Abstract
Background: The Fanconi Anaemia (FA) pathway is responsible for homologous recombination repair of DNA interstrand crosslink damage. This checkpoint in S-phase of the cell cycle is mediated by ATR (Ataxia Telangiectasia Rad-3) and BRCA-1. The role of this tumour suppressor pathway in early oncogenesis is evaluated in oral dysplasia (OED) which transformed into oral squamous cell carcinoma (OSCC) by evaluating expression of FANC-D2 protein.
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