An in vitro carcinogenesis model of human skin keratinocytes has been developed based on the spontaneously immortalized keratinocyte cell line HaCaT. Immortalization, the initial stage in human carcinogenesis in vitro, was induced by ultraviolet-type mutations in the p53 gene followed by further gen
Genetic model of transformation and neoplastic progression in laryngeal epithelium
✍ Scribed by César Álvarez Marcos; Marta Alonso-Guervós; Nuria Rodríguez Prado; Teresa Sampedro Gimeno; Francisco Domínguez Iglesias; Mario Hermsen; José Luis Llorente
- Publisher
- John Wiley and Sons
- Year
- 2011
- Tongue
- English
- Weight
- 702 KB
- Volume
- 33
- Category
- Article
- ISSN
- 1043-3074
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
Background
The aim of this study was to analyze genetic alterations in the transformation‐progression model of laryngeal tumors.
Methods
Copy number changes of 37 genes were analyzed by multiple ligation‐dependent probe amplification (MLPA) in 94 tissue samples.
Results
In the smoker normal mucosa group TP53 loss was predominant, whereas in the precursor lesions CDKN2A loss and CDKN2D gain were most frequent. Precursor lesions with progression presented CTNNB1 loss. In the carcinoma group the most common changes were CDKN2A, MLH1, CTNNB1, and CASP6 losses and RECQL4, CCND1, and EMS1 gains. Positive lymph node primary tumors were related to TP53, IL1A, and RB1 losses and STK11 gain. The lymph node metastases differed from their corresponding primary tumor in LMNA, RECQL4, and IGF1R losses, and N33 and CDKN2D gains.
Conclusions
Genetic changes and new key genes were found to be associated with specific steps. We included new steps, not presented in the classic models: normal mucosa tobacco exposed, positive lymph node primary tumor, and corresponding lymph node metastases. © 2010 Wiley Periodicals, Inc. Head Neck, 2011
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