Status and expression of the p16INK4 gene in human thyroid tumors and thyroid‐tumor cell lines

• Published in: International journal of cancer Vol. 67; no. 1; pp. 29 - 34
• Main Authors: Calabrò, Viola, Strazzullo, Maria, La Mantia, Girolama, Fedele, Monica, Paulin, Christian, Fusco, Alfredo, Lania, Luigi
• Format: Journal Article
• Language: English
• Published: New York Wiley Subscription Services, Inc., A Wiley Company 03-07-1996; Wiley-Liss
• Subjects: Amino Acid Sequence; Base Sequence; Biological and medical sciences; Carrier Proteins - analysis; Carrier Proteins - genetics; Cell Cycle Proteins; Cyclin-Dependent Kinase Inhibitor p15; Cyclin-Dependent Kinase Inhibitor p16; Endocrinopathies; Genes, Tumor Suppressor; Humans; Malignant tumors; Medical sciences; Molecular Sequence Data; Mutation; Polymerase Chain Reaction; RNA, Messenger - analysis; Thyroid Neoplasms - genetics; Thyroid. Thyroid axis (diseases); Tumor Cells, Cultured; Tumor Suppressor Proteins; Endocrinopathy; Human; Carcinoma; Pathogenesis; Thyroid diseases; Thyroid gland; Malignant tumor; Adenoma; Gene expression; Established cell line; Deletion; Benign neoplasm; Mutation; Tumor suppressor gene
• ISSN: 0020-7136; 1097-0215
• DOI: 10.1002/(SICI)1097-0215(19960703)67:1<29::AID-IJC7>3.0.CO;2-1

The p16INK4 tumor‐suppressor gene (also known as CDKN2, CDK41 and MTSI) encodes a negative regulator of the cell cycle. This gene, located in 9p21, is mutated or homozygously deleted in a high percentage of tumor cell lines and specific types of primary tumors. We have examined the status of the p16INK4 gene in 31 thyroid tumors and 7 thyroid cell lines. No DNA abnormalities were found in primary tumors. Conversely, p16INK4 gene structural alterations, deletions and point mutations were found in 4 thyroid cell lines. The expression of the 2 different p16INK4 mRNAs, the p16α and p16β transcripts, was determined by RNA‐PCR experiments. All the primary thyroid tumors expressed the β transcript, while the p16α was barely detectable. The thyroid cell lines always expressed the p16β transcript, while the α transcript was absent or, whenever present, coded for a mutated form of the p16INK4 gene product. Taken together, our results suggest that loss of p16INK4 function is not directly involved in the process of thyroid‐tumor development, but it probably gives cells in tissue culture a selective growth advantage. © 1996 Wiley‐Liss, Inc.