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Steroid/thyroid receptor-like proteins with oncogenic potential: a review

M Sluyser1

  • 1Division of Tumor Biology, The Netherlands Cancer Institute, Amsterdam.

Cancer Research
|February 1, 1990
PubMed

Insights

Mutated steroid/thyroid receptors can act as oncogenes, termed "dononcs," by disrupting normal gene transcription. These aberrant proteins may also cause tumors to lose hormonal responsiveness during progression.

Area of Science:

  • Molecular Biology
  • Genetics
  • Oncology

Background:

  • Certain members of the steroid/thyroid receptor superfamily can exhibit oncogenic potential when mutated or truncated.
  • Aberrant receptor forms interfere with normal transcriptional control by competing for DNA binding sites.

Purpose of the Study:

  • To introduce and define the term "dononcs" for oncogenes arising from dominant-negative mutations.
  • To explore the potential role of these "dononcs" in tumor progression and loss of hormonal responsiveness.

Main Methods:

  • Conceptual analysis of receptor function and mutation.
  • Comparison with recessive oncogenes (e.g., retinoblastoma).

Main Results:

  • Mutated/truncated receptors can function as dominant-negative oncogenes ("dononcs").
  • "Dononcs" disrupt normal transcription by interfering with DNA binding of normal receptors.
  • These oncogenes may contribute to acquired hormone resistance in tumors.

Conclusions:

  • Dominant-negative mutations in steroid/thyroid receptors can create oncogenes ("dononcs").
  • "Dononcs" represent a distinct class of oncogenes with implications for cancer development and treatment resistance.

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