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      Epigenetic disruption of cell signaling in nasopharyngeal carcinoma

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          Abstract

          Nasopharyngeal carcinoma (NPC) is a malignancy with remarkable ethnic and geographic distribution in southern China and Southeast Asia. Alternative to genetic changes, aberrant epigenetic events disrupt multiple genes involved in cell signaling pathways through DNA methylation of promoter CpG islands and/or histone modifications. These epigenetic alterations grant cell growth advantage and contribute to the initiation and progression of NPC. In this review, we summarize the epigenetic deregulation of cell signaling in NPC tumorigenesis and highlight the importance of identifying epigenetic cell signaling regulators in NPC research. Developing pharmacologic strategies to reverse the epigenetic-silencing of cell signaling regulators might thus be useful to NPC prevention and therapy.

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          Genetic instabilities in human cancers.

          C Lengauer, K Kinzler, B Vogelstein (1998)
          Whether and how human tumours are genetically unstable has been debated for decades. There is now evidence that most cancers may indeed be genetically unstable, but that the instability exists at two distinct levels. In a small subset of tumours, the instability is observed at the nucleotide level and results in base substitutions or deletions or insertions of a few nucleotides. In most other cancers, the instability is observed at the chromosome level, resulting in losses and gains of whole chromosomes or large portions thereof. Recognition and comparison of these instabilities are leading to new insights into tumour pathogenesis.
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            Ras superfamily GEFs and GAPs: validated and tractable targets for cancer therapy?

            Dominico Vigil, Jacqueline Cherfils, Kent Rossman … (2010)
            There is now considerable and increasing evidence for a causal role for aberrant activity of the Ras superfamily of small GTPases in human cancers. These GTPases function as GDP-GTP-regulated binary switches that control many fundamental cellular processes. A common mechanism of GTPase deregulation in cancer is the deregulated expression and/or activity of their regulatory proteins, guanine nucleotide exchange factors (GEFs) that promote formation of the active GTP-bound state and GTPase-activating proteins (GAPs) that return the GTPase to its GDP-bound inactive state. In this Review, we assess the association of GEFs and GAPs with cancer and their druggability for cancer therapeutics.
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              Cell cycle control and cancer.

              L. H. Hartwell, M B Kastan (1994)
              Multiple genetic changes occur during the evolution of normal cells into cancer cells. This evolution is facilitated in cancer cells by loss of fidelity in the processes that replicate, repair, and segregate the genome. Recent advances in our understanding of the cell cycle reveal how fidelity is normally achieved by the coordinated activity of cyclin-dependent kinases, checkpoint controls, and repair pathways and how this fidelity can be abrogated by specific genetic changes. These insights suggest molecular mechanisms for cellular transformation and may help to identify potential targets for improved cancer therapies.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Chin J Cancer
                Journal ID (iso-abbrev): Chin J Cancer
                Journal ID (publisher-id): CJC
                Title: Chinese Journal of Cancer
                Publisher: Sun Yat-sen University Cancer Center
                ISSN (Print): 1000-467X
                ISSN (Electronic): 1944-446X
                Publication date (Print): April 2011
                Volume: 30
                Issue: 4
                Pages: 231-239
                Affiliations
                [1 ]Shenzhen Key Laboratory of Cancer Nanotechnology, Institute of Biomedical and Health Engineering, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences-CUHK, Shenzhen, Guangdong 518055, P. R. China;
                [2 ]Cancer Epigenetics Laboratory, Sir YK Pao Center for Cancer, Department of Clinical Oncology, The Chinese University of Hong Kong, Hong Kong and CUHK Shenzhen Research Institute, Shenzhen, Guangdong 518057, P. R. China;
                [3 ]Cancer Research Institute, Xiangya School of Medicine, Central South University, Changsha, Hunan 410078, P. R. China.
                Author notes
                Corresponding Author: Qian Tao, Rm 315, Cancer Center, Department of Clinical Oncology, PWH, The Chinese University of Hong Kong, Shatin, Hong Kong. Tel: +852-2632-1340, Fax: +852-2648-8842 Email: qtao@ 123456clo.cuhk.edu.hk .
                Article
                Publisher ID: cjc-30-04-231
                DOI: 10.5732/cjc.011.10080
                PMC ID: 4013349
                PubMed ID: 21439244
                SO-VID: 184b3114-07de-4580-9e90-a6fde44a05ac
                Copyright © Chinese Journal of Cancer
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported License, which allows readers to alter, transform, or build upon the article and then distribute the resulting work under the same or similar license to this one. The work must be attributed back to the original author and commercial use is not permitted without specific permission.

                History
                Date received : 7 March 2011
                Date revision received : 9 March 2011
                Date accepted : 9 March 2011
                Categories
                Subject: Review

                Keywords: epigenetic,cell signaling,nasopharyngeal neoplasm
                Data availability:
                Keywords: epigenetic, cell signaling, nasopharyngeal neoplasm

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