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Usage Information

Cyclin D1 overexpression and p53 inactivation immortalize primary oral keratinocytes by a telomerase-independent mechanism
Oliver G. Opitz, Yasir Suliman, William C. Hahn, Hideki Harada, Hubert E. Blum, Anil K. Rustgi
Oliver G. Opitz, Yasir Suliman, William C. Hahn, Hideki Harada, Hubert E. Blum, Anil K. Rustgi
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Article

Cyclin D1 overexpression and p53 inactivation immortalize primary oral keratinocytes by a telomerase-independent mechanism

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Abstract

The immortalization of human cells is a critical step in multistep carcinogenesis. Oral-esophageal carcinomas, a model system to investigate molecular mechanisms underlying squamous carcinogenesis, frequently involve cyclin D1 overexpression and inactivation of the p53 tumor suppressor. Therefore, our goal was to establish the functional role of cyclin D1 overexpression and p53 inactivation in the immortalization of primary human oral squamous epithelial cells (keratinocytes) as an important step toward malignant transformation. Cyclin D1 overexpression alone was found to induce extension of the replicative life span of normal oral keratinocytes, whereas the combination of cyclin D1 overexpression and p53 inactivation led to their immortalization. This study also demonstrates that immortalization of oral keratinocytes can be independent of telomerase activation, involving an alternative pathway of telomere maintenance (ALT).

Authors

Oliver G. Opitz, Yasir Suliman, William C. Hahn, Hideki Harada, Hubert E. Blum, Anil K. Rustgi

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Usage data is cumulative from September 2025 through September 2026.

Usage JCI PMC
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PDF 229 5
Figure 654 0
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Citation downloads 204 0
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Usage information is collected from two different sources: this site (JCI) and Pubmed Central (PMC). JCI information (compiled daily) shows human readership based on methods we employ to screen out robotic usage. PMC information (aggregated monthly) is also similarly screened of robotic usage.

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