First description of the t(10;11)(q22;q23)/MLL-TET1 translocation in a T-cell lymphoblastic lymphoma, with subsequent lineage switch to acute myelomonocytic myeloid leukemia

Ittel, Antoine; Jeandidier, Éric; Hélias, Catherine; Perrusson, N; Humbrecht, Catherine; Lioure, Bruno; Mazurier, I.; Mayeur-Rousse, Caroline; Lavaux, Amandine; Thiébault, Sylvie; Lerintiu, Felix; Gervais, Carine; Mauvieux, Laurent

doi:10.3324/haematol.2013.096750

Cited by 31 publications

(18 citation statements)

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“…The TET gene family was first identified because of the involvement of TET1 as a fusion partner of MLL in acute myeloid leukemia (AML) 11 , a translocation event that has also been detected in patients with T cell lymphoma 12 and B-ALL 13 . TET1 mutations are also found at a low frequency in AML (~1%) 14 compared to T cell acute lymphoblastic leukemia (T-ALL) (~14%) 15 although mutations in B cell malignancy have not been reported.…”

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confidence: 99%

TET1 is a tumor suppressor of hematopoietic malignancy

et al. 2015

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The TET methylcytosine dioxygenase 1 (TET1) enzyme is an important regulator of 5-hydroxymethylcytosine (5hmC) in embryonic stem cells. Decreased expression of TET proteins and loss of 5hmC in many tumors suggests a critical role for the maintenance of this epigenetic modification. Here we show that deletion of Tet1 promoted the development of B cell lymphoma in mice. Tet1 was required for maintaining normal content of 5hmC, preventing DNA hypermethylation and in the regulation of B cell lineage, chromosome maintenance and DNA repair genes. Whole-exome sequencing of Tet1-deficient tumors revealed mutations frequently found in Non-Hodgkin B cell lymphoma, where TET1 was hypermethylated and transcriptionally silenced. These findings provide in vivo evidence of TET1 function as a tumor suppressor of hematopoietic malignancy.

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confidence: 99%

TET1 is a tumor suppressor of hematopoietic malignancy

et al. 2015

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“…The fusion of TET1 and MLL has been reported in a number of AML/ALL [24, 25, 31-33]. A recent study indicates that TET1 has essential oncogenic function in the development of MLL-rearranged leukemia, which is through coordination with MLL-fusion proteins in regulating their critical co-targets including homeobox A9 (Hoxa9), myeloid ecotropic viral integration 1 (Meis1), and pre-B-cell leukemia homeobox 3 (Pbx3) genes [19, 78].…”

Section: Tet1 In Human Hematologic Malignanciesmentioning

confidence: 99%

“…In the process of demethylating DNA, TET enzymes further practice 5-hmC to generate 5-fC and 5-caC, both of which can be removed by thymine DNA glycosylase by base excision repair (BER) [22, 23, 30]. In the history of TET proteins, researches demonstrated that fusion of the N-terminal region of MLL H3K4 methyltransferase with the DSBH domain of TET1 is related with acute myeloid/lymphoid leukemias [24, 25, 31-33]. TET2 mutations correlate with many hematologic malignancies, such as myelodysplastic syndromes (MDS), myeloproliferative neoplasms (MPN), CMML, AML, secondary AML, and so on [34-42].…”

Section: Introductionmentioning

confidence: 99%

Epigenetic Function of TET Family, 5-Methylcytosine, and 5-Hydroxymethylcytosine in Hematologic Malignancies

2019

Oncol Res Treat

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DNA methylation plays significant roles in a variety of biological and pathological processes including mammalian development, genomic imprinting, retrotransposon silencing, and X-chromosome inactivation. Recent discoveries indicated that ten-eleven translocation (TET) family of dioxygenases can convert 5-methylcytosine (5-mC) into 5-hydroxymethylcytosine (5-hmC). The TET family includes three members: TET1, TET2, and TET3. With increasing evidence, more and more biological and pathological processes in which 5-hmC and TET family serve unparalleled biological roles are noticed, for example, DNA demethylation and transcriptional regulation of different target genes, which are involved in many human diseases, especially hematologic malignancies, resembling chronic myelomonocytic leukemia, myelodysplastic syndromes, and so on. In this review, we focus on the diverse functions of TET family and the novel epigenetic marks, 5-mC and 5-hmC, in hematologic malignancies. This review will provide valuable insights into the potential targets of hematologic malignancies. Further understanding of the normal and pathological functions of TET family may provide new methods to develop novel epigenetic therapies for treating hematologic malignancies.

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“…myeloid lineages. [8][9][10] We induced the myeloid progenitor cells by growing murine bone marrow mononuclear cells with Iscove modified Dulbecco medium containing 15% fetal bovine serum, interleukin-3, interleukin-6 and stem cell factor for 48 h. During this period, mononuclear cells were activated into myeloid progenitor cells and the number of myeloid progenitor cells was increased. The breakpoint region of the MT1 fusion between exon 9 of MLL and exon 9 of TET1 has been previously identified ( Figure 1A).…”

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confidence: 99%

MLL-TET1 fusion protein promotes immortalization of myeloid progenitor cells and leukemia development

Kim

et al. 2017

Haematologica

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First description of the t(10;11)(q22;q23)/MLL-TET1 translocation in a T-cell lymphoblastic lymphoma, with subsequent lineage switch to acute myelomonocytic myeloid leukemia

Abstract: LETTERS TO THE EDITOR© F e r r a t a S t o r t i F o u n d a t i o n 2 0 1 3

Cited by 31 publications

References 13 publications

TET1 is a tumor suppressor of hematopoietic malignancy

TET1 is a tumor suppressor of hematopoietic malignancy

Epigenetic Function of TET Family, 5-Methylcytosine, and 5-Hydroxymethylcytosine in Hematologic Malignancies

MLL-TET1 fusion protein promotes immortalization of myeloid progenitor cells and leukemia development

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