| Literature DB >> 22359292 |
Qiang Lu1, Dehua Ma, Shuping Zhao.
Abstract
Cervical carcinoma is one of the major causes of death in women worldwide. It is difficult to foresee a dramatic increase in cure rate even with the most optimal combination of cytotoxic drugs, surgery, and radiation; therefore, testing of molecular targeted therapies against this malignancy is highly desirable. Cervical cancer is a multistep process with accumulation of genetic and epigenetic alterations in regulatory genes, leading to activation of oncogenes and inactivation or loss of tumor suppressor genes (TSGs). In the last decade, in addition to genetic alterations, epigenetic inactivation of TSGs by promoter hypermethylation has been recognized as an important and alternative mechanism in tumorigenesis. In cervical cancer, epigenetic alterations can affect the expression of papillomavirus as well as host genes in relation to stages representing the multistep process of carcinogenesis. Here we discuss these epigenetic alterations in cervical cancer focusing on DNA methylation.Entities:
Mesh:
Substances:
Year: 2012 PMID: 22359292 DOI: 10.1007/978-1-61779-612-8_9
Source DB: PubMed Journal: Methods Mol Biol ISSN: 1064-3745