: The 3 cut-off values of LNRs had strong independent prognostic value in a population-based collective of patients with colorectal cancer. The LNR should be routinely reported and included in the American Joint Committee on Cancer staging system. Nevertheless, the benefit of lymphadenectomy on survival is still unclear.
Aberrant subclavian artery (ASA) is one of the most common congenital vascular anomalies of the aortic arch. The incidences of aberrant right subclavian artery (ARSA) and aberrant left subclavian artery (ALSA) are 0.4% to 2.3% and 0.05%, respectively. Approximately 60% of ARSA patients will have a Kommerell's diverticulum at the origin of the ASA. Symptomatic or aneurysmal ASAs need to be treated. Historically, open operation was the favored method to reconstruct ASA anatomy; however, novel endovascular techniques are now available. Following a brief discussion of embryonic development, symptoms, and treatment history of the ASA and Kommerell's diverticulum, the results of a literature review to collect the worldwide experience of endovascular/hybrid treatment of ASA is presented.
Background: Hereditary non-polyposis colorectal cancer (HNPCC) is clinically defined by familial clustering of colorectal cancer and other associated tumours. Methods: By thorough molecular and clinical evaluation of 41 families, two different groups were characterised: group 1, 25 families with truncating mutations in MLH1 or MSH2 (12 novel mutations); and group 2, 16 Amsterdam positive families without mutations in these genes and without microsatellite instability in their corresponding tumours. Results: Significant clinical differences between these two groups were found. Firstly, earlier age of onset for all colorectal cancers (median 41 v 55 years; p,0.001) and all tumours (median 43 v 56 years; p = 0.022) was observed, comparing groups 1 and 2. Secondly, 68% of the index colorectal cancers were localised proximally of the splenic flexure in group 1 compared with 14% in group 2 (p,0.010). Thirdly, more synchronous and metachronous colorectal (p = 0.017) and extracolorectal tumours (p,0.001) were found in group 1. Fourthly, a higher colorectal adenoma/carcinoma ratio (p = 0.030) and a tendency towards more synchronous or metachronous adenomas in group 2 (p = 0.084) was observed, indicating a slower progression of adenomas to carcinomas. As three mutation negative tumours revealed chromosomal instability after comparative genomic hybridisation, these tumours may be caused by one or more highly penetrant disease alleles from the chromosomal instability pathway. Conclusion: These data show that HNPCC includes at least two entities with clinical and molecular differences. This will have implications for surveillance programmes and for cancer research.
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