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Chromosomal location targets different MYC family gene members for oncogenic translocations

Monica Gostissa1, Sheila Ranganath, Julia M Bianco

  • 1The Howard Hughes Medical Institute, Children's Hospital Boston, and Department of Genetics, Harvard Medical School, 300 Longwood Avenue, Boston, MA 02115, USA.

Proceedings of the National Academy of Sciences of the United States of America
|January 29, 2009
PubMed

Insights

The MYC oncogene family drives cell growth and cancer. Researchers found that the c-Myc gene locus is preferentially targeted for translocations and amplifications in specific mouse lymphomas, even when N-myc can substitute its function.

Area of Science:

  • Molecular Biology
  • Oncogenesis
  • Cancer Genetics

Background:

  • The MYC oncogene family (c-Myc, N-myc, L-myc) regulates cell proliferation and death.
  • Aberrant MYC gene activation is linked to specific cancers, such as B lymphoid tumors (c-Myc) and neuroblastomas (N-myc).
  • Tissue-specific expression and functional redundancy between MYC family members may influence oncogenic activation.

Purpose of the Study:

  • To investigate whether the c-Myc locus is preferentially targeted for oncogenic translocations and amplifications.
  • To compare the targeting of wild-type c-Myc versus an N-myc allele (NCR) in a DNA Ligase 4 (Lig4)/p53-deficient pro-B cell lymphoma model.

Main Methods:

  • Utilized a mouse model deficient for DNA Ligase 4 (Lig4) and p53 tumor suppressor.
  • Generated a modified allele (NCR) where N-myc coding sequence replaced c-Myc.
  • Analyzed tumor development, type, and cytological aberrations in mice harboring either wild-type c-Myc or the NCR allele.

Main Results:

  • The N-myc coding sequence (NCR allele) effectively competed with the wild-type c-Myc allele as a target for oncogenic translocations and amplifications.
  • Tumor onset, type, and cytological aberrations were similar between mice with c-Myc or NCR allele targeting.
  • These findings suggest specific features of the c-Myc locus make it a preferred target for translocation/amplification in this lymphoma model.

Conclusions:

  • The c-Myc locus appears to be preferentially targeted for oncogenic aberrations in Lig4/p53-deficient pro-B cell lymphomas.
  • Despite functional redundancy with N-myc, the endogenous N-myc locus is not as readily targeted in this specific cellular context.
  • Locus-specific features, rather than solely functional redundancy, may dictate the susceptibility to oncogenic translocations and amplifications.

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