Different mutational characteristics of TSG in cell lines and surgical specimens
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- 作者：Ewelina Stoczynska-Fidelus (1)
Michal Bienkowski (2)
Marcin Pacholczyk (3)
Marta Winiecka-Klimek (1)
Mateusz Banaszczyk (1)
Jolanta Zieba (1)
Grzegorz Bieniek (4)
Sylwester Piaskowski (1)
Piotr Rieske (1) - 关键词：Tumor suppressor genes ; Quasi ; sufficiency ; Three hits hypothesis ; Two hits hypothesis
- 刊名：Tumor Biology
- 出版年：2014
- 出版时间：November 2014
- 年：2014
- 卷：35
- 期：11
- 页码：11311-11318
- 全文大小：331 KB
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Michal Bienkowski (2)
Marcin Pacholczyk (3)
Marta Winiecka-Klimek (1)
Mateusz Banaszczyk (1)
Jolanta Zieba (1)
Grzegorz Bieniek (4)
Sylwester Piaskowski (1)
Piotr Rieske (1)
1. Department of Tumor Biology, Medical University of Lodz, Lodz, Poland
2. Department of Molecular Pathology and Neuropathology, Medical University of Lodz, Lodz, Poland
3. Institute of Automatic Control, Silesian University of Technology, Gliwice, Poland
4. Department of Orthopedics and Traumatology, Pabianice Medical Center Ltd., Pabianice, Poland - ISSN：1423-0380
文摘
One of the most crucial concerns of cancer research pertains to the differences between the neoplastic cells in tumor specimens in vivo and their counterparts in cell lines. The huge amount of results deposited in cancer genetic databases allows to address this issue from a wider perspective. Our analysis of the Sanger Institute Catalog Of Somatic Mutations In Cancer (COSMIC) database v61 showed a lower percentage of homozygous mutations in a group of tumor suppressor genes in surgical samples (in vivo) in comparison to their frequency in cell lines (in vitro). Similarly, the mutations resulting in the lack of protein (e.g., nonsense mutations or whole gene deletions) of several tumor suppressor genes (TSGs) were more frequently observed in vitro than in vivo. In this article, we suggest two potential explanations of these data. Firstly, TSG heterozygous mutations resulting in the modified protein (e.g., missense mutations) may be gradually (when the specific molecular context is achieved) changed to homozygous mutations resulting in the lack of protein during carcinogenesis. Secondly, among different independent pathways of tumorigenesis, those leading to homozygous nonsense mutations are characteristic for cells which are more efficiently stabilized in vitro. To conclude, these observations may be interesting for researchers working with cell line in vitro models illustrating the extent to which they reflect the tumors in vivo.