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Related Experiment Videos

Cellular oncogenes in neoplasia.

V T Chan1, J O McGee

  • 1University of Oxford, Nuffield Department of Pathology, John Radcliffe Hospital, Oxford.

Journal of Clinical Pathology
|September 1, 1987
PubMed
Summary
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Cellular human and viral DNA detection by nonisotopic in situ hybridization.

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Chromosomal mapping of genes by nonisotopic in situ hybridization.

Methods in molecular biology (Clifton, N.J.)·2012
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Production and use of nonradioactive hybridization probes.

Methods in molecular biology (Clifton, N.J.)·2012
Same author

Cellular human and viral DNA detection by nonisotopic in situ hybridization.

Methods in molecular biology (Clifton, N.J.)·2012
Same author

Chromosomal mapping of genes by nonisotopic in situ hybridization.

Methods in molecular biology (Clifton, N.J.)·2012

Cellular proto-oncogenes, homologous to viral oncogenes, are activated in tumors. Their amplification correlates with poor prognosis, offering potential for improved cancer diagnostics and prognostics.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Cellular proto-oncogenes are homologous to viral oncogenes and implicated in cancer.
  • Proto-oncogene activation can occur through quantitative or qualitative genetic changes.
  • Unlike viral oncogenes, activated cellular oncogenes do not transform normal cells independently.

Purpose of the Study:

  • To explore the role of proto-oncogene activation in carcinogenesis.
  • To investigate the patterns of oncogene activation in human tumors.
  • To assess the diagnostic and prognostic potential of oncogene studies.

Main Methods:

  • Identification and characterization of cellular proto-oncogenes.
  • Analysis of gene structure changes (quantitative and qualitative) in tumor cell lines.

Related Experiment Videos

  • Experimental models to study oncogene cooperation and cell transformation.
  • Examination of proto-oncogene product homology with mitogenic pathway components.
  • Investigation of oncogene activation patterns in various human malignancies.

    • Main Results:

    • Proto-oncogenes are activated in tumor cell lines, but do not transform normal cells alone.
    • Cooperation between oncogenes can induce cell transformation, supporting a multistep carcinogenesis hypothesis.
    • Proto-oncogene products interact with the mitogenic pathway, potentially causing deregulation.
    • Consistent oncogene activation patterns (N-myc, neu, c-myc/N-myc) observed in neuroblastoma, breast, and lung cancers.
    • Gene amplification often correlates with poor prognosis in these cancers.

    Conclusions:

    • Oncogene activation is a significant factor in human tumorigenesis.
    • Specific oncogenes are consistently activated in certain cancers, aiding in classification.
    • Oncogene amplification serves as a prognostic marker.
    • Advancements in studying oncogene transcription and products promise enhanced cancer diagnostics and prognostics.