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Cell Hypothesis (cell + hypothesis)
Selected AbstractsCancer stem cell hypothesis in thyroid cancerPATHOLOGY INTERNATIONAL, Issue 9 2006Ping Zhang There is increasing evidence that many types of cancer contain their own stem cells: cancer stem cells, which are characterized by their self-renewing capacity and differentiation ability. Cancer could be regarded as an abnormal organ initiated by cancer stem cells, and cancer stem cells might play a decisive role in tumor initiation and progression. Dysregulation of stem cell self-renewal is a likely requirement for the development of cancer, and stem cells seem more likely to be the transformed target cells in carcinogenesis. This cancer stem cell model has great implications for understanding of oncogenesis and treatment for cancer. Abundant evidence suggests that, parallel to other solid tumors, cancer stem cells also exist in thyroid cancer, although their characteristics are largely unknown to date. The present review will discuss the potential traits of cancer stem cells in thyroid cancer and their transformation targets: stem cells in the thyroid gland. [source] Mathematical model for the cancer stem cell hypothesisCELL PROLIFERATION, Issue 1 2006R. Ganguly Various genes that regulate self-renewal in normal stem cells are also found in cancer stem cells. This implies that cancers can occur because of mutations in normal stem cells and early progenitor cells. A predictive mathematical model based on the cell compartment method is presented here to pose and validate non-intuitive scenarios proposed through the neural cancer stem cell hypothesis. The growths of abnormal (stem and early progenitor) cells from their normal counterparts are ascribed with separate mutation probabilities. Stem cell mutations are found to be more significant for the development of cancer than a similar mutation in the early progenitor cells. The model also predicts that, as previously hypothesized, repeated insult to mature cells increases the formation of abnormal progeny, and hence the risk of cancer. [source] Origin of multifocal carcinomas of the bladder and upper urinary tract: Molecular analysis and clinical implicationsINTERNATIONAL JOURNAL OF UROLOGY, Issue 8 2005TOMONORI HABUCHI Abstract The simultaneous or metachronous development of multifocal tumors with identical or variable histological features in the urothelial tract in a single patient is a well-known characteristic of urothelial cancer. To explain this phenomenon, two distinct concepts have been proposed: the ,field defect' hypothesis according to which urothelial cells in patients are primed to undergo transformation by previous carcinogenic insults and the ,single progenitor cell' hypothesis, which asserts that the multifocal development is caused by the seeding or intraepithelial spread of transformed cells. Results of recent molecular genetic studies support the ,single progenitor cell' hypothesis, and indicate that the genetic and phenotypic diversity observed in multifocal urothelial tumors is a consequence of clonal evolution from a single transformed cell. An understanding of the mechanism of the heterotopic recurrence of urothelial cancer may provide new prospects for early molecular detection and prevention of heterotopic recurrence of urothelial cancer. [source] | ||||||||||