Oncogene mutations as intermediate markers

David Sidransky, Jay Boyle, Wayne Koch, Peter van der Riet

Research output: Contribution to journalArticlepeer-review

5 Scopus citations


Tumors arise through a series of genetic changes which include activation of protooncogenes and inactivation of tumor suppressor genes. It is now possible to identify rare cells containing genetic mutations in an excess background of normal cells. Theoretically, the identification of a clonal population of cells sharing an early genetic marker for malignant transformation would lead to valuable intermediate endpoints and could diagnose premalignant lesions amenable to chemoprevention. Ideally, these genetic changes would be specific point mutations that occur early in the tumor cascade, prior to the development of a clinically significant tumor. To identify these markers, precise histopathologic and genetic tumor models must be described. Early candidate markers include p53 point mutations in squamous cell carcinoma of the aerodigestive tract.

Original languageEnglish (US)
Pages (from-to)184-187
Number of pages4
JournalJournal of cellular biochemistry
Issue numberS17F
StatePublished - 1993


  • Tumor models
  • molecular markers
  • oncogenic mutations
  • p53

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology


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