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Soon, there will be a time where our scholars & colleagues will not be satisfied with general comments on surgical quality outcomes-instead, they will call any physician charlatan who is incapable to quantify his results."-Theodore Billroth 1860 IntroductionSurgeons' efforts to audit post-operative patient outcomes, in order to measure quality of care systematically, have increased over recent years. National Audits, within the National Clinical Audit Patient Outcomes Program (NCAPOP) provide information on quality of surgical care. The annual reports produced by the National Audits produce are accessible to the public. Cardiothoracic surgeons led the modern era of national audit in a major response to the Bristol Royal Infirmary Inquiry into Paediatric Heart Surgery in the 1980's and 1990's (1).

Background: Predicting malignant transformation in oral epithelial dysplasia(OED) is a clinical challenge. The higher rate of malignant transformation in non-smokers supports an endogenous aetiology. Loss of FANCD2 and associated proteins could lead to genomic instability and oncogenesis.Methods: Longitudinal archival samples from 40 individuals with OED from time of diagnosis to the most recent review in 23 stable OED; or until excision of the SCC in 17 unstable OED undergoing malignant transformation. Histopathological reassessment, immunohistochemistry for FANCD2 and Western blotting for phosphorylation/monubiquitination status of ATR, CHK1, FANCD2 and FANCG were undertaken on each tissue sample.Results: Decreased expression of FANCD2 was observed in the diagnostic biopsy of OED lesions which later underwent malignant transformation. Combining the FANCD2 expression scores with histological grading more accurately predicted malignant transformation (p=0.005) than histology alone and correctly predicted malignant transformation in 10/17 initial biopsies. Significantly reduced expression of total FANCD2, pFANCD2, pATR, pCHK-1 and pFANCG were observed in unstable OED.Discussion: There is good evidence that defects in the DNA damage sensing-signalling-repair cascade are associated with malignant transformation in OED. Loss of post-translational modification in FANCD2 and related proteins, was more predictive of malignant transformation when compared to clinicopathological parameters.

Background: Predicting malignant transformation in oral epithelial dysplasia(OED) is a clinical challenge. The higher rate of malignant transformation in non-smokers supports an endogenous aetiology. Loss of FANCD2 and associated proteins could lead to genomic instability and oncogenesis. Patients & Methods: Longitudinal archival samples from 40 individuals with OED from time of diagnosis to the most recent review in 23 stable OED; or until excision of the SCC in 17 unstable OED undergoing malignant transformation. Histopathological reassessment, immunohistochemistry for FANCD2 and Western blotting for phosphorylation/monubiquitination status of ATR, CHK1, FANCD2 and FANCG were undertaken on each tissue sample. Results:Decreased expression of FANCD2 was observed in the diagnostic biopsy of OED lesions which later underwent malignant transformation. Combining the FANCD2 expression scores with histological grading more accurately predicted malignant transformation (p=0.005) than histology alone and correctly predicted malignant transformation in 10/17 initial biopsies. Significantly reduced expression of total FANCD2, pFANCD2, pATR, pCHK-1 and pFANCG were observed in unstable OED. Discussion: There is good evidence that defects in the DNA damage sensing-signalling-repair cascade are associated with malignant transformation in OED. Loss of post-translational modification in FANCD2 and related proteins, was more predictive of malignant transformation when compared to clinicopathological parameters.