Thyroid cancer is the most
prevalent endocrine malignancy with increasing incidence rate in recent years.
Females are more likely to have thyroid cancer at a ratio of 3:1. The main risk
factors of thyroid cancer are genetic factor, environmental factors and
exposure to ionization radiations at childhood.
Exposure to ionization radiations
cause single strand and double strand breaks and can produce chromosomal
damage and release of reactive oxygen species that causes genomic
instability. In human there are many pathways to repair this DNA damage, out of
which double strand break repair (DSBR) pathway is an important and preferred
pathway to repair such lesion.
This pathway has two types,
non-homologous end joining (NHEJ) and homologous recombinant repair (HRR)
pathway. HRR is an error prone pathway which is template specific and
considered to play a significant role in the repair of DNA double strand damage
produced by ionization radiations. HR encompasses many genes, but major role is
performed by RAD51 and RAD51-like genes such as XRCC2 and XRCC3.
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