Nami Matsuura

Laparoscopic partial adrenalectomy

AbstractBackground: Most laparoscopic adrenalectomies involve total removal of the whole adrenal gland, and reports of laparoscopic partial adrenalectomies have been very few. The criteria for performing a laparoscopic partial adrenalectomy have not been described. Methods: (a) Patients with functioning adrenal tumors smaller than 3 cm in diameter were selected. (b) The solitary adrenal tumors were evaluated by preoperative thin-slice computed tomography (CT) scan. (c) Solitary lesions were reconfirmed with intraoperative ultrasonography. (d) Partial adrenalectomy was performed with at least a 5-mm margin using a vascular stapler. Results: Laparoscopic partial adrenalectomy was performed in five patients using the vascular stapler. Hemostasis was perfect in all five patients. The tumor was located in the inferior part of the right adrenal gland in three cases and in the upper pole of the left adrenal gland in two cases. The postoperation pathologic diagnosis was adrenocortical adenoma in all five patients, and excessive hormonal levels or symptoms all disappeared. Conclusions: Laparoscopic partial adrenalectomy can be performed safely using a vascular stapler.

Alteration of integrins by heparin-binding EGF-like growth factor in human breast cancer cells

The adhesion of cancer cells to the vascular endothelium is an important step in the hematogenous metastasis of cancer. Human breast cancer cells adhere to human umbilical vein endothelial cells (HUVECs) through the interaction of E selection on HUVECs and the carbohydrate ligand sialyl Lewisx on the cancer cells. We investigated the alteration of integrin expression on human breast cancer cells, following selectin-mediated initial adhesion to HUVECs. Four cell lines derived from human breast cancer expressed alpha 2-, alpha 3-, alpha 5-, alpha 6- and beta 1-integrins. The expression of alpha 2 beta 1- and alpha 3 beta 1-integrins on BT-20 cells, strongly expressing epidermal growth factor (EGF) receptors, was markedly increased by addition of the heparin-binding EGF-like growth factor (HB-EGF). The expression of alpha 2 beta 1-integrin on SK-BR-3 cells also was increased by the addition of HB-EGF. However, no such effect of HB-EGF on the expression of integrins was observed in T-47D and MCF-7 cells, nor on expression of the EGF receptor. The increase of integrin expression in BT-20 cells was inhibited by the addition of the tyrosine kinase inhibitor genistein. HB-EGF treatment of BT-20 or SK-BR-3 cells resulted in the augmentation of cancer cell adhesion to immobilized collagen. When BT-20 cells were cocultured with HUVECs, a similar level of augmentation of cancer cell adhesion to collagen was observed. The augmentation of cancer cell adhesion to collagen was inhibited by addition of an anti-HB-EGF-neutralizing antibody. Our interpretation of the results described above is that the cancer cells receive stimulation from cytokines, such as HB-EGF, produced by vascular endothelial cells, following the initial adhesion of cancer cells via selectins. This results in a secondary increase in the expression of cell adhesion molecules, such as the beta 1-integrin family, and leads to augmentation in the adhesive activities of cancer cells at the vessel walls. We postulate that these events are the ones involved in the enhanced transmigration of cancer cells to extravascular tissues following the selectin-mediated adhesion to the endothelium.

Induction of E-selectin expression on vascular endothelium by digestive system cancer cells

The adhesion of circulating cancer cells to the vascular endothelium is an important step in the hematogenous metastasis of cancer. Carbohydrate antigens, such as sialyl Le x and sialyl Le a, are expressed on the surface of cancer cells, and E-selectin is expressed on the surface of endothelial cells to effect this adhesion. ~ 3 The expression of E-selectin on endothelial cells is enhanced by inflammatory cytokines, such as IL-1 ~ or TNF or. 4 In this connection, a report has been found stating that certain cytokines promote tumor cell adhesion to endothelial cellsr Recent evidence suggests that Eselectin is expressed on the endothelial cells of small vessels adjacent to cancer nests, and that serum Eselectin levels are elevated in patients with metastatic cancer. 6 Accordingly, it is surmised that cancer cells induce the expression of E-selectin on the endothelium either directly or indirectly. However, there are few studies of the interaction between cancer and endothelial cells. 7,8 Hence, our investigation focused on this interaction, i.e., the cancer cells of the digestive system acting upon vascular endothelium in the expression of E-selectin.

Adhesion of human breast cancer cells to vascular endothelium mediated by Sialyl Lewisx/E-selectin

The adhesion molecules involved in the attachment of breast cancer cells to endothelial cells were investigated in vitro. All six human breast cancer cell lines expressed sialyl Lewisx antigen (s-Lex). Only two cell lines expressed sialyl Lewisa antigen. A correlation was found between the degree of s-Lex expression and the attachment of cancer cells to human umbilical vein endothelial cells (HUVECs) activated by IL-1β. Monoclonal antibodies against s-Lex or E-selectin inhibited this adhesion. These findings suggest that s-Lex on the surface of cancer cells and E selectin on the surface of endothelial cells play roles in adhesion of breast cancer cells to vascular endothelium.

Successful surgical treatment of a solitary parapharyngeal metastasis from thyroid cancer, using the mandibular swing-transcervical approach: report of a case.

A 72-year-old man presented with a right parapharyngeal mass, 4 cm in diameter, which was subsequently diagnosed as a metastasis originating from papillary carcinoma of the thyroid gland. The parapharyngeal tumor was successfully removed by the mandibular swing-transcervical approach with pharyngeal reconstruction, performed using a buccal mucosal island flap based on the facial artery. His postoperative course was uneventful, and the preoperative clinical symptoms such as dysphagia and head-aches completely resolved after surgery.

Parathyroid hormone suppression by 22-oxacalcitriol in the severe parathyroid hyperplasia

The suppression of parathyroid hormone (PTH) secretion by the administration of 1,25-dihydroxyvitamin D [1,25(OH)2D3] and 22-oxacalcitriol (OCT) was evaluated in nude mice transplanted with human hyperplastic parathyroid tissue. The parathyroid tissue was obtained for transplantation from a patient with severe secondary hyperparathyroidism who had undergone a parathyroidectomy. Tissue specimens were transplanted into the gluteus muscle of female nude mice. Animals were divided into two groups; one group was fed a normal diet, and the other group was fed a low calcium diet during the administration of OCT and 1,25(OH)2D3. OCT and 1,25(OH)2D3 were intraperitoneally administered two times every week, for a total of eight times. Serum calcium and phosphate levels were significantly higher in the mouse administered 1,25(OH)2D3 than in the mouse administered OCT. Serum alkaline phosphatase activity was elevated similarly in the mouse administered either OCT or 1,25(OH)2D3. OCT strongly suppressed human PTH secretion from the graft in mice with normal serum calcium levels as did 1,25(OH)2D3. However, human PTH secretion from the graft was stimulated by the administration of a low-calcium diet, despite OCT and 1,25(OH)2D3 administration. In summary, OCT and 1,25(OH)2D3 suppress PTH secretion even from severe secondary hyperplastic parathyroid tissue only in mice with normal or high calcium serum levels.