Lessons from Using Genetically Engineered Mouse Models of MYC-Induced Lymphoma

Cells. 2022 Dec 22;12(1):37. doi: 10.3390/cells12010037.

Abstract

Oncogenic overexpression of MYC leads to the fatal deregulation of signaling pathways, cellular metabolism, and cell growth. MYC rearrangements are found frequently among non-Hodgkin B-cell lymphomas enforcing MYC overexpression. Genetically engineered mouse models (GEMMs) were developed to understand MYC-induced B-cell lymphomagenesis. Here, we highlight the advantages of using Eµ-Myc transgenic mice. We thoroughly compiled the available literature to discuss common challenges when using such mouse models. Furthermore, we give an overview of pathways affected by MYC based on knowledge gained from the use of GEMMs. We identified top regulators of MYC-induced lymphomagenesis, including some candidates that are not pharmacologically targeted yet.

Keywords: B-cells; Eµ-Myc transgene; MYC; genetically engineered mouse models; lymphoma.

Publication types

  • Review
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • B-Lymphocytes / metabolism
  • Lymphoma* / pathology
  • Lymphoma, B-Cell* / metabolism
  • Mice
  • Mice, Transgenic
  • Proto-Oncogene Proteins c-myc / genetics
  • Proto-Oncogene Proteins c-myc / metabolism

Substances

  • Proto-Oncogene Proteins c-myc

Grants and funding

This research was funded by the Carl Zeiss Foundation (to R.W.), the Deutsche Forschungsgemeinschaft (DFG, German Research Foundation), GRK 1715/grant number 177710919 (to C.K.) and by a Landesgraduiertenstipendium, Friedrich Schiller University Jena (to E.-M.P.).