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Review
. 2004 Feb;25(1):31-7.
doi: 10.1007/s00292-003-0673-2.

[Phosphoinositide 3-kinase (PI3-K) expression. Tumorigenesis of epithelial carcinoma of the mouth]

[Article in German]
U Stahl  1 , J Wenk, F Wagener, J Woenckhaus, U Gamerdinger, A Battmann, T Dreyer
Affiliations
Review

[Phosphoinositide 3-kinase (PI3-K) expression. Tumorigenesis of epithelial carcinoma of the mouth]

[Article in German]
U Stahl et al. Pathologe. 2004 Feb.

Abstract

Phosphoinositide 3-kinase (PI3-K) is a heterodimeric enzyme involved in the regulation of mitogenesis, apoptosis, cell adhesion, and motility. PI3-K was suggested as a protooncogene in human cancer. To determine the expression of PI3-K during cancerogenesis and tumor invasion of HNSCC, we investigated normal and dysplastic epithelium of the oral cavity, squamous cell carcinoma and lymph node metastasis by immunohistochemistry. The strongest immunoreactivity for p85alpha and p110alpha was found in invasive tumors and their metastases. Carcinomas in situ showed a focal positivity. Dysplasias and normal epithelium reacted predominantly negatively. The PI3-K inhibitor LY294002 inhibited proliferation and invasion of the HNSCC cell line CAL-27 and induced apoptosis in vitro. Our data suggest PI3-K as a marker of malignancy and tumor invasion. We suggest including PI3-K in the multistep carcinogenesis model of HNSCC. In addition, PI3-K is a potential target for pharmacological intervention.

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References

    1. Cell. 1997 May 2;89(3):457-67 - PubMed
    1. Pathol Res Pract. 2003;199(6):391-7 - PubMed
    1. J Biol Chem. 2002 Nov 1;277(44):41556-62 - PubMed
    1. Carcinogenesis. 2002 Oct;23(10):1759-65 - PubMed
    1. Langenbecks Arch Surg. 2001 Jul;386(4):293-301 - PubMed

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