Chiba Cancer Center Hospital

Chūō-ku, Japan

Chiba Cancer Center Hospital

Chūō-ku, Japan
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Yamada C.,Aichi Cancer Center Research Institute | Yamada C.,Chiba University | Ozaki T.,Aichi Cancer Center Research Institute | Ando K.,Aichi Cancer Center Research Institute | And 10 more authors.
Journal of Biological Chemistry | Year: 2010

Although it has been shown that the gastric tumor suppressor RUNX3 has a growth inhibitory activity, the precise molecular mechanisms behind RUNX3-mediated tumor suppression remained unclear. In this study, we found that RUNX3 is closely involved in DNA damage-dependent phosphorylation of tumor suppressor p53 at Ser-15 and acts as a co-activator for p53. The small interference RNA-mediated knockdown of RUNX3 inhibited adriamycin (ADR)-dependent apoptosis in p53-proficient cells but not in p53-deficient cells in association with a significant reduction of p53-target gene expression as well as phosphorylation of p53 at Ser-15. In response to ADR, RUNX3 was induced to accumulate in the cell nucleus and co-localized with p53. Immunoprecipitation experiments demonstrated that RUNX3 forms a complex with p53 in cells. In vitro pulldown assays revealed that the COOH-terminal portion of p53 is required for the interaction with RUNX3. Forced expression of RUNX3 enhanced p53-mediated transcriptional activation. Additionally, RUNX3 had an ability to induce the phosphorylation of p53 at Ser-15, thereby promoting p53-dependent apoptosis. Intriguingly, RUNX3 interacted with phosphorylated forms of ataxia telangiectasia-mutated in response to ADR; however, it did not affect the extent of DNA damage. From the clinical point of view, coordinated p53 mutation and decreased expression of RUNX3 in 105 human lung adenocarcinomas were significantly associated with the poor outcome of patients (p = 0.0203). Thus, our present results strongly suggest that RUNX3 acts as a novel co-activator for p53 through regulating its DNA damage-induced phosphorylation at Ser-15 and also provide a clue to understanding the molecular mechanisms underlying RUNX3-mediated tumor suppression. © 2010 by The American Society for Biochemistry and Molecular Biology, Inc.


Suzuki T.,Chiba University | Okamoto Y.,Chiba University | Yonekura S.,Chiba University | Okuma Y.,Chiba University | And 2 more authors.
Annals of Allergy, Asthma and Immunology | Year: 2016

Background People with allergic rhinitis often have laryngeal symptoms (LSs) in addition to nasal symptoms during the pollen-scattering season. Objective To clarify the characteristics of the LSs induced by pollen exposure using an environmental challenge chamber. Methods Cypress pollen exposure using an environmental challenge chamber for 25 participants with cypress pollen-induced allergic rhinitis was performed for 3 hours for 2 consecutive days in 3 study courses: namely, pollen exposure under normal nasal breathing and pollen or sham pollen exposure with nasal blockage, which eliminated any allergic reactions in the nasal mucosa. The nasal and LSs scores and the levels of serum inflammatory mediators, including eosinophil cationic protein (ECP), were monitored. Laryngeal examinations and physiologic lung tests were also conducted. Results Various LSs were reported, and these LSs were significantly elevated during pollen exposure and even under sham exposure with artificial nasal blockage. The pollen exposure with artificial nasal blockage exaggerated the LSs in 32% of the participants and also increased the serum ECP levels. The serum ECP levels did not change after sham exposure. The findings of both laryngeal examinations and lung tests failed to reveal any significant changes. Conclusion Nasal obstruction could induce significant LSs even without pollen exposure. LSs were enhanced by pollen exposure and allergic reactions in the larynx could thus be involved in this enhancement. Trial Registration clinicaltrials.gov Identifier: UMIN000015667. © 2016 American College of Allergy, Asthma & Immunology.


Suzuki M.,Chiba University | Sakurada T.,Chiba University | Gotoh K.,St Lukes International Hospital | Watanabe S.,Chiba Cancer Center Hospital | Satoh N.,Chiba University
American Journal of Hospice and Palliative Medicine | Year: 2013

Morphine and oxycodone are widely used in the therapy for cancer pain. Although some previous studies have reported that morphine induces immunosuppression and oxycodone does not, whether this is true for human infections is unclear. We performed a retrospective study on the correlation between the administration of morphine or oxycodone and the development of infections in patients with cancer pain. This study was undertaken in 841 inpatients receiving only 1 opioid continuously for more than 10 days. Development of infections was based on (1) antibiotic administration and (2) diagnosis of infections, positive microbial culture test, or increase in white blood cells or C-reactive protein. Liver, kidney, and hematological cancer, antineoplastic drugs, radiotherapy, steroid, immunosuppressive agents, granulocyte colony-stimulating factor, and thyroid inhibitors were defined as the exclusion criteria in consideration of influence on immune system or metabolism and excretion of morphine and oxycodone. A total of 60 morphine and 74 oxycodone cases were included, which resulted in 18 and 10 infection cases. Significantly more patients treated with morphine developed infections than those patients treated with oxycodone (odds ratio = 3.60, 95% confidence interval = 1.40-9.26). No significant differences were seen in the other variables analyzed. Although perhaps some confounding variables were included because this was an observational rather than randomized study, these results suggested that morphine's immunosuppressive effect may contribute to the development of infections in patients with cancer pain. © The Author(s) 2012.


The high reliability and utility of core needle biopsy (CNB) have been previously described. Our aim in this study was to clarify the host and histopathological factors influencing the discrepancies in ER, PgR, and HER2 status between CNB and surgically excised tumors (SET).All patients diagnosed with operable invasive breast cancer in our hospital between January 2005 and April 2015 were included in the study; patients who required neoadjuvant chemotherapy were excluded. ER, PgR, and HER2 expression were assessed between paired CNB and SET samples. ER and PgR status were determined using immunohistochemistry(IHC). HER2 status was determined using IHC and scored from 0 to 3+. Fluorescence in-situ hybridization analysis was carried out in HER2 2+ cases. The cut off point for ER and PgR positivity was set at 1%.A total of 1307 patients were assessed. The concordance rates of ER, PgR, and HER2 status in CNB and SET were 95%, 84% and 97%, respectively. Factors of discrepancy were nuclear grade, histological type, and menopausal status for ER and PgR, and none detected for HER2. The discrepancy factors were assessed with univariate and multivariate analysis.Using the largest known dataset to date of paired samples from a single institution, we evaluated the accuracy of CNB and the discrepancy factors between CNB and SET in breast cancer patients. We conclude that CNB for ER and PgR assessment in postmenopausal patients before treatment should be used with caution. Further research will contribute to increased CNB accuracy, improving patient treatment decisions.


Shimozato O.,Aichi Cancer Center Research Institute | Waraya M.,Aichi Cancer Center Research Institute | Nakashima K.,Aichi Cancer Center Research Institute | Souda H.,Chiba Cancer Center Hospital | And 11 more authors.
Oncogene | Year: 2015

Although CD133 has been considered to be a molecular marker for cancer stem cells, its functional roles in tumorigenesis remain unclear. We here examined the molecular basis behind CD133-mediated signaling. Knockdown of CD133 resulted in the retardation of xenograft tumor growth of colon cancer-derived HT-29 and LoVo cells accompanied by hypophosphorylation of AKT, which diminished β-cateninT-cell factor-mediated CD44 expression. As tyrosine residues of CD133 at positions 828 and 852 were phosphorylated in HT-29 and SW480 cells, we further addressed the significance of this phosphorylation in the tumorigenesis of SW480 cells expressing mutant CD133, with substitution of these tyrosine residues by glutamate (CD133-EE) or phenylalanine (CD133-FF). Forced expression of CD133-EE promoted much more aggressive xenograft tumor growth relative to wild-type CD133-expressing cells accompanied by hyperphosphorylation of AKT; however, CD133-FF expression had negligible effects on AKT phosphorylation and xenograft tumor formation. Intriguingly, the tyrosine phosphorylation status of CD133 was closely linked to the growth of SW480-derived spheroids. Using yeast two-hybrid screening, we finally identified receptor-type protein tyrosine phosphatase κ (PTPRK) as a binding partner of CD133. In vitro studies demonstrated that PTPRK associates with the carboxyl-terminal region of CD133 through its intracellular phosphatase domains and also catalyzes dephosphorylation of CD133 at tyrosine-828tyrosine-852. Silencing of PTPRK elevated the tyrosine phosphorylation of CD133, whereas forced expression of PTPRK reduced its phosphorylation level markedly and abrogated CD133-mediated AKT phosphorylation. Endogenous CD133 expression was also closely associated with higher AKT phosphorylation in primary colon cancer cells, and ectopic expression of CD133 enhanced AKT phosphorylation. Furthermore, lower PTPRK expression significantly correlated with the poor prognosis of colon cancer patients with high expression of CD133. Thus, our present findings strongly indicate that the tyrosine phosphorylation of CD133, which is dephosphorylated by PTPRK, regulates AKT signaling and has a critical role in colon cancer progression. © 2015 Macmillan Publishers Limited. All rights reserved.


Cho A.,Chiba Cancer Center Hospital
Asian journal of endoscopic surgery | Year: 2012

INTRODUCTION: Laparoscopic hemihepatectomy has not yet become widely accepted because of the technical difficulties in controlling each Glissonean pedicle laparoscopically. MATERIALS AND SURGICAL TECHNIQUE: The subjects in the present study included 12 patients who underwent laparoscopic left hemihepatectomy between August 2007 and June 2011. Arantius' ligament was divided. Retracting the caudal stump of the ligament revealed a space between the left Glissonean pedicle and the liver parenchyma. The left Glissonean pedicle could be easily encircled by using an Endo Retract Maxi. No Glissonean injuries, including bleeding or biliary leakage, occurred in any of the 12 patients. DISCUSSION: Therefore, the Arantius' ligament approach for the left extrahepatic Glissonean pedicle appears to be feasible and safe for successfully performing pure laparoscopic left hemihepatectomy. © 2012 Japan Society for Endoscopic Surgery, Asia Endosurgery Task Force and Wiley Publishing Asia Pty Ltd.


Cho A.,Chiba Cancer Center Hospital | Yamamoto H.,Chiba Cancer Center Hospital | Kainuma O.,Chiba Cancer Center Hospital | Muto Y.,Chiba Cancer Center Hospital | And 3 more authors.
World Journal of Gastroenterology | Year: 2014

The use of minimally invasive surgery has become widely accepted in many gastrointestinal fields, even in patients with malignancy. However, performing laparoscopic resection for the treatment of hilar cholangiocarcinoma is still not universally accepted as an alternative approach to open surgery, and only a limited number of such procedures have been reported due to the difficulty of performing oncologic resection and the lack of consensus regarding the adequacy of this approach. Laparoscopy was initially limited to staging, biopsy and palliation. Recent technological developments and improvements in endoscopic procedures have greatly expanded the applications of laparoscopic liver resection and lymphadenectomy, and some reports have described the use of laparoscopic or robot-assisted laparoscopic resection for hilar cholangiocarcinoma as being feasible and safe in highly selected cases, with the ability to obtain an adequate surgical margin. However, the benefits of major laparoscopic surgery have yet to be conclusively proven, and carefully selecting patients is essential for successfully performing this procedure. © 2014 Baishideng Publishing Group Inc. All rights reserved.


Cho A.,Chiba Cancer Center Hospital
Nippon Geka Gakkai zasshi | Year: 2011

Laparoscopic pancreatic resection of pancreatic cancer is still not universally accepted as an alternative approach to open surgery because of technical difficulties and a lack of consensus regarding the adequacy of this approach for malignancy. Ten patients with pancreatic cancer underwent laparoscopic pancreatic resection, including pancreaticoduodenectomy and distal pancreatectomy in our institution. Eight of the 10 patients recovered without any complications and were discharged on the 10-29th postoperative day. The remaining 2 patients developed pancreatic fistula and were discharged on the 46 and 60th postoperative day, respectively. All lesions were well clear of surgical margins in 6 patients (R0). In the remaining 4 patients, microscopic neoplastic change was found at the surgical margin (R1). Those 4 patients developed tumor recurrence, including liver metastases or peritoneal dissemination, and 3 of the 4 died of the primary disease. Although experience is limited, laparoscopic pancreatic resection of pancreatic cancer can be feasible, safe, and effective in carefully selected patients. However, the benefit of this procedure has yet to be confirmed. Not only adequate experience in pancreatic surgery but also expertise in laparoscopy is mandatory, and careful selection of patients is essential for successful application of this procedure.


Cho A.,Chiba Cancer Center Hospital | Yamamoto H.,Chiba Cancer Center Hospital | Kainuma O.,Chiba Cancer Center Hospital
Journal of Hepato-Biliary-Pancreatic Sciences | Year: 2014

In previous reports of laparoscopic pancreaticoduodenectomy, the Kocher maneuver with a wide mobilization of the right colonic flexure is carried out in the early phase, and dissection of the superior mesenteric artery is performed in the last phase of resection. This report describes laparoscopic superior mesenteric artery first approach, in which the superior mesenteric artery is dissected in the early phase of resection. Through the ligament of Treitz, the retroperitoneum is widely opened and the superior mesenteric artery is isolated just superior to the left renal vein. The periarterial connective tissue and nerve plexuses surrounding the superior mesenteric artery are dissected longitudinally to identify the inferior pancreaticoduodenal artery, which is then tied and divided. The superior mesenteric artery first approach and early ligation of the inferior pancreaticoduodenal artery is considered to be a feasible, safe, and effective method for performing pure laparoscopic pancreaticoduodenectomy. © 2013 Japanese Society of Hepato-Biliary- Pancreatic Surgery.


Cho A.,Chiba Cancer Center Hospital | Yamamoto H.,Chiba Cancer Center Hospital | Kainuma O.,Chiba Cancer Center Hospital | Souda H.,Chiba Cancer Center Hospital | And 3 more authors.
Surgical Endoscopy and Other Interventional Techniques | Year: 2011

Background: Although recent technological developments and improved endoscopic procedures have further spread the application of laparoscopic liver resection, laparoscopic anatomical liver resection still presents major technical difficulties, such as pedicle control. Methods: Subjects comprised 27 patients who underwent laparoscopic anatomical liver resection using an extrahepatic Glissonean pedicle transaction between August 2005 and February 2010. Results: A total of 61 Glissonean pedicles could be encircled en bloc extrahepatically, as planned. No serious complications, including major bleeding or injury of the portal triad, were encountered during procedures. Conclusions: Extrahepatic Glissonean access seems to be feasible and safe for laparoscopic anatomical resection of the liver. © 2010 Springer Science+Business Media, LLC.

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