Natural history of intracavernous aneurysms: a consecutive single-center study of 250 patients with 276 aneurysms.

OBJECTIVE: The natural history of cavernous carotid aneurysms (CCAs) is not fully understood. For robust clinical decision-making, the behavior of CCAs needs to be fully understood. The objective of this paper was to calculate the mortality and morbidity rates of patients with diagnosed but untreated CCAs from a relatively large single-center cohort. METHODS: The authors identified 250 patients with 276 CCAs from August 1946 to August 2017 from an aneurysm database including 12,000 intracranial aneurysm patients. Patient and aneurysm characteristics were extracted for further analysis. RESULTS: The cumulative patient follow-up was 1560 years, with a mean of 6.3 years. For patients presenting with a cranial nerve deficit caused by a CCA, those with a ruptured CCA, and patients who received treatment for a CCA, the cumulative patient follow-up was 121 years, with a mean of 1.3 years. For patients with symptom-free or conservatively treated CCAs, the cumulative patient follow-up was 1093 years, with a mean of 7.2 years. Of the 276 aneurysms, 57 (21%) caused cranial nerve deficits and 18 (6.5%) other symptoms, while 201 (73%) remained symptom free. A total of 264 (96%) of the CCAs remained unruptured, and 2 were considered possibly ruptured. Ten (3.6%) ruptures of the CCAs were found. However, none of the ruptured aneurysms caused subarachnoid hemorrhage or death of the patient. Of the CCAs, 51 were multiple, and 131 patients had ≥ 1 intradural aneurysm. The CCAs were analyzed separately. CONCLUSIONS: The majority of the CCAs were asymptomatic during follow-up, and none caused the death of the patient. The incidence of symptoms increased with aneurysm size. Because CCAs have a benign natural course, treatment should be considered mainly if the CCA is symptomatic or grows during follow-up.

Tumour Suppressor Neuron Navigator 3 and Matrix Metalloproteinase 14 are Co-expressed in Most Melanomas but Downregulated in Thick Tumours.

Melanoma is a highly metastatic tumour originating from neural crest-derived melanocytes. The aim of this study was to analyse the expression of neuron navigator 3 (NAV3) in relation to membrane type-1 matrix metalloproteinase MMP14, a major regulator of invasion, in 40 primary melanomas, 15 benign naevi and 2 melanoma cell lines. NAV3 copy number changes were found in 18/27 (67%) primary melanomas, so that deletions dominated (16/27 of samples, 59%). NAV3 protein was found to be localized at the leading edge of migrating melanoma cells in vitro. Silencing of NAV3 reduced both melanoma cell migration in 2-dimensional conditions, as well as sprouting in 3-dimensional collagen I. NAV3 protein expression correlated with MMP14 in 26/37 (70%) primary melanomas. NAV3 and MMP14 were co-expressed in all tumours with Breslow thickness < 1 mm, in 11/23 of mid-thickness tumours (1-5 mm), but in only 1/6 samples of thick (> 5 mm) melanomas. Altogether, NAV3 number changes are frequent in melanomas, and NAV3 and MMP14, while expressed in all thin melanomas, are often downregulated in thicker tumours, suggesting that the lack of both NAV3 and MMP14 favours melanoma progression.