Absence of PTEN/MMAC1 gene mutations in lung adenocarcinomas induced by N-nitrosobis(2-hydroxypropyl)amine in rats

T Tsujiuchi1, Y Sasaki, M Tsutsumi

  • 1Department of Oncological Pathology, Cancer Center, Nara Medical University, Kashihara, Nara 634-8521, Japan. ttujiuch@nmu-gw.naramed-u.ac.jp

Cancer Letters
|January 9, 2001
PubMed

Insights

Investigating the phosphatase and tensin homolog deleted on chromosome ten (PTEN) gene in rat lung adenocarcinomas revealed no mutations. These findings suggest PTEN alterations are not involved in BHP-induced lung cancer development.

Area of Science:

  • Oncology
  • Molecular Biology
  • Toxicology

Background:

  • The phosphatase and tensin homolog deleted on chromosome ten (PTEN) gene is a critical tumor suppressor.
  • PTEN mutations are implicated in various human cancers, but its role in chemically induced lung adenocarcinomas is less understood.

Purpose of the Study:

  • To investigate mutations and expression alterations of the PTEN/MMAC1 gene in N-nitrosobis(2-hydroxypropyl)amine (BHP)-induced rat lung adenocarcinomas.

Main Methods:

  • Male Wistar rats were exposed to BHP in drinking water for 12 weeks.
  • Total RNA was extracted from 15 induced lung adenocarcinomas.
  • PTEN/MMAC1 gene mutations were analyzed using reverse transcription-polymerase chain reaction-restriction-single-strand conformation polymorphism (RT-PCR-SSCP).

Main Results:

  • No mutations in the PTEN/MMAC1 gene were detected in any of the analyzed lung adenocarcinomas.
  • Loss or decrease in PTEN/MMAC1 mRNA expression was also not observed in any of the samples.

Conclusions:

  • Alterations in the PTEN/MMAC1 gene do not appear to play a significant role in the development of BHP-induced lung adenocarcinomas in this rat model.
  • Further research may be needed to explore other genetic or molecular pathways involved in this specific cancer model.

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