Miyagi Cancer Center Research Institute

Natori, Japan

Miyagi Cancer Center Research Institute

Natori, Japan
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Minami Y.,Tohoku University | Nishino Y.,Miyagi Cancer Center Research Institute | Kawai M.,Tohoku University | Kakugawa Y.,Miyagi Cancer Center Hospital
Cancer Causes and Control | Year: 2012

Objective: Being breastfed in infancy has been hypothesized to influence subsequent breast cancer risk. In a hospital-based case-control study, we investigated the relationship between having been breastfed and breast cancer risk, both overall and separately among female subjects with different birth years. Methods: The study subjects included 571 cases and 2,155 controls admitted to a single hospital in Miyagi Prefecture, Japan, between 1997 and 2005. History of having been breastfed was assessed with a self-administered questionnaire. Odds ratios (ORs) and 95% confidence interval (CI) were estimated using logistic regression. Results: After adjustment for known risk factors, no association for having been breastfed was observed overall (OR = 1.20; 95% CI: 0.82-1.76). Analysis stratified according to birth year (<1950, ≥1950) demonstrated heterogeneity in the association for having been breastfed between the two birth-year groups (p for interaction = 0.0006); having been breastfed was significantly associated with a decreased risk among subjects who were born before 1950 (OR = 0.59; 95% CI: 0.35-0.99), whereas no such risk reduction was observed for subjects born after 1950 (OR = 1.60; 95% CI: 0.88-2.90). Conclusion: Although having been breastfed is not related to overall risk, birth year may modify the association between having been breastfed in infancy and breast cancer risk. In Japan, sociodemographic changes have occurred since the end of World War II. The use of standard formula supplement began to spread around 1950. The difference of breast cancer risk between birth-year groups may be attributable to these environmental changes. © 2011 Springer Science+Business Media B.V.


Patent
Chugai Seiyaku Kabushiki Kaisha and Miyagi Cancer Center Research Institute | Date: 2014-06-23

The present inventors successfully produced therapeutic agents for non-small cell lung cancer except adenocarcinoma, comprising as active ingredient an anti-Epiregulin antibody that shows cross-species reactivity between the human animal and cynomolgus which is a non-human animal, an anti-Epiregulin antibody with suppressed chemical degradation, an anti-Epiregulin antibody with reduced isoelectric point, an anti-Epiregulin antibody with increased midpoint temperature of thermal denaturation, or an anti-Epiregulin antibody with reduced amount of aggregates, generated by appropriately substituting amino acid residues in the variable-region sequences of a humanized EP27 antibody that inhibits cancer cell proliferation by exerting a cytotoxicity and a neutralizing activity against human Epiregulin-expressing cancer cells.


Patent
Chugai Seiyaku Kabushiki Kaisha and Miyagi Cancer Center Research Institute | Date: 2016-05-04

The present inventors successfully produced therapeutic agents for non-small cell lung cancer except adenocarcinoma, comprising as active ingredient an anti-Epiregulin antibody that shows cross-species reactivity between the human animal and cynomolgus which is a non-human animal, an anti-Epiregulin antibody with suppressed chemical degradation, an anti-Epiregulin antibody with reduced isoelectric point, an anti-Epiregulin antibody with increased midpoint temperature of thermal denaturation, or an anti-Epiregulin antibody with reduced amount of aggregates, generated by appropriately substituting amino acid residues in the variable-region sequences of a humanized EP27 antibody that inhibits cancer cell proliferation by exerting a cytotoxicity and a neutralizing activity against human Epiregulin-expressing cancer cells.


Hamada S.,Tohoku University | Masamune A.,Tohoku University | Miura S.,Tohoku University | Satoh K.,Miyagi Cancer Center Research Institute | Shimosegawa T.,Tohoku University
Cellular Signalling | Year: 2014

The poor prognosis of invasive ductal adenocarcinoma of the pancreas is mainly due to its resistance against therapeutic agents. The molecular mechanism by which morbidity enhances cell survival has been extensively studied, but radical improvements in the therapeutic strategy have not yet been achieved. Recent reports have indicated the substantial contribution of miRNA in multiple cell functions by comprehensively targeting clusters of genes. We identified several miRNAs highly expressed in invasive ductal adenocarcinoma in our previous study, and clarified their contribution to the epithelial-mesenchymal transition. Among the differentially expressed miRNAs, miR-365 was highly expressed in invasive ductal adenocarcinoma, whose functional role has not been reported. In the current study, we found that miR-365 induced gemcitabine resistance in pancreatic cancer cells. MiR-365 directly targeted adaptor protein Src Homology 2 Domain Containing 1 (SHC1) and apoptosis-promoting protein BAX. The siRNA-based knockdown of SHC1 and BAX increased gemcitabine resistance, indicating the miR-365/SHC1/BAX axis influences the survival of pancreatic cancer cells. In addition, miR-365 up-regulated cancer-promoting molecules such as Inhibitor of DNA binding 2 and S100P, suggesting the existence of cross-talk with other cancer-promoting signals. MiR-365 could exert orchestrated effects on pancreatic cancer cell survival. © 2013 Elsevier Inc.


Hamada S.,Tohoku University | Satoh K.,Miyagi Cancer Center Research Institute | Masamune A.,Tohoku University | Shimosegawa T.,Tohoku University
Frontiers in Physiology | Year: 2012

Pancreatic cancer is a leading cause of cancer-related death due to its invasive nature. Despite the improvement of diagnostic strategy, early diagnosis of pancreatic cancer is still challenging. Surgical resection is the only curative therapy, while vast majority of patients are not eligible for this therapeutic option. Complex biological processes are involved in the establishment of invasion and metastasis of pancreatic cancer and epithelial-mesenchymal transition (EMT) has been reported to play crucial role. EMT is part of the normal developmental processes which mobilizes epithelial cells and yields mesenchymal phenotype. Deregulation of EMT inducing molecules in pancreatic cancer is reported, such as multiple cytokines, growth factors and downstream transcriptional factors. In addition to these molecules, non-coding RNA including miRNAalso contributes to EMT. EMT of cancer cell also correlates with cancer stem cell (CSC) properties such as chemoresistance or tumorigenicity, therefore these upstream regulators of EMT could be attractive therapeutic targets and several candidates are examined for clinical application. This review summarizes recent advances in this field, focusing the regulatory molecules of EMT and their downstream targets. Further understanding and research advances will clarify the cryptic mechanism of cancer metastasis and delineate novel therapeutic targets. © 2012 Hamada, Satoh, Masamune and Shimosegawa.


Satoh K.,Miyagi Cancer Center Research Institute | Hamada S.,Tohoku University | Shimosegawa T.,Tohoku University
Journal of Gastroenterology | Year: 2014

Pancreatic ductal adenocarcinoma (PDAC) is an intractable disease as a result of its rapid dissemination and resistance to conventional chemotherapy and radiotherapy. Surgical resection is the only curative therapy, but most of the tumors are unresectable at the time of diagnosis. The molecular mechanisms underlying the biological aggressiveness of this tumor type remain to be clarified. Epithelial to mesenchymal transition (EMT) is a developmental process that leads the phenotype shift from an epithelial morphology to a motile, fibroblast-like morphology. Recent studies showed that EMT is involved in the invasion and metastasis of many types of carcinomas including PDAC. In addition, PDAC cells with the EMT phenotype also exhibit chemoresistance and the cancer stem cell property. Various factors such as cytokines, growth factors, or transcriptional factors were found to promote the EMT program in PDAC cells. In this review, we summarize the current knowledge about the EMT in PDAC cells, focusing on the involvement of this process and its regulatory molecules including microRNA during the development of PDAC cells. © 2014, Springer Japan.


Satoh K.,Miyagi Cancer Center Research Institute | Hamada S.,Tohoku University | Shimosegawa T.,Tohoku University
Frontiers in Physiology | Year: 2012

MSX2, a member of the homeobox genes family, is demonstrated to be the downstream target for ras signaling pathway and is expressed in a variety of carcinoma cells, suggesting its relevance to the development of ductal pancreatic tumors since pancreatic ductal adenocarcinoma (PDAC) and intraductal papillary-mucinous neoplasia (IPMN) harbor frequent K-ras gene mutations. Recent studies revealed the roles of MSX2 in the development of carcinoma of various origins including pancreas. Among gastrointestinal tumors, PDAC is one of the most malignant. PDAC progresses rapidly to develop metastatic lesions, frequently by the time of diagnosis, and these tumors are usually resistant to conventional chemotherapy and radiation therapy. The molecular mechanisms regulating the aggressive behavior of PDAC still remain to be clarified. On the other hand, IPMN of the pancreas is distinct from PDAC because of its intraductal growth in the main pancreatic duct or secondary branches with rare invasion and metastasis to distant organs. However, recent evidence indicated that once IPMN showed stromal invasion, it progresses like PDAC. Therefore, it is important to determin how IPMN progresses to malignant phenotype. In this review, we focus on the involvement of MSX2 in the enhancement of malignant behavior in PDAC and IPMN, and further highlight the clinical approach to differentiate PDAC from chronic pancreatitis by evaluating MSX2 expression level. © 2012 Satoh, Hamada and Shimosegawa.


Miyagi T.,Tohoku Pharmaceutical University | Yamaguchi K.,Miyagi Cancer Center Research Institute
Glycobiology | Year: 2012

Sialic acids are terminal acidic monosaccharides, which influence the chemical and biological features of glycoconjugates. Their removal catalyzed by a sialidase modulates various biological processes through change in conformation and creation or loss of binding sites of functional molecules. Sialidases exist widely in vertebrates and also in a variety of microorganisms. Recent research on mammalian sialidases has provided evidence for great importance of these enzymes in various cellular functions, including lysosomal catabolism, whereas microbial sialidases appear to play roles limited to nutrition and pathogenesis. Four types of mammalian sialidases have been identified and characterized to date, designated as NEU1, NEU2, NEU3 and NEU4. They are encoded by different genes and differ in major subcellular localization and enzymatic properties including substrate specificity, and each has been found to play a unique role depending on its particular properties. This review is an attempt to concisely summarize current knowledge concerning mammalian sialidases, with an especial focus on their properties and physiological and pathological roles in cellular functions. © 2012 The Author.


Miyagi T.,Tohoku Pharmaceutical University | Takahashi K.,Tohoku Pharmaceutical University | Hata K.,Tohoku Pharmaceutical University | Shiozaki K.,Kagoshima University | Yamaguchi K.,Miyagi Cancer Center Research Institute
Glycoconjugate Journal | Year: 2012

Aberrant glycosylation is a characteristic feature of cancer cells. In particular, altered sialylation is closely associated with malignant properties, including invasiveness and metastatic potential. To elucidate the molecular mechanisms underlying the aberrancy, our studies have focused on mammalian sialidase, which catalyzes the removal of sialic acid residues from glycoproteins and glycolipids. The four types of mammalian sialidase identified to date show altered expression and behave in different manners during carcinogenesis. The present review briefly summarizes results on altered expression of sialidases and their possible roles in cancer progression. These enzymes are indeed factors defining cancer malignancy and thus potential targets for cancer diagnosis and therapy. © Springer Science+Business Media, LLC 2012.


Nishino Y.,Miyagi Cancer Center Research Institute
Japanese Journal of Cancer and Chemotherapy | Year: 2015

The national cancer registry in Japan will commence operations in January 2016 under the Cancer Registry Promotion Act, which was established in December 2013. Although data on cancer incidence and survival rates in Japan have been available for limited regions for a long time, accurate nationwide data obtained from the national cancer registry database will contribute to the planning and evaluation of cancer control in Japan. It is expected that this database will be utilized in evaluating the quality of medical care for cancer patients, in assessing the accuracy of cancer screening, and in follow-up surveys in nationwide cohort studies. Furthermore, under the Cancer Registry Promotion Act, hospitals will be permitted to obtain vital patient information from data registered in the national cancer registry database, which will promote the publication of survival rates for cancer patients and accelerate research at hospitals. The founding of the Japanese national cancer registry is a landmark development in the promotion of cancer control and cancer research in Japan and it is essential that the Japanese population benefits from the information obtained from this database.

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