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Diagnosis and Pathobiology
Published in Franklyn De Silva, Jane Alcorn, The Elusive Road Towards Effective Cancer Prevention and Treatment, 2023
Franklyn De Silva, Jane Alcorn
All cells of the body generally contain the same genome. However, it is the information stored within the epigenetic code that regulates many aspects of the genome and reveals itself across various physiological, pathological, and developmental stages including cellular/tissue differentiation and lineage commitment [364–366]. Epigenetics, a term coined by Waddington in 1942, is the study of heritable changes in gene expression that occur independently of the basic DNA sequence and results in a phenotype modification without genotype modification [366, 367]. Since genetic material is not physically changed, epigenetic programming guarantees the inheritance of untouched genomic information from parents to offspring [296, 364] The epigenetic code is cell- and tissue-specific, and the literature identifies over 90,000 individual and over 400 different types of epigenetic modifications [368]. Epigenetics plays a seminal role in cancer. The ‘two-hit' model proposed by Knudson suggests cancer initiation follows from the interconnection of independent epimutations (a heritable change in DNA that does not involve an actual DNA mutation) that silence tumor-suppressor genes (the first hit) and deleterious genetic mutations or deletions (the second hit) that disrupt normal cellular processes [369]. Furthermore, in cancer progression, signals from the tumor microenvironment influence cancer epigenomes because stress induced by the tumor environment (e.g., inflammation, hypoxia) and/or by the therapeutic intervention may reshape the chromatin landscape, engendering epigenetic plasticity. This can promote intrinsic cellular reprogramming and cancer stemness, the molecular processes governing the fundamental stem cell properties of self-renewal and propagation of differentiated daughter cells [370, 371]) by way of a slow-cycling or semiquiescent phenotype persister state (where cells are resistant to a wide range of treatments and remain viable under conditions that kill surrounding cells [371]), as well as epithelial-mesenchymal plasticity (i.e., the ability to reversibly switch between a static adherent state and detached mobile state [372]), messenger RNA epitranscriptomic regulation (different RNA modifications such as covalent modifications like methylation that are added to individual nucleotides to regulate the stability, translation, and immunogenicity of RNA molecules [373]), and resistance to therapy [268, 272, 283, 371, 374–376]. Therefore, it is both the nucleotide sequence and these additional epigenetic modifications that regulate the function of the mRNAs transcribed from a given gene [373].
Nomogram prediction of vulnerable periodontal condition before orthodontic treatment in the anterior teeth of Chinese patients with skeletal Class III malocclusion
Published in Acta Odontologica Scandinavica, 2021
Jian Jiao, Wu-Di Jing, Jian-Xia Hou, Xiao-Tong Li, Xiao-Xia Wang, Xiao Xu, Ming-Xin Mao, Li Xu
However, to the best of our knowledge, there was no proper model for assessing the condition of periodontal soft and hard tissues and the risk for periodontal damage before orthodontic treatment. Nomograms enabled calculation of the probability of a specific clinical outcome for an individual patient and facilitate risk estimation, clinical decision-making, and patient communication. We developed simple and easy-to-use prediction nomograms based on multivariate regressions predicting the thin periodontal phenotype and alveolar dehiscence and fenestration. Reasonable clinical decisions, for example whether a phenotype modification therapy is needed, can be made by clinicians according to the model predictions [26].