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Mice have long served as models for studying human biology and pathology because of their phylogenetic and physiological similarity with humans. They are also easy to maintain and breed in the laboratory, and hence, many inbred strains are now available for research. Studies on mice have contributed immeasurably to our understanding of cancer biology.
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Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...
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Related Experiment Video

Updated: Jun 27, 2026

Assessing Somatic Hypermutation in Ramos B Cells after Overexpression or Knockdown of Specific Genes
08:12

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Published on: November 1, 2011

Uncoupling between Ig somatic hypermutation and oncogene mutation in mouse lymphoma.

Christelle Vincent1, Véronique Truffinet, Remi Fiancette

  • 1UMR CNRS 6101, Centre National de la Recherche Scientifique, Université de Limoges, France.

Biochimica Et Biophysica Acta
|November 26, 2008
PubMed
Summary

Mice engineered with a c-myc gene linked to the immunoglobulin heavy chain locus develop Burkitt lymphoma (BL). This process involves specific mutations in the c-myc gene, driving lymphoma development independently of antigen selection.

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11:06

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Published on: February 24, 2014

Area of Science:

  • Oncology
  • Molecular Biology
  • Immunology

Background:

  • Burkitt lymphoma (BL) is characterized by c-myc translocations with the immunoglobulin heavy chain (IgH) locus.
  • Understanding the mechanisms driving BL pathogenesis is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the role of the 3'IgH locus control region (LCR) in c-myc-driven lymphomagenesis.
  • To elucidate the mutational processes affecting the c-myc oncogene in lymphoma development.

Main Methods:

  • Generation of transgenic c-myc-3'LCR mice that develop lymphoma.
  • Analysis of BCL-6 expression and somatic hypermutation (SHM) in lymphoma cells.
  • Sequencing of the transgenic c-myc gene to identify mutations.

Main Results:

  • c-myc-3'LCR mice develop clonal BL or diffuse anaplastic lymphoma.
  • Lymphoma cells exhibit high levels of SHM specifically targeting the c-myc oncogene, particularly in regulatory elements.
  • Mutations lead to constitutive c-myc expression, independent of antigen selection.

Conclusions:

  • The c-myc-3'IgH LCR association drives lymphoma from naive B cells by recruiting AID activity to c-myc.
  • Lymphoma development relies on AID-driven mutations in c-myc regulatory regions, circumventing antigen-driven selection.
  • This model recapitulates key features of human BL, offering insights into oncogene deregulation.