Does coronary heart disease risk equivalence in diabetes depend on concomitant risk factors?
Our results and comparisons with other available data show wide variation in the rate of CHD in diabetes, depending on the population and existing risk factors. Most individuals had a 10-year cumulative incidence >20%, but only those with multiple risk factors had a 10-year cumulative incidence that was equivalent to that of patients with CHD. Until more data are available, it may be prudent to consider targets based on the entire risk factor profile rather than just the presence of diabetes.
These findings demonstrate that: (i) mutations of the cell cycle regulatory genes p16 and p21 and the S100A4 gene are infrequent and might be unnecessary in development and/or progression of oropharyngeal SCCs, (ii) the results were not found to relate to previous results of p53, (iii) loss of p21 and/or p53 might not predict for prognosis in these cancers, (iv) the absence of mutations of the three genes examined in the cases previously found mutated for p53 might suggest that these mutations are complementary to p53 mutations in the development of these cancers, but the lack of these mutations in the cases with no mutations in p53 might suggest that the pathogenesis of these cancers may follow other independent pathways. Since p53 and pRb (p16/pRb/cyclin-D1) pathways represent the two main mechanisms for cell cycle control at the G1-S checkpoint, further studies are necessary to examine the possible alterations in the pRb (p16/pRb/cyclin-D1) and the p53 pathways in oropharyngeal SCCs.