyaDepartment of Hematology, Rheumatology, and Infectious Disease, Kumamoto University Graduate School of Medicine, Kumamoto, Japan.
Koichi AkashiDepartment of Medicine and Biosystemic Science, Kyushu University Graduate School of Medicine, Fukuoka, Japan.
Daniel G TenenHarvard Medical School, Harvard Stem Cell Institute, Boston, Massachusetts, USA.
Jun-Ichirou YasunagaDepartment of Hematology, Rheumatology, and Infectious Disease, Kumamoto University Graduate School of Medicine, Kumamoto, Japan.ORCID https://orcid.org/0000-0002-7939-2080
Masao MatsuokaDepartment of Hematology, Rheumatology, and Infectious Disease, Kumamoto University Graduate School of Medicine, Kumamoto, Japan.ORCID https://orcid.org/0000-0002-0473-754X
Yutaka OkunoDepartment of Hematology, Rheumatology, and Infectious Disease, Kumamoto University Graduate School of Medicine, Kumamoto, Japan.ORCID https://orcid.org/0000-0003-2108-5157
Hiro TatetsuDepartment of Hematology, Rheumatology, and Infectious Disease, Kumamoto University Graduate School of Medicine, Kumamoto, Japan.ORCID https://orcid.org/0000-0001-8131-3401

Funding

Japan Society for the Promotion of Science 21K08420Japan Society for the Promotion of Science 26461427
6 · The paper itself

Abstract

Diffuse large B-cell lymphoma (DLBCL) is the most common subtype of lymphoma, accounting for 30% of non-Hodgkin lymphomas. Although comprehensive analysis of genetic abnormalities has led to the classification of lymphomas, the exact mechanism of lymphomagenesis remains elusive. The Ets family transcription factor, PU.1, encoded by Spi1, is essential for the development of myeloid and lymphoid cells. Our previous research illustrated the tumor suppressor function of PU.1 in classical Hodgkin lymphoma and myeloma cells. In the current study, we found that patients with DLBCL exhibited notably reduced PU.1 expression in their lymphoma cells, particularly in the non-germinal center B-cell-like (GCB) subtype. This observation suggests that downregulation of PU.1 may be implicated in DLBCL tumor growth. To further assess PU.1's role in mature B cells in vivo, we generated conditional Spi1 knockout mice using Cγ1-Cre mice. Remarkably, 13 of the 23 knockout mice (56%) showed splenomegaly, lymphadenopathy, or masses, with some having histologically confirmed B-cell lymphomas. In contrast, no wild-type mice developed B-cell lymphoma. In addition, RNA-seq analysis of lymphoma cells from Cγ1-Cre Spi1

Indexed as

B-LymphocytesLymphoma, Large B-Cell, DiffuseMice, KnockoutProto-Oncogene ProteinsTrans-ActivatorsAnimalsCell Line, TumorGene Expression Regulation, NeoplasticHumansMiceProto-Oncogene Protein Spi-1Proto-Oncogene ProteinsProto-Oncogene Protein Spi-1Trans-Activatorsdiffuse large B‐cell lymphomaDLBCLlymphomagenesisPU.1Spi1

Identifiers

PMID39321027
PMCPMC11611758

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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.