Hotspots of MLV integration in the hematopoietic tumor genome

Tsuruyama, Tatsuaki; Hiratsuka, Toru; Yamada, Norishige

doi:10.1038/onc.2016.285

Cited by 13 publications

(10 citation statements)

References 74 publications

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“…MLV genomes were integrated into Stat5, c-Myc, ZFP521, and other oncogenes in the lymphoma cell genome. Upregulation in expression of Stat5 and ZFP521 are not sufficient, as pre-B cell lymphomagenesis and a strain-dependent background are required [50,51].…”

Section: Methodsmentioning

confidence: 99%

Signaling Pathway for the Development of Pre-B Cells

Tsuruyama¹

2019

Lymphocytes

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Pre-B cells represent the immature stage of the B cell lineage and express genes for the pre-B cell receptor (preBCR). PreBCR consists of lambda 5 and VpreB and its expression elicits a rearrangement of the immunoglobulin heavy chain prior to rearrangement of the immunoglobulin light chain. The lambda 5 and VpreB form a surrogate light chain, which is a premature type of light chain immunoglobulin. PreBCR may cooperate or interact with the IL-7 receptor, which contributes to pre-B cell development. The preBCR distal signaling pathway recruits several adaptor proteins and protein kinases. This review aims to illustrate the framework of the signaling pathway that contributes to B cell lineage development and reconsiders the relationship between the preBCR and IL-7 receptors.

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Section: Methodsmentioning

confidence: 99%

Signaling Pathway for the Development of Pre-B Cells

Tsuruyama¹

2019

Lymphocytes

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“…Second, the inserted retroviral element has the promoter or enhancer activity of the host proto-oncogene. The genome of human papilloma virus (HPV), hepatitis B virus (HBV), human T-cell adult leukemia virus (HTLV) [5], avian sarcoma virus (ASV) [6], feline leukemia virus (FeLV) [7], murine leukemia virus (MLV) [8][9][10][11][12][13], and mouse mammary tumor virus (MMTV) can be integrated in the host genome. As a survival strategy, the inserted retroviral genome (provirus) is thereafter replicated during host cell division.…”

Section: Viral Genome Integrationmentioning

confidence: 99%

“…Through the recognition of open chromatin structure, BET proteins have been suggested to contribute to the tethering of the MLV PIC to the host chromatin [10,12]. Furthermore, it has been shown that the cell-permeable small molecule JQ-1, a pan-BET bromodomain inhibitor, prevents the BRD4-acetylated lysine interaction by competitively binding to BRD4 and reduces MLV integration frequencies at transcription start sites [4,13,14]. These findings suggest that BET proteins navigate the MLV genome and promote efficient MLV integration around transcription start sites associated with a chromatin structure characteristic of an open, transcriptionally active domain [3].…”

Section: Interaction Partners For MLV Integrase and Recent Developmenmentioning

confidence: 99%

Basic Research and Clinical Examination of Tumor Virus

Tsuruyama¹,

Ogawa²,

Yamada³

2020

Viruses and Viral Infections in Developing Countries

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Tumor viruses cause cancer; thus, extensive studies are being conducted on them. In this article, we will review the basic medical research on the current clinical genetic tests for tumor viruses such as human papilloma virus, hepatitis B virus, and T-cell leukemia virus. Recently, clinical genetic tests have been developed for quick diagnosis of the tumor virus infection. Additionally, we will review the mutagenesis of murine leukemia retrovirus. In particular, we will focus on the insertional mutagenesis. This will help in deciding the direction of future virus research by combining clinical and basic research.

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“…In the experimental model, transgenic mice carrying chimera genes, such as Emu-myc mice, MT-BCR-ABL Lymphocyte Updates -Cancer, Autoimmunity and Infection mice, [6,7], and TEL/AML1 mice rapidly develop pre-B LBL [8][9][10]. Unlike these models, the SL/Kh mouse develops spontaneously in the absence of artificially introduced gene mutation; however, Zfp521 is the gene that is spontaneously and constitutively mutated by MLV insertion after the birth [11,12].…”

Section: The Characterization Of Spontaneous Pre-b-cell Lymphoma In Smentioning

confidence: 99%

Signal Pathway in Precursor B-Cell Lymphoblastic Leukemia/Lymphoma

Tsuruyama¹,

Hiratsuka²

2017

Lymphocyte Updates - Cancer, Autoimmunity and Infection

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Stat5, c-myc, Hipk2, Fiz1, and ZFP521 to lymphomagenesis precursor B-cell lymphoblastic lymphoma/leukemia have been previously identified as a putative gene involved in the induction of B-cell lymphomagenesis. In this review, we summarize the role of ZFP521 in B-cell lymphomagenesis. Zinc finger protein 521 (Zfp521) is a novel identified gene that is responsible for pre-B-lymphoblastic lymphomagenesis through activation of pre-B-cell receptor (pre-BCR)-signaling by upregulation of adaptor genes and related kinases in the signaling downstream. The pre-BCR-signaling molecules, FLT3, CD43, and IL-7 receptor (IL-7R) were positively regulated by these genes. Stimulation of pre-BCR and/or IL-7R signaling caused aberrant upregulation of other oncogene sets such as cyclin genes, thereby inducing the growth of pre-B cells. IL-7R/Janus kinase (JAK)/STAT signaling cascade is one of the key signaling pathways that are activated in precursor B-cell lymphoblastic lymphoma/ leukemia. FLT3, CD43, and pre-BCR cascades crosstalk with JAK/STAT cascade. FLT3 and CD43 cascades have the potential to enhance JAK/STAT cascade effect on pre-B cell growth. On the other hand, pre-BCR and interleukin (IL)-7 receptor exerted competitive effects on pre-B-cell growth; thus, precursor B-cell lymphoblastic lymphomagenesis is a consequence through interaction with these cascades.

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Hotspots of MLV integration in the hematopoietic tumor genome

Cited by 13 publications

References 74 publications

Signaling Pathway for the Development of Pre-B Cells

Signaling Pathway for the Development of Pre-B Cells

Basic Research and Clinical Examination of Tumor Virus

Signal Pathway in Precursor B-Cell Lymphoblastic Leukemia/Lymphoma

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