A rare eicosanoid precursor analogue, sciadonic acid (5Z,11Z,14Z-20:3), detected in vivo in hormone positive breast cancer tissue.

Numerous genetic alterations of HSA 11q13 are found frequently in several cancer types, including breast cancer (BC). The 11q13 locus harbors FADS2 encoding Δ6 desaturation which is not functional in several cancer cell lines, including hormone positive MCF7 BC cells. In vitro, the non-functional FADS2 activity unmasks 18:2n-6 elongation to 20:2n-6 and Δ5 desaturation by FADS1 to yield 5Z,11Z,14Z-20:3 (sciadonic acid) rather than 5Z,8Z,11Z,14Z-20:4 (arachidonic acid). In this pilot study we aimed to determine whether 5,11,14-20:3 appears in vivo in hormone positive human BC tissue. Fatty acids were profiled in surgically removed human breast tumor and adjacent normal tissue (n = 9). Sciadonic acid was detected in three of nine breast tumor samples and was below detect limits in normal breast tissue. The internal Δ8 double bond of arachidonic acid is required for normal eicosanoid synthesis but is missing in sciadonic acid. This pilot study demonstrates for the first time in vivo sciadonic acid in hormone positive BC tissue, warranting a larger survey study to further evaluate its appearance and the functional implications.

Eversion technique increases the risk for post-carotid endarterectomy hypertension.

OBJECTIVE: The incidence of postoperative hypertension (HTN) after eversion carotid endarterectomy (e-CEA) was compared with that after standard carotid endarterectomy (s-CEA). METHODS: In a retrospective analysis from January 1998 to January 2000, 217 patients underwent 219 CEAs for symptomatic (68) or asymptomatic (151) high-grade (>80%) carotid artery stenosis by either standard (137) or eversion (82) techniques. The eversion technique involves an oblique transection of the internal carotid artery at the carotid bulb and a subsequent endarterectomy by everting the internal carotid artery over the atheromatous plaque. All procedures were done under general anesthesia, and somatosensory-evoked potentials were used for cerebral monitoring. Patients with s-CEA were compared with those with e-CEA for postoperative hemodynamic instability, carotid sinus nerve block, requirement for intravenous vasodilators or vasopressors, stroke, and death. RESULTS: Patients who underwent e-CEA had a significantly (P <.005) increased postoperative blood pressure and required more frequent intravenous antihypertensive medication (24%), compared with patients having an s-CEA (6%). Furthermore, postoperative vasopressors were required after 10% of s-CEAs, but after none of the e-CEAs. No statistically significant difference was noted in the morbidity or mortality of patients after s-CEA and e-CEA. CONCLUSION: e-CEA is a substantial risk factor for HTN in the immediate postoperative period, when compared with the s-CEA. This difference would be even more remarkable in the absence of antihypertensive medications in the e-CEA group and vasopressors in the s-CEA group. Therefore, particular attention should be focused on diagnosing and controlling postoperative HTN in patients after e-CEA.