title: Relative quantification of PIK3CA gene expression level in fine-needle aspiration biopsy thyroid specimens collected from patients with papillary thyroid carcinoma and non-toxic goitre by real-time RT-PCR.
abstract: BACKGROUND
  Recent studies have shown that the phosphatidylinositol 3-kinase (PI3K) signaling pathway is important regulator of many cellular events, including apoptosis, proliferation and motility. PI3K pathway alterations (PIK3CA gene mutations and/or amplification) have been observed in various human tumours. In the majority of diagnosed cases, mutations are localized in one of the three "hot spots" in the gene, responsible for coding catalytic subunit α of class I PI3K (PIK3CA). Mutations and amplification of PIK3CA gene are characteristic for thyroid cancer, as well.
  
  
  METHODS
  The aim of our study was to examine a gene expression level of PIK3CA in fine-needle aspiration biopsy (FNAB) thyroid specimens in two types of thyroid lesions, papillary thyroid carcinoma (PTC) and non-toxic goitre (NTG). Following conventional cytological examination, 42 thyroid FNAB specimens, received from patients with PTC (n = 20) and NTG (n = 22), were quantitatively evaluated regarding PIK3CA expression level by real-time PCR in the ABI PRISM® 7500 Sequence Detection System.
  
  
  RESULTS
  Significantly higher expression level (RQ) of PIK3CA in PTC group has been noted in comparison with NTG group (p < 0.05).
  
  
  CONCLUSIONS
  These observations may suggest role of PIK3CA alterations in PTC carcinogenesis.
authors.affiliation: Department of Endocrinology and Metabolic Diseases, Medical University of Lodz, Polish Mother's Memorial Hospital - Research Institute, Lodz, Poland. kacha80@poczta.fm.
authors.forename: Katarzyna
authors.initials: K
authors.lastname: Wojciechowska-Durczyńska
authors.forename: Kinga
authors.initials: K
authors.lastname: Krawczyk-Rusiecka
authors.forename: Anna
authors.initials: A
authors.lastname: Cyniak-Magierska
authors.forename: Arkadiusz
authors.initials: A
authors.lastname: Zygmunt
authors.forename: Elzbieta
authors.initials: E
authors.lastname: Gałecka
authors.forename: Andrzej
authors.initials: A
authors.lastname: Lewiński
references.citation: Nat Genet. 1999 Jan;21(1):99-102
references.pmid: 9916799
references.citation: Cell Cycle. 2004 Oct;3(10):1221-4
references.pmid: 15467468
references.citation: J Clin Endocrinol Metab. 2005 Aug;90(8):4688-93
references.pmid: 15928251
references.citation: Cancer Biol Ther. 2004 Aug;3(8):772-5
references.pmid: 15254419
references.citation: Cancer Res. 2005 Nov 15;65(22):10199-207
references.pmid: 16288007
references.citation: Br J Cancer. 2006 Feb 27;94(4):455-9
references.pmid: 16449998
references.citation: Curr Opin Oncol. 2006 Jan;18(1):77-82
references.pmid: 16357568
references.citation: J Clin Endocrinol Metab. 2008 Feb;93(2):611-8
references.pmid: 18000091
references.citation: Endocr J. 2003 Feb;50(1):77-83
references.pmid: 12733712
references.citation: J Clin Endocrinol Metab. 2007 Jun;92(6):2387-90
references.pmid: 17426084
references.citation: Trends Biochem Sci. 2007 Oct;32(10):450-6
references.pmid: 17920279
references.citation: Clin Cancer Res. 2007 Feb 15;13(4):1161-70
references.pmid: 17317825
references.citation: Trends Biochem Sci. 2007 Jul;32(7):342-9
references.pmid: 17561399
references.citation: Thyroid. 2010 Jul;20(7):697-706
references.pmid: 20578891
references.citation: Oncogene. 2000 May 25;19(23):2739-44
references.pmid: 10851074