For the Mouse gene set with the same name, see DAWSON_METHYLATED_IN_LYMPHOMA_TCL1

Systematic name M1238
Brief description Genes hypermethylated in at least one of the lymphoma tumors of transgenic mice overexpressing TCL1 [GeneID=8115] in germinal center B lymphocytes.
Full description or 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.
Collection C2: Curated
      CGP: Chemical and Genetic Perturbations
Source publication Pubmed 17260020   Authors: 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 MA
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Source species Mus musculus
Contributed by Arthur Liberzon (MSigDB Team)
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Version history 3.1: First introduced

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