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P53 mutation predicts intravesical adriamycin instillation failure in superficial transitional cell carcinoma of bladder.

AbstractBACKGROUND:
We studied whether p53 status has any predictive value on the outcome of intravesical adriamycin (ADR) instillation for superficial transitional cell carcinoma (TCC) of the bladder.
MATERIALS AND METHODS:
Paraffin-embedded specimens were obtained from 70 consecutive patients by transurethral resection (TUR). All patients received intravesical instillation with either Epirubicin (n = 45) or Pirarubicin (n = 25). P53 mutation and overexpression were examined for single-strand conformation polymorphism (SSCP) and immunohistochemistry (IHC), respectively.
RESULTS:
In 18.2% of tumors, mutation was observed, including exon 5, 6 or 7. P53 overexpression was observed in 22.9% of tumors. High concordance between SSCP and IHC was shown (p = 0.0001), while there was a certain number of discrepant cases. The recurrence-free rate was significantly different between the group with and without p53 mutation, but not stage, grade or p53 IHC.
CONCLUSION:
P53 mutation predicts the failure of intravesical ADR instillation. Aggressive therapeutic approaches following initial TUR should be considered for patients with p53 mutation.
AuthorsKoji Shiraishi, Satoshi Eguchi, Jun Mohri, Yoriaki Kamiryo
JournalAnticancer research (Anticancer Res) 2003 Jul-Aug Vol. 23 Issue 4 Pg. 3475-8 ISSN: 0250-7005 [Print] Greece
PMID12926093 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Antibiotics, Antineoplastic
  • Tumor Suppressor Protein p53
  • Doxorubicin
Topics
  • Administration, Intravesical
  • Adult
  • Aged
  • Aged, 80 and over
  • Antibiotics, Antineoplastic (administration & dosage)
  • Carcinoma, Transitional Cell (drug therapy, genetics, metabolism)
  • Disease-Free Survival
  • Doxorubicin (administration & dosage)
  • Female
  • Humans
  • Immunohistochemistry
  • Male
  • Middle Aged
  • Mutation
  • Polymorphism, Single-Stranded Conformational
  • Tumor Suppressor Protein p53 (biosynthesis, genetics)
  • Urinary Bladder Neoplasms (drug therapy, genetics, metabolism)

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