Absence of frameshift mutations in the bax gene in renal cell cancer (RCC) and transitional cell cancer (TCC)

Anticancer Res. 1998 May-Jun;18(3A):1655-9.

Abstract

Background: Bax protein, a member of the Bcl-2 family, regulates the apoptotic pathway that involves both Bcl-2 and p53. bax mutations are found in hematological malignancies, colon cancer with microsatellite mutator phenotype, and some other cancers. We evaluated the possibility that Bax functions as a TCC or RCC tumor suppressor gene.

Materials and methods: Using Western blot and polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) we looked for somatic mutations in a tract of eight deoxyguanosines (G)8 within third exon of bax in TCC and RCC cell lines and tumor specimens.

Results: We failed to reveal genetic alterations, at least in this specific region of bax gene in urological cancers.

Conclusion: Alterations of bax, at least at investigated specific region, do not play considerable role in RCC or TCC tumorigenesis.

MeSH terms

  • Adult
  • Aged
  • Aged, 80 and over
  • Carcinoma, Renal Cell / genetics*
  • Carcinoma, Renal Cell / pathology
  • Carcinoma, Transitional Cell / genetics*
  • Carcinoma, Transitional Cell / pathology
  • Cell Line
  • Child, Preschool
  • Female
  • Frameshift Mutation
  • Genes, Tumor Suppressor
  • Humans
  • Kidney Neoplasms / genetics*
  • Kidney Neoplasms / pathology
  • Male
  • Middle Aged
  • Neoplasm Staging
  • Polymerase Chain Reaction
  • Polymorphism, Single-Stranded Conformational*
  • Proto-Oncogene Proteins / genetics*
  • Proto-Oncogene Proteins c-bcl-2*
  • Proto-Oncogenes*
  • Tumor Cells, Cultured
  • Urinary Bladder Neoplasms / genetics*
  • Urinary Bladder Neoplasms / pathology
  • bcl-2-Associated X Protein

Substances

  • BAX protein, human
  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-bcl-2
  • bcl-2-Associated X Protein