Abstract
p53plays a central role in prevention of normal cell from the development of the malignant phenotype. Somatic alterations (mutations, loss of heterozygosity, deletions) in p53are a hallmark of most human cancers and cause defects in normal p53function. However, in the tumors harboring wild-type p53, there are alterations in the regulation of the p53. Thus, understanding why p53is unable to perform its role as a tumor suppressor in these wild-type tumors is very crucial. Germ-line polymorphisms in p53are also anticipated to cause measurable disturbance in p53function. Over-expression as well as polymorphic variants of MDM2might have effects on cancer development. In addition, degradation of p53by E6protein of high risk human papillomavirus is also suggested as one of the mechanisms which attenuate p53responses in oral carcinogenesis. p53has also been demonstrated to mediate cellular responses upon various DNA damaging cancer therapies, importantly, apoptosis. These responses have been implicated in an individual's ability to respond to these cancer therapies. Thus, exploring mechanisms by which normal function of p53is affected in the comprehensive way in oral cancer might aid in the identification of tumor characteristics, prognosis and thus in the development of a new approach to treat the oral cancer.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
