Publications by authors named "Masayuki Nakau"

Background: Minimally invasive esophagectomy (MIE) is increasingly performed to expect lower complication rate compared to open esophagectomy. Studies of minimally invasive Ivor Lewis esophagectomy (MIILE) with circular staplers have reported better outcomes compared to MIE with cervical anastomosis, but frequent anastomotic complications have also been reported. MIILE with linear staplers is a promising alternative, but the long-term functional and oncological outcomes are uncertain.

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We aimed to histologically observe portal venous gas (PVG)-causing intestinal pneumatosis (IP) and evaluate pathogenic mechanisms and therapeutic strategies, including decisions on whether emergency surgery should be performed. Autopsy was performed in two cases of nonocclusive mesenteric ischemia (NOMI). We directly histologically observed the pathogenic mechanisms of IP caused by gas-producing bacteria and IP considered to be caused by mechanical damage to the intestinal mucosa.

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We report a case of recurrent gallbladder cancer in which the patient's tumor showed a remarkable response to gemcitabine( GEM)plus cisplatin(CDDP)therapy. In January 2007, the patient underwent curative resection for gallbladder cancer (T2N1M0, Stage III), and tegafur/uracil was administered for a year as adjuvant chemotherapy. In September 2009, elevated serum CA19-9 levels were observed, and para-aortic lymph node swelling was seen on CT scans.

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The development of hepatocellular carcinomas (HCC) appears to be a multistep process that takes several decades in humans. However, the identities of specific gene alterations and their contribution to HCC pathogenesis remain poorly understood. We previously reported that Lkb1(+/-) mice spontaneously develop multiple hepatic nodular foci (NdFc) followed by HCC, and that the conditional activation of beta-catenin in Catnb(lox(ex3)) mouse livers alone does not cause tumor formation.

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We performed a right transthoracic subtotal esophagectomy with systemic three-field lymph node dissection, followed by reconstruction with a gastric tube shifted retrosternally into the left side of the neck, for esophageal cancer in a 62-year-old woman. The patient had an uneventful postoperative course until postoperative day (POD) 9, when a venous thrombosis originating from the left brachiocephalic vein and elongating to the left subclavian vein was detected occasionally on computed tomography scans, although there were no clinical symptoms. The left brachiocephalic vein seemed narrowed by compression from the reconstructed gastric tube, and this was considered the cause of the thrombosis.

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Germline mutations of the LKB1 gene are associated with Peutz-Jeghers syndrome, which is characterized by mucocutaneous pigmentation and gastrointestinal hamartoma with an increased risk of cancer development. To investigate the role of LKB1 in vivo, we have recently constructed Lkb1 gene knockout mice. Because of Lkb1 gene haploinsufficiency, the heterozygous Lkb1 mice develop gastrointestinal polyps of which the histological characteristics resemble those of the Peutz-Jeghers syndrome hamartomas.

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Dendritic cells (DCs) from cancer patients, as well as tumor-infiltrating DCs, are reported to have suppressed immunostimulatory capacity. One of the major problems in the clinical use of DCs for treating tumors is that the DCs must be autologous ones obtained from patients. Compared with normal DCs (nDCs), flow-cytometric analysis and allogeneic mixed lymphocyte reaction (MLR) have revealed lower expression of the costimulatory molecules and suppressed T-cell-stimulatory activity in DCs derived from tumor-bearing mice (tDCs) despite of culture.

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Peutz-Jeghers syndrome (PJS) is a hereditary disorder characterized by gastrointestinal hamartomatous polyposis associated with mucocutaneous pigmentation. Germ-line mutations of the gene encoding LKB1 (STK11), a serine/threonine kinase, are identified in most PJS patients. To investigate the role of LKB1 in the PJS phenotypes, we introduced a germ-line mutation in the mouse Lkb1 gene by homologous recombination in mouse embryonic stem cells.

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