Genetic/epigenetic signatures of radiation-induced thyroid cancer in post-Chernobyl samples

Ahmed Kamar ElZaman Mona


Willems Luc, (ULg),

SCK•CEN Mentor

Derradji Hanane
+32 14 33 21 51

SCK•CEN Co-mentor

Baatout Sarah
+32 14 33 27 29

Expert group


PhD started


Short project description

The increase of thyroid cancer as a consequence of the Chernobyl accident caused a passionate societal debate on the risk of developing thyroid cancer after low dose exposure. Recently, the Fukushima accident re-launched the questioning about the consequences of both acute external radiation exposure (at low doses) or internal contamination by radionuclides, which could be present in the environment.

Either external radiation exposure or contamination by 131I during childhood is a well demonstrated pro-tumourigenic factor for thyroid tissues. Epidemiologic studies showed an increased risk to develop thyroid cancer, significant for doses as low as 0.1Gy (1). The reported excess relative risk (ERR) of thyroid cancer after exposure to radiation is the highest after exposure during childhood and varies with age at exposure, gender and other factors (2,3).

For radiation protection purposes, a linear non-threshold model is applied to extrapolate the risk observed from high dose exposure to low doses (4,5). However, for doses lower than 100 mSv, the risk estimate becomes so low that it falls outside the limits of conventional epidemiology studies. Therefore, research in molecular epidemiology in the low dose region is considered of particular interest (6). At low doses, only a very low number of radiation-induced thyroid tumours would be expected and this number would be masked by the high number of sporadic tumours (Representing 3.8% of all new cancer cases). The same can be expected in long-term follow-up of exposed populations once the frequency of radiation-induced thyroid tumours decreases with time and starts then to be masked by the increase of tumours due to ageing.

Until now, classical epidemiology studies have no tools to discriminate between sporadic and radiation induced thyroid cancer at low doses. Therefore, a better knowledge of radiation-induced thyroid tumourigenesis and the development of innovative tools for a case-by-case molecular epidemiology will allow an appropriate management of medically, occupationally and accidentally exposed populations.

Full references:

  1. Ron et al., Thyroid cancer after exposure to external radiation: a pooled analysis of seven studies. Radiat Res. 1995 Mar;141(3):259-77.
  2. Ron, Thyroid cancer incidence among people living in areas contaminated by radiation from the Chernobyl accident. Health Phys. 2007 Nov;93(5):502-11.
  3. Cardis et al., The Chernobyl accident--an epidemiological perspective. Clin Oncol. 2011 May;23(4):251-60.
  4. Land, Low-dose extrapolation of radiation health risks: some implications of uncertainty for radiation protection at low doses. Health Phys. 2009, Nov;97(5):407-15.
  5. Mobbs et al., Risks from ionising radiation: an HPA viewpoint paper for Safegrounds. J Radiol Prot. 2011 Sep;31(3):289-307.
  6. Christodouleas et al., Short-term and long-term health risks of nuclear-power-plant accidents. N Engl J Med. 2011 Jun 16;364(24):2334-41.



The overall objectives of this PhD proposal is to equip classical epidemiology with sensitive and new molecular tools (genetic and epigenetic signatures) to discriminate radiation-induced thyroid tumours from sporadic counterparts and to investigate further the molecular mechanisms underlying radiation-induced thyroid cancer. To achieve these overall objectives, specific objectives are formulated:

  1. Identification of new discriminating signatures of radiation-induced thyroid cancer at the transcriptomic (alternative splicing) and epigenetic (methylation) levels
  2. Identification of genetic and epigenetic signatures of radiation-exposure
  3. Investigation of the link between initial radiation stress and the development of thyroid cancer
  4. Study of the influence of specific genes on thyroid cancer risk development through functional studies using in vitro and in vivo models
  5. Analysis of DNA repair efficiency in human thyroid cells following radiation exposure