In advanced-stage NSCLC, KRAS, and CMET mutations suggest poor prognosis, whereas EGFR and p53 mutations do not seem to have survival impact. Mutations in EGFR, KRAS and p53 are unlikely to be responsible for the progression of NSCLC from early- to late-stage disease. WGA may be used to expand starting deoxyribonucleic acid from low-volume lung biopsies for further analysis of advanced-stage NSCLC.
Acquiring a separate low-volume lung biopsy sample for mutational analysis in lung cancer patients during the diagnostic procedure is feasible and may be a valuable complement to the usual diagnostic workflow in future.
The conventional treatment of traumatic thoracic aortic transection is open surgical repair but it is associated with high rates of morbidity and mortality, particularly in patients with multiple injuries. We reviewed our experience of endovascular repair of traumatic thoracic aortic transection. Between March 2002 and December 2007, 7 patients (male 6, female 1; mean age 40 years) with multiple injuries secondary to blunt trauma underwent endovascular stenting. One patient required adjunctive surgery to facilitate endovascular stenting. Mean intensive care unit stay was 8.6 days (range, 3-16 days). Arterial access in all patients was obtained by femoral cut-down. The mean operating time was 122 min. Technical success was achieved in all cases. There was no mortality. One patient suffered a right parietal stroke, but none developed procedure-related paralysis. The mean follow-up period was 18.6 months (range, 6-48 months). There was no evidence of endoleak, stent migration, or late pseudoaneurysm formation on follow-up computed tomography. Endovascular stents can be used to treat traumatic thoracic aortic transection, with low rates of morbidity and mortality. Although early and midterm results are promising, the long-term durability of endovascular stenting for traumatic thoracic aortic transection remains unknown.
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