Evidence map›Paper›PMID 38734786›Full record

ArticleLeukemia2024

TIF1β activates leukemic transcriptional program in HSCs and promotes BCR::ABL1-induced myeloid leukemia.

Mariko Morii, Sho Kubota, Mihoko Iimori, Takako Yokomizo-Nakano, Ai Hamashima, Jie Bai, Akiho Nishimura, Masayoshi Tasaki, Yukio Ando, Kimi Araki and 1 more

Abstract read
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In one paragraph

Article in Leukemia, 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. KAP1 in antiviral immunity: dual roles in viral silencing and immune regulation.Frontiers in cellular and infection microbiology · 2025
    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

11 authors.

Mariko MoriiLaboratory of Transcriptional Regulation in Leukemogenesis, International Research Center for Medical Sciences, Kumamoto University, Kumamoto, Japan.
Sho KubotaLaboratory of Transcriptional Regulation in Leukemogenesis, International Research Center for Medical Sciences, Kumamoto University, Kumamoto, Japan.ORCID 0000-0001-6119-1259
Mihoko IimoriLaboratory of Transcriptional Regulation in Leukemogenesis, International Research Center for Medical Sciences, Kumamoto University, Kumamoto, Japan.
Takako Yokomizo-NakanoLaboratory of Transcriptional Regulation in Leukemogenesis, International Research Center for Medical Sciences, Kumamoto University, Kumamoto, Japan.ORCID 0000-0003-3879-7046
Ai HamashimaLaboratory of Transcriptional Regulation in Leukemogenesis, International Research Center for Medical Sciences, Kumamoto University, Kumamoto, Japan.ORCID 0000-0002-1683-4443
Jie BaiLaboratory of Transcriptional Regulation in Leukemogenesis, International Research Center for Medical Sciences, Kumamoto University, Kumamoto, Japan.ORCID 0000-0002-7485-4450
Akiho NishimuraGastrointestinal Cancer Biology, International Research Center of Medical Sciences, Kumamoto University, Kumamoto, 860-0811, Japan.
Masayoshi TasakiDepartment of Biomedical Laboratory Sciences, Graduate School of Health Sciences, Kumamoto University, Kumamoto, Japan.
Yukio AndoDepartment of Amyloidosis Research, Nagasaki International University, Sasebo, Japan.
Kimi ArakiInstitute of Resource Development and Analysis, Kumamoto University, Kumamoto, Japan.
Goro SashidaLaboratory of Transcriptional Regulation in Leukemogenesis, International Research Center for Medical Sciences, Kumamoto University, Kumamoto, Japan. sashidag@kumamoto-u.ac.jp.ORCID 0000-0003-2318-5987

Funding

MEXT | Japan Society for the Promotion of Science (JSPS) 15K19545MEXT | Japan Society for the Promotion of Science (JSPS) 18H02842MEXT | Japan Society for the Promotion of Science (JSPS) 20K17383MEXT | Japan Society for the Promotion of Science (JSPS) 21H02952MEXT | Japan Society for the Promotion of Science (JSPS) 21K06870MEXT | Japan Society for the Promotion of Science (JSPS) 22J40054
6 · The paper itself

Abstract

TIF1β/KAP1/TRIM28, a chromatin modulator, both represses and activates the transcription of genes in normal and malignant cells. Analyses of datasets on leukemia patients revealed that the expression level of TIF1β was increased in patients with chronic myeloid leukemia at the blast crisis and acute myeloid leukemia. We generated a BCR::ABL1 conditional knock-in (KI) mouse model, which developed aggressive myeloid leukemia, and demonstrated that the deletion of the Tif1β gene inhibited the progression of myeloid leukemia and showed longer survival than that in BCR::ABL1 KI mice, suggesting that Tif1β drove the progression of BCR::ABL1-induced leukemia. In addition, the deletion of Tif1β sensitized BCR::ABL1 KI leukemic cells to dasatinib. The deletion of Tif1β decreased the expression levels of TIF1β-target genes and chromatin accessibility peaks enriched with the Fosl1-binding motif in BCR::ABL1 KI stem cells. TIF1β directly bound to the promoters of proliferation genes, such as FOSL1, in human BCR::ABL1 cells, in which TIF1β and FOSL1 bound to adjacent regions of chromatin. Since the expression of Fosl1 was critical for the enhanced growth of BCR::ABL1 KI cells, Tif1β and Fosl1 interacted to activate the leukemic transcriptional program in and cellular function of BCR::ABL1 KI stem cells and drove the progression of myeloid leukemia.

Indexed as

Fusion Proteins, bcr-ablLeukemia, Myelogenous, Chronic, BCR-ABL PositiveTripartite Motif-Containing Protein 28AnimalsGene Expression Regulation, LeukemicHumansMiceTranscription, GeneticFusion Proteins, bcr-ablTRIM28 protein, humanTrim28 protein, mouseTripartite Motif-Containing Protein 28

Identifiers

PMID38734786

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.