YY1 Control of AID-Dependent Lymphomagenesis

Abstract

We hypothesize that YY1 levels control AID nuclear accumulation, AID mutation rates, and subsequent AIDmediated B cell lymphomagenesis. We are testing this hypothesis by exploring the impact of YY1 overexpression, or deletion, in mouse lines that spontaneously develop AID-dependent B cell lymphoma. In the initial granting period this year, we have bred the mice that spontaneously develop B cell lymphoma and have initiated YY1- overexpression studies. Our results are still preliminary but suggest that overexpression of YY1 leads to higher mortality. Second, we have bred the yy1 f/f and gamma1-CRE alleles onto the background of the mice that spontaneously develop AID-dependent B cell lymphoma. These mice will enable us to test in the coming year if YY1 knock-out reduces B cell lymphoma. Finally, we have demonstrated that knock-out of YY1 results in reduced AID-mediated mutagenesis, supporting our main hypothesis. In the coming year we anticipate being able to complete experiments to test the role of YY1 in controlling AID-dependent lymphoma.

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Document Details

Document Type
Technical Report
Publication Date
Jul 01, 2015
Accession Number
ADA624305

Entities

People

  • Michael Atchison

Organizations

  • University of Pennsylvania

Tags

DTIC Thesaurus Topics

  • Biological Staining And Labeling
  • Biomedical Research
  • Bone Marrow
  • Bones
  • Electronic Mail
  • Genes
  • Genetic Phenomena
  • Histology
  • Lymph Nodes
  • Lymphatic System
  • Medical Personnel
  • Microarray Analysis
  • Mutations
  • Neoplasms
  • Patent Applications
  • Pathology
  • Phenotypes

Fields of Study

  • Biology

Readers

  • Military Logistics and Supply Chain Management
  • Molecular and Cellular Biology
  • Oncology