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Related Experiment Videos

The transgenic window on lymphoid malignancy.

J M Adams1, A W Harris, D L Vaux

  • 1Walter and Eliza Hall Institute of Medical Research, Post Office Royal Melbourne Hospital, Victoria, Australia.

Princess Takamatsu Symposia
|January 1, 1989
PubMed
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Transgenic mice expressing oncogenes like myc, N-myc, ras, v-abl, and bcl-2 reveal cancer development pathways. Spontaneous genetic alterations cooperate with these oncogenes to trigger lymphoid neoplasia and tumors.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Transgenic mice are valuable tools for studying oncogene function in specific tissues.
  • Lymphoid neoplasia research requires understanding oncogene-driven tumorigenesis.
  • The immunoglobulin heavy chain enhancer (E mu) drives oncogene expression in lymphocytes.

Purpose of the Study:

  • To investigate the role of various oncogenes in lymphoid neoplasia using transgenic mouse models.
  • To delineate the pathways to malignancy driven by specific oncogenes.
  • To identify cooperating genetic events in oncogene-induced tumorigenesis.

Main Methods:

  • Generation of transgenic mouse strains expressing different oncogenes (myc, N-myc, N-ras, v-abl, bcl-2) under the E mu enhancer.
  • Analysis of tumor development, cell lineage specificity, and preneoplastic phases.

Related Experiment Videos

  • Investigation of spontaneous genetic alterations cooperating with trans-oncogenes, including mutations and rearrangements.
  • Utilizing insertional mutagenesis with a retrovirus lacking an oncogene to identify novel cooperating oncogenes.

    • Main Results:

    • E mu-myc mice developed pre-B and B cell lymphomas; E mu-N-myc mice showed similar outcomes, suggesting overlapping functions.
    • E mu-N-ras mice developed T lymphomas and macrophage tumors, indicating lineage-specific oncogenic potential of ras.
    • E mu-v-abl mice were predisposed to plasmacytomas, possibly stage-specific oncogenesis.
    • E mu-bcl-2 mice produced excess resting B lymphocytes, highlighting bcl-2's role in cell survival.
    • Tumorigenesis often involved spontaneous genetic alterations cooperating with the introduced oncogene, such as myc rearrangements in E mu-v-abl plasmacytomas or ras mutations in E mu-myc lymphomas.

    Conclusions:

    • Different oncogenes induce distinct lymphoid and myeloid malignancies in a lineage-specific manner.
    • Tumorigenesis in these models requires cooperation between the introduced oncogene and spontaneous genetic alterations.
    • The study provides a framework for identifying cooperating oncogenes and understanding the genetic events leading to malignant transformation.