Senescence as a modulator of oral squamous cell carcinoma development

Summary Senescence of somatic cells in vitro can occur through the gradual erosion of the chromosomal telomeres following multiple rounds of cell division, or more acutely following cellular stresses connected with oncogene activation, tumour suppressor loss, ageing and migration. These various form...

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Bibliographic Details
Published in:Oral oncology 2010-12, Vol.46 (12), p.840-853
Main Author: Parkinson, E. Kenneth
Format: Article
Language:English
Subjects:
Biological and medical sciences
Carcinoma, Squamous Cell - genetics
Carcinoma, Squamous Cell - pathology
Cell Line, Tumor
Cellular Senescence - genetics
Cellular Senescence - physiology
Dermatology
Dysplasia
Female
Genes, p16 - physiology
Hematology, Oncology and Palliative Medicine
Humans
Keratinocyte
Male
Medical sciences
Mouth Neoplasms - genetics
Mouth Neoplasms - pathology
Otolaryngology
Otorhinolaryngology. Stomatology
Senescence
Squamous cell carcinoma
Telomere
Tumor Suppressor Protein p53 - genetics
Tumor Suppressor Protein p53 - physiology
Tumors
Tumors of the skin and soft tissue. Premalignant lesions
Upper respiratory tract, upper alimentary tract, paranasal sinuses, salivary glands: diseases, semeiology
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Summary:Summary Senescence of somatic cells in vitro can occur through the gradual erosion of the chromosomal telomeres following multiple rounds of cell division, or more acutely following cellular stresses connected with oncogene activation, tumour suppressor loss, ageing and migration. These various forms of senescence are associated with the activation of DNA damage checkpoints, the over-expression of p16INK4A and the secretion of cytokines, all of which are detected in pre-malignant lesions but muted upon malignant conversion. The various senescence signals are integrated by p16INK4A and p53 to produce the permanent cell cycle arrest associated with senescence. Both pRB/p16INK4A and p53 are dysfunctional in many cancers, including the most common type of oral cancer, squamous cell carcinoma (OSCC) and other evidence is accumulating in support of the idea that senescence acts as a barrier to tumour development and/or progression. However, senescence of the non-epithelial component of developing human tumours has been shown to enhance growth and invasion of the pre-malignant epithelial component and so senescence may well enhance cancer as well as suppress it depending on the context.
ISSN:1368-8375
1879-0593
DOI:10.1016/j.oraloncology.2009.09.009