Differentiation arrest by autologously replicating DNA loops formed along differentiation pathway: an hypothesis of carcinogenesis.
The current hypothesis attempts to explain tumor development from the perspective of deoxyribonucleic acid structural changes rather than mutational alterations of single or multiple genes. The hypothesis postulates that stable deoxyribonucleic acid loops capable of autologous replication, translation and expression cause cell-differentiation arrest and contribute to the carcinogenesis and various abnormal biological behaviors of tumor. The formation of deoxyribonucleic acid loops at particular steps along the differentiation pathway determines tumor phenotype, grade and behavior. The outcome of deoxyribonucleic acid loop-formation in a cell is highly affected by the differentiation signals imposed by the cell's differentiation microenvironment which is considered as a very important regulatory factor during tumor development in this hypothesis. The incompatibility of adhesion molecules between tumor cells and surrounding normal cells is proposed in this hypothesis as a major reason for separation of tumor cells from primary lesions and thus metastasis. This hypothesis also postulates that tumor invasion is caused by the expression of proteins related to the transient invasive phenotype of normal cells in physiologic process that is controlled by the genes within autologous deoxyribonucleic acid loops.
Xue
B H
BH
Department of Medicine, Loyola University Medical Center, Maywood, IL 60153, USA.
D000818:Animals; D002454:Cell Differentiation; D002471:Cell Transformation, Neoplastic; D004247:DNA / Q000737:chemistry / Q000378:metabolism; D004261:DNA Replication; D015870:Gene Expression; D006801:Humans; D008954:Models, Biological; D009361:Neoplasm Invasiveness; D009362:Neoplasm Metastasis; D009369:Neoplasms / Q000235:genetics* / Q000473:pathology* / Q000503:physiopathology; D010641:Phenotype
D004247:DNA