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
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...
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Published in | Thyroid research Vol. 3; no. 1; p. 5 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
England
BioMed Central Ltd
30.08.2010
BioMed Central BMC |
Subjects | |
Online Access | Get full text |
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Summary: | 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.
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.
Significantly higher expression level (RQ) of PIK3CA in PTC group has been noted in comparison with NTG group (p < 0.05).
These observations may suggest role of PIK3CA alterations in PTC carcinogenesis. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 |
ISSN: | 1756-6614 1756-6614 |
DOI: | 10.1186/1756-6614-3-5 |