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From the book Polyploidization and Cancer

Polyploidy:
Mechanisms and Cancer Promotion in Hematopoietic and Other Cells

Hao G. Nguyen and Katya Ravid

Polyploidy, the state of having greater than a diploid content of DNA (e.g., tetraploid, octaploid, etc) has been recognized in a large variety of both, plant and animal cells. Human and murine megakaryocytes, hepatocytes, arterial smooth muscle cells and cardiac myocytes, all develop a certain degree of polyploidy during their normal lifespan. In addition, polyploid cells may be found in some tissues under conditions of stress, including uterine smooth muscle during pregnancy, aortic vascular smooth muscle cells during aging and hypertension, beta‑cells in diabetic human or mouse thyroid cells in hyperthyroidism and cells in seminal vesicles with aging. Polyploid cells are also found in malignant tissues in which they are believed to contribute to the development of cells with intermediate DNA content values (e.g., 3n, 4.5n, etc.) (reviewed in refs. 1,2). With the use of micro‑array, researchers have demonstrated that genetically identical yeast strains (Saccharomyces cerevisiae) with differences only in ploidy status (from haploid to tetraploid) display a substantial difference in gene expression, including of the G1 cyclins. This finding has suggested that DNA content per se might affect cellular functions. Currently, the relationships between polyploidy and aneuploidy has not been studied extensively considering the prominent role of genetic instability in tumorigenesis. An understanding of the biochemical, gene expression and signaling pathways that drive normal and abnormal polyploidization could lead to useful insights with respect to novel anti‑cancer therapeutic approaches. The occurrence of polyploidy in normal and transformed cells poses a number of questions. Is polyploidy a protective mechanism upon stress, as suggested, or rather a maladaptive response? What mechanisms or signaling pathways are employed by normal developing polyploid cells (e.g., megakaryocytes) to safeguard them from becoming aneuploid.

Taken from the book

Polyploidization and Cancer

Edited by: Randy Y.C. Poon

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