Abstract:
:Most human lymphomas originate from transformed germinal center (GC) B lymphocytes. While activating mutations and translocations of MYC, BCL2 and BCL6 promote specific GC lymphoma subtypes, other genetic and epigenetic modifications that contribute to malignant progression in the GC remain poorly defined. Recently, aberrant expression of the TCL1 proto-oncogene was identified in major GC lymphoma subtypes. TCL1 transgenic mice offer unique models of both aggressive GC and marginal zone B-cell lymphomas, further supporting a role for TCL1 in B-cell transformation. Here, restriction landmark genomic scanning was employed to discover tumor-associated epigenetic alterations in malignant GC and marginal zone B-cells in TCL1 transgenic mice. Multiple genes were identified that underwent DNA hypermethylation and decreased expression in TCL1 transgenic tumors. Further, we identified a secreted isoform of EPHA7, a member of the Eph family of receptor tyrosine kinases that are able to influence tumor invasiveness, metastasis and neovascularization. EPHA7 was hypermethylated and repressed in both mouse and human GC B-cell non-Hodgkin lymphomas, with the potential to influence tumor progression and spread. These data provide the first set of hypermethylated genes with the potential to complement TCL1-mediated GC B-cell transformation and spread.
journal_name
Oncogenejournal_title
Oncogeneauthors
Dawson DW,Hong JS,Shen RR,French SW,Troke JJ,Wu YZ,Chen SS,Gui D,Regelson M,Marahrens Y,Morse HC 3rd,Said J,Plass C,Teitell MAdoi
10.1038/sj.onc.1210211subject
Has Abstractpub_date
2007-06-21 00:00:00pages
4243-52issue
29eissn
0950-9232issn
1476-5594pii
1210211journal_volume
26pub_type
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