## Background: D-type cyclins, in association with the cyclin-dependent kinases cdk4 and cdk6, promote progression through the g1 phase of the cell cycle. cdk activity is modulated by inhibitors such as p15ink4b and p16ink4a. loss of function of p15ink4b and p16ink4a (multiple tumor suppressor-i an
Status and expression of the p16INK4 gene in human thyroid tumors and thyroid-tumor cell lines
✍ Scribed by Viola Calabrò; Maria Strazzullo; Girolama La Mantia; Monica Fedele; Christian Paulin; Alfredo Fusco; Luigi Lania
- Publisher
- John Wiley and Sons
- Year
- 1996
- Tongue
- French
- Weight
- 648 KB
- Volume
- 67
- Category
- Article
- ISSN
- 0020-7136
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✦ Synopsis
The p 16INK4 tumor-suppressor gene (also known as CDKNZ, CDK41 and MTSI) encodes a negative regulator of the cell cycle. This gene, located in 9pZ I, 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 p16lNK4 mRNAs, the p Ibo! and p 168 transcripts, was determined by RNA-PCR experiments. All the primary thyroid tumors expressed the 8 transcript, while the p I6a was barely detectable. The thyroid cell lines always expressed the p168 transcript, while the o! transcript was absent or, whenever present, coded for a mutated form of the p16INK4 gene roduct. Taken directly involved in the process of thyroid-tumor development, but it probably gives cells in tissue culture a selective growth advantage. o 1996 Wilq-Liss, Inc. together, our results suggest that loss of pl6INK . Y function is not
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