The incidence of thyroid cancer is currently on the rise worldwide. This could be attributed to advances in screening technologies that enables the detection of small tumors, increased exposure to Ionizing Radiation (IR) for medical purposes and to the persisting Iodine Deficiency (ID) worldwide health problem. IR and ID are two risk factors of thyroid cancer that can influence the development of thyroid cancer as seen in epidemiological studies after the Chernobyl nuclear accident. However, the molecular mechanisms from combined IR and ID are unknown and hence the need for our study. Our hypothesis is that low dose IR and ID would have an additive negative effect on thyrocytes via the induction of higher levels of oxidative stress, potentially leading to activation of precancerous pathways. Our data indicates that PCCL3 cells are resistant to ID and IR, especially at low doses as we observed cell death mostly at intermediate and high doses after 48 and 72 hours. Furthermore, we observed no significant DNA damage at all doses. Apparently, the cell death observed is not enough to stop cell division as we observed enhanced cell proliferation. However, the mechanisms behind this potential proliferation are still unknown. Based on these data, we can conclude that PCCL3 cell line are highly resistant to the double stress of IR and ID at low doses.
|Qualification||Master of Science|
|State||Published - 9 Jun 2017|