Genomic gain of PIK3CA and increased expression of pI I 0alpha are associated with progression of dysplasia into invasive squamous cell carcinoma

Journal of Pathology

Volumn 198, Issue 3, 2002, Pages 335-342

  Woenckhaus, Joachim ^a   Steger, Klaus ^a   Werner, Eva ^a   Fenic, Irina ^a   Gamerdinger, Ulrike ^a   Dreyer, Thomas ^a   Stahl, Ulrich ^a  

^a JUSTUS LIEBIG UNIVERSITY   (Germany)

Author keywords

Amplification of 3q26; HNSCC; p110 ; PIK3CA; Tumourigenesis

Indexed keywords

FORMALDEHYDE; MESSENGER RNA; PHOSPHATIDYLINOSITOL 3 KINASE; PROTEIN;

ADULT; AGED; ARTICLE; CARCINOGENESIS; CELL NUCLEUS; CHROMOSOME 3Q; CHROMOSOME NUMBER; CLINICAL ARTICLE; CONTROLLED STUDY; DATA ANALYSIS; DYSPLASIA; ENZYME ACTIVATION; ENZYME ACTIVE SITE; FEMALE; FLUORESCENCE IN SITU HYBRIDIZATION; GENE AMPLIFICATION; GENE EXPRESSION; GENE MUTATION; HEAD AND NECK CARCINOMA; HUMAN; HUMAN TISSUE; IMMUNOHISTOCHEMISTRY; INTERPHASE; INVASIVE CARCINOMA; MALE; MALIGNANT NEOPLASTIC DISEASE; MALIGNANT TRANSFORMATION; MORPHOLOGY; PRIORITY JOURNAL; PROTEIN EXPRESSION; SQUAMOUS CELL CARCINOMA; TISSUE FIXATION; TISSUE SECTION; YEAST ARTIFICIAL CHROMOSOME;

1-PHOSPHATIDYLINOSITOL 3-KINASE; ADULT; AGED; CARCINOMA, SQUAMOUS CELL; CHROMOSOME ABERRATIONS; DISEASE PROGRESSION; FEMALE; GENE EXPRESSION REGULATION, NEOPLASTIC; HEAD AND NECK NEOPLASMS; HUMANS; IN SITU HYBRIDIZATION, FLUORESCENCE; MALE; MIDDLE AGED; NEOPLASM INVASIVENESS; NEOPLASM PROTEINS; PRECANCEROUS CONDITIONS; RNA, MESSENGER; RNA, NEOPLASM; TONSIL;

EID: 0036841057     PISSN: 00223417     EISSN: None     Source Type: Journal    
DOI: 10.1002/path.1207     Document Type: Article

References (33)

1. Becker N, Wahrendorf J (eds). In Atlas of Cancer Mortality in the Federal Republic of Germany (3rd edn). Springer-Verlag: New York, 1998; 68-98.
2. Wolff E, Girod S, Liehr T, et al. Oral squamous cell carcinomas are characterized by a rather uniform pattern of genomic imbalances detected by comparative genomic hybridisation. Oral Oncol 1998; 34: 186-190.
3. Bockmühl U, Schwendel A, Dietel M, Petersen I. Distinct patterns of chromosomal alterations in high- and low-grade head and neck squamous cell carcinomas. Cancer Res 1996; 1: 5325-5329.
4. Weber RG, Scheer M, Born IA, et al. Recurrent chromosomal imbalances detected in biopsy material from oral premalignant and malignant lesions by combined tissue microdissection, universal DNA amplification, and comparative genomic hybridization. Am J Pathol 1998; 153: 295-303.
5. Redon R, Muller D, Caulee K, Wanherdrick K, Abecassis J, du Manoir S. A simple specific pattern of chromosomal aberrations at early stages of head and neck squamous cell carcinomas: PIK3CA but not p63 gene as a likely target of 3q26-qter gains. Cancer Res 2001; 15: 4122-4129.
6. Heselmeyer K, Schröck E, du Manoir S, et al. Gains of chromosome 3q define the transition from severe dysplasia to invasive carcinoma of the uterine cervix. Proc Natl Acad Sci U S A 1996; 93: 479-484.
7. Heselmeyer K, Macville M, Schröck E, et al. Advanced-stage cervical carcinoma is defined by a recurrent pattern of chromosomal aberration revealing high genetic instability and consistent gain of chromosome arm 3q. Genes Chromosomes Cancer 1997; 19: 233-240.
8. Balsara BR, Sonoda G, du Manoir S, Siegfried JM, Gabrielson E, Testa JR. Comparative genomic hybridization analysis detects frequent, often high-level, overrepresentation of DNA sequences at 3q, 5p, 7p, and 8q in human non-small cell lung carcinomas. Cancer Res 1997; 1: 2116-2120.
9. Liehr T, Ries J, Wolff E, et al. Gain of DNA copy number on chromosomes 3q26-qter and 5p14-pter is a frequent finding in head and neck squamous cell carcinomas. Int J Mol Med 1998; 2: 173-179.
10. Kettunen E, el-Rifai W, Bjorkqvist AM, et al. A broad amplification pattern at 3q in squamous cell lung cancer - a fluorescence in situ hybridization study. Cancer Genet Cytogenet 2000; 117: 66-70.
11. Bockmühl U, Schluns K, Kuchler I, Petersen S, Petersen I. Genetic imbalances with impact on survival in head and neck cancer patients. Am J Pathol 2000; 157: 369-375.
12. Volinia S, Hiles I, Ormondroyd E, et al. Molecular cloning, cDNA sequence, and chromosomal localisation of the human phosphatidylinositol 3-kinase p110 alpha (PI3KCA) gene. Genomics 1994; 24: 472-477.
13. Keely PJ, Westwick JK, Whitehead IP, Der CJ, Parise LV. Cdc42 and Rac1 induce integrin-mediated cell motility and invasiveness through PI(3)K. Nature 1997; 390: 622-636.
14. Rameh LE, Cantley LC. The role of phosphoinositide 3-kinase lipid products in cell function. J Biol Chem 1999; 26: 8347-8350.
15. Vanhaesebroeck B, Waterfield MD. Signaling by distinct classes of phosphoinositide 3-kinases. Exp Cell Res 1999; 25: 239-254.
16. Shayesteh L, Lu Y, Kuo WL, et al. PIK3CA is implicated as an oncogene in ovarian cancer. Nature Genet 1999; 21: 99-103.
17. Aoki M, Schetter C, Himly M, Batista O, Chang HW, Vogt PK. The catalytic subunit of phosphoinositide 3-kinase: requirements for oncogenicity. J Biol Chem 2000; 275: 6267-6275.
18. Benistant C, Chapuis H, Roche S. A specific function for phosphatidylinositol 3-kinase alpha (p85-p110 alpha) in cell survival and for phosphatidylinositol 3-kinase beta (p85alpha-p110 beta) in de novo DNA synthesis of human colon carcinoma. Oncogene 2000; 19: 5083-5090.
19. Ma YY, Wei SJ, Lin YC, et al. PIK3CA as an oncogene in cervical cancer. Oncogene 2000; 19: 2739-2744.
20. WHO. Histological typing of upper respiratory tract tumors. In International Histological Classification of Tumors, Vol. 19, Shanmugaratnam K, Sobin LH (eds). Springer-Verlag: Geneva, 1978; 27-31.
21. Sobin LH, Wittekind C (eds). TNM classification of Malignant Tumors, 5th edn. Union International Contre le Cancer. Wiley-Liss: New York, 1997.
22. Poetsch M, Woenckhaus C, Dittberner T, Pambor M, Lorenz G, Herrmann FH. Differences in chromosomal aberrations between nodular and superficial spreading malignant melanoma detected by interphase cytogenetics. Lab Invest 1998; 78: 883-888.
23. Jackson MP. Detection of Shiga toxin-producing Shigella dysenteriae type 1 and Escherichia coli by using polymerase chain reaction with incorporation of dioxigenin-11-dUTP. J Clin Microbial 1991; 29: 1910-1914.
24. Lewis FA, Wells M. Detection of virus in infected human tissue by in-situ hybridization. In In-situ Hybridization, a Practical Approach, Wilkinson DG (ed.) Oxford University Press: Oxford, 1992; 121-135.
25. Brzoska PM, Levin NA, Fu KK, et al. Frequent novel DNA copy number increase in squamous cell head and neck tumors. Cancer Res 1995; 15: 3055-3059.
26. Warnakulasuriya S. Lack of molecular markers to predict malignant potential of precancer [editorial; comment]. J Pathol 2000; 190: 407-409.
27. Subo J, Bryne M, Johannessen AC, Kildal W, Danielsen HE, Reith A. Comparison of histological grading and large-scale genomic status (DNA ploidy) as prognostic tools in oral dysplasia. J Pathol 2001; 194: 303-310.
28. Ried T, Heselmeyer-Haddad K, Blegen H, Schrock E, Auer G. Genomic changes defining the genesis, progression, and malignancy potential in solid human tumors: a phenotype/genotype correlation. Genes Chromosomes Cancer 1999; 25: 195-204.
29. Taubald A, Liehr T, Ries J, Girod S, Hassfurter E, Gebhart E. CGH-detected DNA sequence copy number amplifications can be confirmed by interphase-FISH: new possibilities for prognostic approaches in oral squamous cell carcinomas. Int J Mol Med 1998; 2: 555-560.
30. Soder AI, Hoare SF, Muir S, Going JJ, Parkinson EK, Keith WN. Amplification, increased dosage and in situ expression of the telomerase RNA gene in human cancer. Oncogene 1997; 6: 1013-1021.
31. Kaelin WG Jr. The p53 gene family. Oncogene 1999; 18: 7701-7705.
32. Kim NW, Piatyszek MA, Prowse KR, et al. Specific association of human telomerase activity with immortal cells and cancer. Science 1994; 23: 2011-2015.
33. Imoto I, Pimkhaokham A, Fukuda Y, et al. Sno is a probable target for gene amplification at 3q26 in squamous-cell carcinomas of the esophagus. Biochem Biophys Res Commun 2001; 24: 559-565.