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Citations to this article

Transcription intermediary factor 1γ is a tumor suppressor in mouse and human chronic myelomonocytic leukemia
Romain Aucagne, … , Jean-Noël Bastie, Laurent Delva
Romain Aucagne, … , Jean-Noël Bastie, Laurent Delva
Published May 2, 2011
Citation Information: J Clin Invest. 2011;121(6):2361-2370. https://doi.org/10.1172/JCI45213.
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Research Article Hematology Article has an altmetric score of 12

Transcription intermediary factor 1γ is a tumor suppressor in mouse and human chronic myelomonocytic leukemia

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Abstract

Transcription intermediary factor 1γ (TIF1γ) was suggested to play a role in erythropoiesis. However, how TIF1γ regulates the development of different blood cell lineages and whether TIF1γ is involved in human hematological malignancies remain to be determined. Here we have shown that TIF1γ was a tumor suppressor in mouse and human chronic myelomonocytic leukemia (CMML). Loss of Tif1g in mouse HSCs favored the expansion of the granulo-monocytic progenitor compartment. Furthermore, Tif1g deletion induced the age-dependent appearance of a cell-autonomous myeloproliferative disorder in mice that recapitulated essential characteristics of human CMML. TIF1γ was almost undetectable in leukemic cells of 35% of CMML patients. This downregulation was related to the hypermethylation of CpG sequences and specific histone modifications in the gene promoter. A demethylating agent restored the normal epigenetic status of the TIF1G promoter in human cells, which correlated with a reestablishment of TIF1γ expression. Together, these results demonstrate that TIF1G is an epigenetically regulated tumor suppressor gene in hematopoietic cells and suggest that changes in TIF1γ expression may be a biomarker of response to demethylating agents in CMML.

Authors

Romain Aucagne, Nathalie Droin, Jérôme Paggetti, Brice Lagrange, Anne Largeot, Arlette Hammann, Amandine Bataille, Laurent Martin, Kai-Ping Yan, Pierre Fenaux, Régine Losson, Eric Solary, Jean-Noël Bastie, Laurent Delva

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Total citations by year

Year: 2025 2024 2023 2022 2021 2020 2019 2018 2017 2016 2015 2014 2013 2012 2011 Total
Citations: 1 6 2 2 5 6 5 4 5 2 9 4 3 6 4 64
Citation information
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Citations to this article in year 2015 (9)

Title and authors Publication Year
A Comprehensive Overview on Myositis-Specific Antibodies: New and Old Biomarkers in Idiopathic Inflammatory Myopathy
M Satoh, S Tanaka, A Ceribelli, SJ Calise, EK Chan
Clinical Reviews in Allergy & Immunology 2015
Chronic myelomonocytic leukemia: Forefront of the field in 2015
CB Benton, A Nazha, N Pemmaraju, G Garcia-Manero
Critical Reviews in Oncology/Hematology 2015
Repression of TIF1γ by SOX2 promotes TGF-β-induced epithelial–mesenchymal transition in non-small-cell lung cancer
L Wang, H Yang, Z Lei, J Zhao, Y Chen, P Chen, C Li, Y Zeng, Z Liu, X Liu, HT Zhang
Oncogene 2015
Tumour suppressor TRIM33 targets nuclear β-catenin degradation
J Xue, Y Chen, Y Wu, Z Wang, A Zhou, S Zhang, K Lin, K Aldape, S Majumder, Z Lu, S Huang
Nature Communications 2015
The transcriptional cofactor TRIM33 prevents apoptosis in B lymphoblastic leukemia by deactivating a single enhancer: ( A ) Negative selection shRNA screen targeting chromatin regulators in murine B cell acute lymphoblastic leukemia (B-ALL). shRNAs are rank ordered by the fold-change in GFP positivity over 10 days in culture, which represents a competition-based assay in which loss of GFP positivity reflects shRNA-postive cells becoming outcompeted by shRNA-negative cells. ( B – E ) Competition-based assays and Western blotting to evaluate the effect of TRIM33 shRNAs on B-ALL, 38B9, acute myeloid leukemia (AML), or T-cell acute lymphoblastic leukemia (T-ALL) cells. GFP percentages are normalized to day 2 measurements. Results are the average of three biological replicates. ( F ) Annexin V/DAPI staining following transduction of B-ALL cells with the indicated MLS shRNAs on day 3 post-transduction. Representative experiment of three biological replicates is shown. ( G ) shRNA transgenic mouse strategy. TRE: tet(doxycycline) response element; rtTA-M2: reverse tet transactivator M2 variant (tet-on). ( H ) Western blotting performed of indicated tissue lysates prepared from mice treated with dox for 4 weeks. Representative experiment of three biological replicates is shown. ( I – J ) Flow cytometry analysis using the indicated antibody stainings of whole bone marrow or spleen. B220 and Cd19: B lymphoid, Ter119: erythroid, Gr1 and Mac1: myeloid, Cd3: T lymphoid. Gating was performed on GFP + /shRNA + cells prior to quantifying marker positivity. The GFP + percentage in bone marrow was ∼75% and in the spleen was ∼15%. Mice were administered dox for 1 week or 4 weeks, with both timepoints giving similar results. Results shown are the average 4 or 5 mice. All error bars in this figure represent S.E.M
E Wang, S Kawaoka, JS Roe, J Shi, AF Hohmann, Y Xu, AS Bhagwat, Y Suzuki, JB Kinney, CR Vakoc
eLife 2015
TIF1γ interferes with TGFβ1/SMAD4 signaling to promote poor outcome in operable breast cancer patients
L Kassem, M Deygas, L Fattet, J Lopez, T Goulvent, E Lavergne, S Chabaud, N Carrabin, N Chopin, T Bachelot, G Gillet, I Treilleux, R Rimokh
BMC Cancer 2015
Characteristic repartition of monocyte subsets as a diagnostic signature of chronic myelomonocytic leukemia
D Selimoglu-Buet, O Wagner-Ballon, V Saada, V Bardet, R Itzykson, L Bencheikh, M Morabito, E Met, C Debord, E Benayoun, AM Nloga, P Fenaux, T Braun, C Willekens, B Quesnel, L Ades, M Fontenay, P Rameau, N Droin, S Koscielny, E Solary
Blood 2015
The HSP90 inhibitor, 17AAG, protects the intestinal stem cell niche and inhibits graft versus host disease development
AL Joly, A Deepti, A Seignez, A Goloudina, S Hebrard, E Schmitt, S Richaud, E Fourmaux, A Hammann, A Collura, M Svrcek, G Jego, E Robinet, E Solary, O Demidov, E Kohli, C Garrido
Oncogene 2015
TRIM66 overexpresssion contributes to osteosarcoma carcinogenesis and indicates poor survival outcome
Y Chen, Y Guo, H Yang, G Shi, G Xu, Y Na, J Shi, D Chen
Oncotarget 2015

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