Primary small-cell neuroendocrine carcinoma of the breast is a rare and aggressive neoplasm without an established treatment protocol because so few cases have been described. We report a case of primary small-cell neuroendocrine carcinoma in a 31-year-old woman. The patient came to our hospital 10 days after consulting another clinic, where a diagnosis of locally advanced breast cancer suitable for neoadjuvant chemotherapy had been made. Core needle biopsy under ultrasonographic guidance revealed invasive carcinoma. The doubling time of the tumor progression was calculated as 12 days based on ultrasonographic measurement. After three cycles of chemotherapeutic regimens consisting of adriamycin plus docetaxel, the disease was judged to be progressive and the patient underwent surgery. Definitive histopathological examination revealed primary small-cell neuroendocrine carcinoma. Local and mediastinal recurrence with multiple liver metastases developed only 5 weeks after surgery. Cisplatin plus irinotecan combination chemotherapy was started; however, the patient died of aggressive recurrent tumor progression 6 months after surgery, in spite of the transient tumor regression achieved by chemotherapy. This case reinforces the importance of an early correct diagnosis and the standardization of a treatment regimen for this very rare tumor.

Carotid plaque with hemorrhage leads to cerebral embolism and ischemic stroke. Plaque angiogenesis and angiogenetic factors such as vascular endothelial growth factor (VEGF) are critical in the progression of atherosclerotic carotid plaque and intraplaque hemorrhage. The correlation between plaque angiogenesis and presence of clinical symptoms was studied in 41 specimens obtained during carotid endarterectomy from 20 symptomatic and 21 asymptomatic patients treated for carotid artery stenosis. Histological findings using hematoxylin-eosin and immunohistochemical staining against von Willebrand factor and VEGF were examined. Intraplaque hemorrhage, calcification, necrosis, and invasion of foam cells were frequently observed in the carotid plaques from symptomatic patients compared with asymptomatic patients. Higher microvessel density was found in the carotid plaques with necrosis and invasion of foam cells compared with plaques without necrosis and/or foam cell invasion, and higher expression of VEGF was found from symptomatic patients compared with asymptomatic patents. These results suggest that plaque angiogenesis and higher level of VEGF expression may enhance the progression of ischemic symptoms in patients with carotid artery stenosis. Invasive macrophages in the plaque of symptomatic patients increase levels of VEGF and might enhance plaque angiogenesis and atherosclerosis progression.

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We report a rare case of a huge cavernous hemangioma arising in a male breast. A 60-year-old man first noticed 1 x 2 cm elastic hard nodule just below his right nipple ten years previously. It enlarged 5 x 5 cm over six years. When he came to our clinic, it was size of child head (510 mm in circumference),was an elastic hard with a rather smooth surface, and firmly fixed to the chest wall. Magnetic resonance imaging (MRI) and multidetectocomputed tomography (MDCT)showed a large mass infiltrating into the chest wall. Fine needle aspiration cytology (FNA) and core needle biopsy (CNB) failed to obtain proper material except for old bloody fluid or necrotic connective tissue, precluding a correct diagnosis preoperatively. Mastectomy with partial resection of the chest wall was subsequently performed. Histologically, it was found to be a cavernous hemangioma without cellular atypia. In such a case, complete excision is recommended to exclude the possibility of an underlying malignant lesion.