Radiation-induced molecular modulations in thyroid cells cultured under iodine-deficiency

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@phdthesis{b8d50f3be1ad40b28e8e7fc302434725,
title = "Radiation-induced molecular modulations in thyroid cells cultured under iodine-deficiency",
abstract = "Iodine Deficiency (ID) and Ionizing Radiation (IR) are known risk factors for thyroid cancer, however there is little knowledge on their combined effects on thyroid cells especially when considering low radiation doses. To investigate their combined effects, a normal thyroid cells were subjected to low, intermediate and high doses of radiation under iodine sufficient or deficient condition, and different endpoints were investigated: Apoptosis/cell death, ROS production, DNA damage and precancerous proteins expression. The co-treatment induced apoptosis only at high dose of radiation. After co-treatment, activation of markers of apoptosis (active caspase 3), cell survival (NF-κB p65 and pIKKa), cell growth (STAT-3) and cell cycle regulator (Cyclin-D1) were only observed at the highest dose of radiation. In addition, the co-treatment increased ROS production in a dose dependent manner and induced DNA damage starting from 0.1 Gy. These data suggest that thyroid cells are relatively resistant to apoptosis, and show little DNA damage as induced by the co-treatment even when the latter involves intermediate or high doses of radiation. It should be noted that the majority of the cells remained alive after the co-treatment and this population may bear chromosomal aberrations of cancer related genes which may promote their malignant transformation.",
keywords = "Thyroid cancer- Radiation-Iodine deficiency- apoptosis- DNA damage- ROS- Precancerous pathways",
author = "Raghda Ramadan and Hanane Derradji and Sarah Baatout",
note = "Score=2",
year = "2015",
month = "6",
day = "9",
language = "English",
publisher = "UHasselt - Universiteit Hasselt",
school = "Uhasselt - Hasselt University",

}

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TY - THES

T1 - Radiation-induced molecular modulations in thyroid cells cultured under iodine-deficiency

AU - Ramadan, Raghda

A2 - Derradji, Hanane

A2 - Baatout, Sarah

N1 - Score=2

PY - 2015/6/9

Y1 - 2015/6/9

N2 - Iodine Deficiency (ID) and Ionizing Radiation (IR) are known risk factors for thyroid cancer, however there is little knowledge on their combined effects on thyroid cells especially when considering low radiation doses. To investigate their combined effects, a normal thyroid cells were subjected to low, intermediate and high doses of radiation under iodine sufficient or deficient condition, and different endpoints were investigated: Apoptosis/cell death, ROS production, DNA damage and precancerous proteins expression. The co-treatment induced apoptosis only at high dose of radiation. After co-treatment, activation of markers of apoptosis (active caspase 3), cell survival (NF-κB p65 and pIKKa), cell growth (STAT-3) and cell cycle regulator (Cyclin-D1) were only observed at the highest dose of radiation. In addition, the co-treatment increased ROS production in a dose dependent manner and induced DNA damage starting from 0.1 Gy. These data suggest that thyroid cells are relatively resistant to apoptosis, and show little DNA damage as induced by the co-treatment even when the latter involves intermediate or high doses of radiation. It should be noted that the majority of the cells remained alive after the co-treatment and this population may bear chromosomal aberrations of cancer related genes which may promote their malignant transformation.

AB - Iodine Deficiency (ID) and Ionizing Radiation (IR) are known risk factors for thyroid cancer, however there is little knowledge on their combined effects on thyroid cells especially when considering low radiation doses. To investigate their combined effects, a normal thyroid cells were subjected to low, intermediate and high doses of radiation under iodine sufficient or deficient condition, and different endpoints were investigated: Apoptosis/cell death, ROS production, DNA damage and precancerous proteins expression. The co-treatment induced apoptosis only at high dose of radiation. After co-treatment, activation of markers of apoptosis (active caspase 3), cell survival (NF-κB p65 and pIKKa), cell growth (STAT-3) and cell cycle regulator (Cyclin-D1) were only observed at the highest dose of radiation. In addition, the co-treatment increased ROS production in a dose dependent manner and induced DNA damage starting from 0.1 Gy. These data suggest that thyroid cells are relatively resistant to apoptosis, and show little DNA damage as induced by the co-treatment even when the latter involves intermediate or high doses of radiation. It should be noted that the majority of the cells remained alive after the co-treatment and this population may bear chromosomal aberrations of cancer related genes which may promote their malignant transformation.

KW - Thyroid cancer- Radiation-Iodine deficiency- apoptosis- DNA damage- ROS- Precancerous pathways

UR - http://ecm.sckcen.be/OTCS/llisapi.dll/open/ezp_139704

UR - http://knowledgecentre.sckcen.be/so2/bibref/12706

M3 - Master's thesis

PB - UHasselt - Universiteit Hasselt

CY - Hasselt, Belgium

ER -

ID: 133024