ABSTRACT
<p>A 74-year-old woman presented to our hospital with complaints of dysphagia. On examination, we diagnosed extensive thoracic aortic aneurysm and esophageal compression due to a descending thoracic aortic aneurysm. We planned a two-stage approach for repairing the extensive thoracic aortic aneurysm ; the first stage involving the repair of the ascending and arch segments, and the second stage involving the repair of the descending aorta. In the first stage, we performed the Bentall procedure and total arch replacement with a long elephant trunk. Following this, her dysphagia resolved, although the size of the descending aortic aneurysm was the same as that before the procedure (49 mm in diameter). We decided to treat her conservatively in the outpatient clinic without the second stage, because the descending aorta was asymptomatic and not sufficiently large. One year later, she presented with a sudden recurrence of dysphagia and swelling of buttocks. She was diagnosed with an expansion of the descending aortic aneurysm (62 mm in diameter) and a hematoma in the gluteal muscle due to aneurysm-induced disseminated intravascular coagulation (DIC). After emergency admission, she underwent a successful thoracic endovascular aortic repair and was discharged following a smooth recovery from dysphagia and aneurysm-induced DIC. We report this case along with a review of the literature.</p>
ABSTRACT
Cyclin D1 gene (<i>CCND1</i>) numerical aberrations are independent prognostic indicators of head and neck squamous cell carcinomas (HNSCCs). High epidermal growth factor receptor gene (<i>EGFR</i>) copy number is associated with poor prognosis in lung cancer, but such findings are controversial in oral SCCs (OSCCs). We analyzed copy number status in <i>CCND1</i> and <i>EGFR</i> in OSCC patients and its association with clinical outcome.<i>EGFR</i> and <i>CCND1</i> statuses were analyzed in 85 OSCC patients by fluorescence <i>in situ</i> hybridization (FISH) of specimens obtained by fine-needle aspiration biopsy.<i>CCND1</i> numerical aberration was found in 35 of 85 tumors (41%), and aberrant <i>EGFR</i> copy number was observed in 36 (42%). Gene amplification (GA) was dominant among <i>CCND1</i> copy number changes (14/35:40%). Balanced trisomy (BT) was the most frequently observed <i>EGFR</i> aberration (17/36:47%). In a multivariate Cox's proportional hazards analysis, <i>CCND1</i> GA was correlated with disease-free survival (<i>P</i><0.001), whereas <i>EGFR</i> BT was significantly correlated with overall survival (<i>P</i>=0.001). Patients with a combination of <i>CCND1</i> GA and/or <i>EGFR</i> BT had significantly poorer clinical outcome.<i>CCND1</i> and <i>EGFR</i> copy number changes were frequent in OSCC and had differing aberration patterns. <i>CCND1</i> GA and <i>EGFR</i> BT statuses by dual-color FISH were the predominant predictors of clinical outcome. Further investigation is needed to determine the implications for EGFR inhibitor therapy in OSCC.