Carcinogenesis and the hypothesis of phylogenetic reversion. Export

@article{citeulike:2739961, abstract = {Chemoprevention must target early molecular events involved in malignant transformation. The sequence of events leading from a normally functioning interphase cell to an uncontrolled tumor cell is only partially understood, impeding systematic design of chemopreventive agents. The respective roles of mutagenic and epigenetic mechanisms have not been definitively established. Also, traditional models do not appear to incorporate cellular response to events leading to carcinogenesis. A perspective on system response offered by complexity science elucidates the roles of feedback and control in maintaining functional stability during carcinogenesis. Carcinogenesis is seen as a process of epigenetic redifferentiation resulting in a cell behaving like an archetypal karyocyte free of growth restraints (phylogenetic reversion). Genes that evolved during the development of multicellular organisms, restraining uncontrolled growth and regulating intercell communication may be systematically silenced during carcinogenesis. The formation of heterochromatin, which results in epigenetic silencing by hypermethylation in CpG-dense islands, finds expression in the nuclear chromatin pattern. Karyometry is an integrating biomarker of chromatin pattern information that accommodates the possibility of multiple, differently ordered pathways and provides exquisite sensitivity, allowing detection of very early transformation events. Its use can monitor the impact of chemopreventive agents on the earliest events in progression to cancer.}, address = {Optical Sciences Center and Arizona Cancer Center, Division of Epidemiology and Arizona Cancer Center, University of Arizona, Tucson, Arizona 85724, USA. jrangerm@azcc.arizona.edu}, author = {Bartels, P. H. and Ranger-Moore, J. and Alberts, D. and Hess, L. and Scarpelli, M. and Montironi, R.}, citeulike-article-id = {2739961}, citeulike-linkout-0 = {http://view.ncbi.nlm.nih.gov/pubmed/17067006}, citeulike-linkout-1 = {http://www.hubmed.org/display.cgi?uids=17067006}, issn = {0884-6812}, journal = {Analytical and quantitative cytology and histology / the International Academy of Cytology [and] American Society of Cytology}, keywords = {cancer, epigenetics, evolution, hypothesis}, month = {October}, number = {5}, pages = {243--252}, posted-at = {2008-04-30 20:58:59}, priority = {5}, title = {Carcinogenesis and the hypothesis of phylogenetic reversion.}, url = {http://view.ncbi.nlm.nih.gov/pubmed/17067006}, volume = {28}, year = {2006} }

TY - JOUR ID - citeulike:2739961 L3 - citeulike-article-id:2739961 N2 - Chemoprevention must target early molecular events involved in malignant transformation. The sequence of events leading from a normally functioning interphase cell to an uncontrolled tumor cell is only partially understood, impeding systematic design of chemopreventive agents. The respective roles of mutagenic and epigenetic mechanisms have not been definitively established. Also, traditional models do not appear to incorporate cellular response to events leading to carcinogenesis. A perspective on system response offered by complexity science elucidates the roles of feedback and control in maintaining functional stability during carcinogenesis. Carcinogenesis is seen as a process of epigenetic redifferentiation resulting in a cell behaving like an archetypal karyocyte free of growth restraints (phylogenetic reversion). Genes that evolved during the development of multicellular organisms, restraining uncontrolled growth and regulating intercell communication may be systematically silenced during carcinogenesis. The formation of heterochromatin, which results in epigenetic silencing by hypermethylation in CpG-dense islands, finds expression in the nuclear chromatin pattern. Karyometry is an integrating biomarker of chromatin pattern information that accommodates the possibility of multiple, differently ordered pathways and provides exquisite sensitivity, allowing detection of very early transformation events. Its use can monitor the impact of chemopreventive agents on the earliest events in progression to cancer. IS - 5 JF - Analytical and quantitative cytology and histology / the International Academy of Cytology [and] American Society of Cytology SN - 0884-6812 AD - Optical Sciences Center and Arizona Cancer Center, Division of Epidemiology and Arizona Cancer Center, University of Arizona, Tucson, Arizona 85724, USA. jrangerm@azcc.arizona.edu EP - 252 TI - Carcinogenesis and the hypothesis of phylogenetic reversion. VL - 28 SP - 243 KW - cancer KW - epigenetics KW - evolution KW - hypothesis AU - Bartels, PH AU - Ranger-Moore, J AU - Alberts, D AU - Hess, L AU - Scarpelli, M AU - Montironi, R PY - 2006/10// UR - http://view.ncbi.nlm.nih.gov/pubmed/17067006 ER -