Tnfrsf13c (Baffr) is Mis-expressed in Tumors with Murine Leukemia Virus Insertions at Lvis22

Hentges, Kathryn E.; Yarlagadda, Sujatha; Justice, Monica J.

doi:10.1006/geno.2002.6812

Cited by 5 publications

(2 citation statements)

References 14 publications

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“…36,37 The murine homologs of PANE1 and TNFRSF13C are likewise immediately adjacent to one another in the syntenic region of the mouse genome on chromosome 15. 38 The product of the human TNFRSF13C gene, also known as BAFF-R-B-cell activation factor receptor-encodes a membrane-bound receptor for BAFF (B-cell activation factor), and is the principal receptor for BAFF-mediated mature B-cell survival. Deficiency of BAFF and/or BAFF-R results in almost complete loss of follicular and marginal zone B lymphocytes in secondary lymphoid organs in For personal use only.…”

Section: Discussionmentioning

confidence: 99%

The PANE1 gene encodes a novel human minor histocompatibility antigen that is selectively expressed in B-lymphoid cells and B-CLL

Brickner¹

2006

Blood

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Section: Discussionmentioning

confidence: 99%

The PANE1 gene encodes a novel human minor histocompatibility antigen that is selectively expressed in B-lymphoid cells and B-CLL

Brickner¹

2006

Blood

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“…These sites may be specific to a lymphoid subset of tumors, and, in particular, many may be unique to the B-cell lineage. Several of these novel sites have been validated as novel cancer-causing genes by gene expression in tumors or by oncogenicity after bone marrow transductions, or in transgenic mice, including Hex (George et al 2003 ), Evi3 (Hentges et al 2005 ), Tnfrsr13c (Hentges et al 2002 ), Evi1 (Boyd et al, 2006 ), Sox4 (Boyd et al 2006 ), and Eg5 (Castillo et al, unpublished). Of note, the Lvis24 ( Tnfrsf13c ) site was first detected as only a single hit in our VST database, but was pursued because it was commonly overexpressed in human lymphoid tumors in the Cancer Genome Anatomy Project (CGAP) database, showing that some unclustered single insertions are true positives.…”

Section: Discussionmentioning

confidence: 99%

Retroviral insertions in the VISION database identify molecular pathways in mouse lymphoid leukemia and lymphoma

et al. 2007

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AKXD recombinant inbred (RI) strains develop a variety of leukemias and lymphomas due to somatically acquired insertions of retroviral DNA into the genome of hematopoetic cells that can mutate cellular proto-oncogenes and tumor suppressor genes. We generated a new set of tumors from nine AKXD RI strains selected for their propensity to develop B-cell tumors, the most common type of human hematopoietic cancers. We employed a PCR technique called viral insertion site amplification (VISA) to rapidly isolate genomic sequence at the site of provirus insertion. Here we describe 550 VISA sequence tags (VSTs) that identify 74 common insertion sites (CISs), of which 21 have not been identified previously. Several suspected proto-oncogenes and tumor suppressor genes lie near CISs, providing supportive evidence for their roles in cancer. Furthermore, numerous previously uncharacterized genes lie near CISs, providing a pool of candidate disease genes for future research. Pathway analysis of candidate genes identified several signaling pathways as common and powerful routes to blood cancer, including Notch, E-protein, NFjB, and Ras signaling. Misregulation of several Notch signaling genes was confirmed by quantitative RT-PCR. Our data suggest that analyses of insertional mutagenesis on a single genetic background are biased toward the identification of cooperating mutations. This tumor collection represents the most comprehensive study of the genetics of B-cell leukemia and lymphoma development in mice. We have deposited the VST sequences, CISs in a genome viewer, histopathology, and molecular tumor typing data in a public web database called VISION (Viral Insertion Sites Identifying Oncogenes), which is located at

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The Pathogenetic Role of Oncogenes Deregulated by Chromosomal Translocation in B-Cell Malignancies

Dyer

2003

Int J Hematol

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Chromosomal translocations involving the immunoglobulin (IG) loci play a pivotal role in the pathogenesis of many subtypes of mature B-cell malignancy. Although all the common IG translocations have been cloned, cloning of rare but nonetheless recurrent translocations continues to allow identification of genes of importance to the development of both normal and malignant B-cells. Clustering of breakpoints within the IG gene segments has allowed development of polymerase chain reaction methods that facilitate cloning. IG translocations result in overexpression of a wide variety of genes ranging from cell surface receptors to transcriptional repressors. Genes recently shown to be involved in such translocations include BCL11A and MALT1. As with the acute leukemias, different translocations in B-cell lymphomas may target different proteins that interact directly. A common endpoint for several translocations is activation of the nuclear factor kappaB pathway. Analysis of the mechanisms of transformation may define new therapeutic strategies.

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Tnfrsf13c (Baffr) is Mis-expressed in Tumors with Murine Leukemia Virus Insertions at Lvis22

Cited by 5 publications

References 14 publications

The PANE1 gene encodes a novel human minor histocompatibility antigen that is selectively expressed in B-lymphoid cells and B-CLL

The PANE1 gene encodes a novel human minor histocompatibility antigen that is selectively expressed in B-lymphoid cells and B-CLL

Retroviral insertions in the VISION database identify molecular pathways in mouse lymphoid leukemia and lymphoma

The Pathogenetic Role of Oncogenes Deregulated by Chromosomal Translocation in B-Cell Malignancies

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