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19. TP53 codon 72 polymorphism and cervical cancer: a pooled analysis of individual data from 49 studies

Author

Klug, Stefanie J, Ressing, Meike, Koenig, Jochem, Abba, Martin C, Agorastos, Theodoros, Brenna, Sylvia MF, Ciotti, Marco, Das, BR, Del Mistro, Annarosa, Dybikowska, Aleksandra, Giuliano, Anna R, Gudleviciene, Zivile, Gyllensten, Ulf, Haws, Andrea LF, Helland, Aslaug, Herrington, C Simon, Hildesheim, Alan, Humbey, Olivier, Jee, Sun H, Kim, Jae Weon, Madeleine, Margaret M, Menczer, Joseph, Ngan, Hextan YS, Nishikawa, Akira, Niwa, Yoshimitsu, Pegoraro, Rosemary, Pillai, MR, Ranzani, Gulielmina, Rezza, Giovanni, Rosenthal, Adam N, Roychoudhury, Susanta, Saranath, Dhananjaya, Schmitt, Virginia M, Sengupta, Sharmila, Settheetham-Ishida, Wannapa, Shirasawa, Hiroshi, Snijders, Peter JF, Stoler, Mark H, Suárez-Rincón, Angel E, Szarka, Krisztina, Tachezy, Ruth, Ueda, Masatsugu, van der Zee, Ate GJ, von Knebel Doeberitz, Magnus, Wu, Ming-Tsang, Yamashita, Tsuyoshi, Zehbe, Ingeborg, and Blettner, Maria

Published
2009
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21. Essential role of gastric gland mucin in preventing gastric cancer in mice

Author

Karasawa, Fumitoshi, Shiota, Akira, Goso, Yukinobu, Kobayashi, Motohiro, Sato, Yoshiko, Masumoto, Junya, Fujiwara, Maiko, Yokosawa, Shuichi, Muraki, Takashi, Miyagawa, Shinichi, Ueda, Masatsugu, Fukuda, Michiko N., Fukuda, Minoru, Ishihara, Kazuhiko, and Nakayama, Jun

Subjects
Prevention, Physiological aspects, Research, Health aspects, Stomach cancer -- Health aspects -- Prevention -- Research, Mucins -- Physiological aspects -- Research, Helicobacter pylori -- Health aspects -- Research
Abstract

Introduction Gel-forming mucins covering the gastric mucosa are heavily glycosylated glycoproteins that form a barrier between the stomach and the external environment. Gastric mucins are divided into surface mucin and [...], Gastric gland mucin secreted from the lower portion of the gastric mucosa contains unique O-linked oligosaccharides (O-glycans) having terminal α 1,4-linked N-acetylglucosamine residues (α GlcNAc). Previously, we identified human α 1,4-N-acetylglucosaminyltransferase (α 4GnT), which is responsible for the O-glycan biosynthesis and characterized α GlcNAc function in suppressing Helicobacter pylori in vitro. In the present study, we engineered [A4gnt.sup.-/-] mice to better understand its role in vivo. [A4gnt.sup.-/-] mice showed complete lack of α GlcNAc expression in gastric gland mucin. Surprisingly, all the mutant mice developed gastric adenocarcinoma through a hyperplasia-dysplasia-carcinoma sequence in the absence of H. pylori infection. Microarray and quantitative RT-PCR analysis revealed upregulation of genes encoding inflammatory chemokine ligands, proinflammatory cytokines, and growth factors, such as Ccl2, Il-11, and Hgf in the gastric mucosa of [A4gnt.sup.-/-] mice. Further supporting an important role for this O-glycan in cancer progression, we also observed significantly reduced α GlcNAc in human gastric adenocarcinoma and adenoma. Our results demonstrate that the absence of α GlcNAc triggers gastric tumorigenesis through inflammation-associated pathways in vivo. Thus, α GlcNAc-terminated gastric mucin plays dual roles in preventing gastric cancer by inhibiting H. pylori infection and also suppressing tumor-promoting inflammation.

Published
2012
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25. Proceedings of The 28th Annual Meeting of the Japan Human Cell Society 23 August 2009 Tsukuba, Ibaraki, Japan

Author

Abei, Masato, Kameoka, Yosuke, Nakamura, Yukio, Era, Takumi, Masui, Tohru, Akaike, Toshihiro, Akutsu, Hidenori, Eto, Koji, Tamagawa, Tomoharu, Ishiwata, Isamu, Tokieda, Yuko, Iguchi, Megumi, Nakahara, Taka, Kurihara, Kunihiro, Watanabe, Yoshitaka, Kuwahata, Norihiro, Oyama, Akihiro, Ishikawa, Hiroshi, Fukushima, Tsuyoshi, Yokogami, Kiyotaka, Takeshima, Hideo, Kataoka, Hiroaki, Danjoh, Inaho, Araki, Yasuyuki, Sato, Takuya, Katagiri, Kumiko, Kubota, Yoshinobu, Araki, Yasuhisa, Ogawa, Takehiko, Ide, Yoshiaki, Tamaki, Yuichi, Tominaga, Noriko, Kawakami, Miyuki, Yasuda, Makoto, Suzuki, Minako, Nasu, Masanori, Ueda, Masatsugu, Toji, Eisaku, Yamamoto, Michiko, Kunifuji, Noriko, Nishiyama, Hiromi, Nakagawa, Tomomi, Nunobiki, Osamu, Sato, Naomi, Izuma, Shinji, Torii, Kiyo, Okamoto, Yoshiaki, Noda, Sadamu, Li, Yi, Qiang, Li, Kawaguchi, Takuya, Yamahara, Takahiro, Seno, Toshitaka, Numa, Yoshihiro, Asai, Akio, Kawamoto, Keiji, Tanaka, Nobuyuki, Miyajima, Akira, Kosaka, Takeo, Shirotake, Suguru, Hasegawa, Masanori, Kosugi, Michio, Kikuchi, Eiji, Oya, Mototsugu, Gondo, Tatsuo, Horiguchi, Yutaka, Hashimoto, Takeshi, Suzuki, Eriko, Nakashima, Jun, Umezawa, Kazuo, Tachibana, Masaaki, Tanaka, Masamitsu, Kinoshita, Manabu, Yoshihara, Yasuo, Shinomiya, Nariyoshi, Seki, Shuji, Nemoto, Koichi, Morimoto, Yuji, Nakayama, Akiyoshi, Matsuo, Hirotaka, Fujita, Masanori, Suzuki, Shinya, Ishikawa, Mayumi, Ito, Toshihide, Tsuboi, Kumiko, Tachibana, Toshiaki, Shibuya, Kazutoshi, and Yoshino, Gen

Published
2010
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26. Evidence-based guidelines for treatment of cervical cancer in Japan: Japan Society of Gynecologic Oncology (JSGO) 2007 edition

Author

Nagase, Satoru, Inoue, Yoshiki, Umesaki, Naohiko, Aoki, Daisuke, Ueda, Masatsugu, Sakamoto, Hideki, Kobayashi, Shigemitsu, Kitagawa, Ryo, Toita, Takafumi, Nagao, Shoji, Hasegawa, Kiyoshi, Fukasawa, Ichio, Fujiwara, Keiichi, Watanabe, Yoh, Ito, Kiyoshi, Niikura, Hitoshi, Iwasaka, Tsuyoshi, Ochiai, Kazunori, Katabuchi, Hidetaka, Kamura, Toshiharu, Konishi, Ikuo, Sakuragi, Noriaki, Tanaka, Tadao, Hirai, Yasuo, Hiramatsu, Yuji, Mukai, Makio, Yoshikawa, Hiroyuki, Takano, Tadao, Yoshinaga, Kosuke, Otsuki, Takeo, Sakuma, Michiko, Inaba, Noriyuki, Udagawa, Yasuhiro, and Yaegashi, Nobuo

Published
2010
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29. Progressive polyuria without vasopressin neuron loss in a mouse model for familial neurohypophysial diabetes insipidus

Author

Hayashi, Masayuki, Arima, Hiroshi, Ozaki, Noriyuki, Morishita, Yoshiaki, Hiroi, Maiko, Ozaki, Nobuaki, Nagasaki, Hiroshi, Kinoshita, Noriaki, Ueda, Masatsugu, Shiota, Akira, and Oiso, Yutaka

Subjects
Diabetes insipidus -- Risk factors, Diabetes insipidus -- Research, Neurons -- Physiological aspects, Neurons -- Research, Urination disorders -- Risk factors, Urination disorders -- Research, Vasopressin -- Physiological aspects, Vasopressin -- Research, Biological sciences
Abstract

Familial neurohypophysial diabetes insipidus (FNDI), an autosomal dominant disorder, is mostly caused by mutations in the gene of neurophysin II (NPII), the carrier protein of arginine vasopressin (AVP). Previous studies suggest that loss of AVP neurons might be the cause of polyuria in FNDI. Here we analyzed knockin mice expressing mutant NPII that causes FNDI in humans. The heterozygous mice manifested progressive polyuria as do patients with FNDI. Immunohistochemical analyses revealed that inclusion bodies that were not immunostained with antibodies for mutant NPII, normal NPII, or AVP were present in the AVP cells in the supraoptic nucleus (SON), and that the size of inclusion bodies gradually increased in parallel with the increases in urine volume. Electron microscopic analyses showed that aggregates existed in the endoplasmic reticulum (ER) as well as in the nucleus of AVP neurons in 1-mo-old heterozygous mice. At 12 too, dilated ER filled with aggregates occupied the cytoplasm of AVP cells, while few aggregates were found in the nucleus. Analyses with in situ hybridization revealed that expression of AVP mRNA was significantly decreased in the SON in the heterozygous mice compared with that in wild-type mice. Counting cells expressing AVP mRNA in the SON indicated that polyuria had progressed substantially in the absence of neuronal loss. These data suggest that cell death is not the primary cause of polyuria in FNDI, and that the aggregates accumulated in the ER might be involved in the dysfunction of AVP neurons that lead to the progressive polyuria. hereditary disease; arginine vasopressin; endoplasmic reticulum; inclusion bodies

Published
2009

35. Disruption of genetic interaction between two autosomal regions and the X chromosome causes reproductive isolation between mouse strains derived from different subspecies

Author

Oka, Ayako, Aoto, Toshihiro, Totsuka, Yoshikazu, Takahashi, Riichi, Ueda, Masatsugu, Mita, Akihiko, Sakurai-Yamatani, Noriko, Yamamoto, Hiromi, Kuriki, Satoshi, Takagi, Nobuo, Moriwaki, Kazuo, and Shiroishi, Toshihiko

Subjects
Isolating mechanisms -- Research, X chromosome -- Research, Biological sciences
Abstract

Reproductive isolation that initiates speciation is likely caused by incompatibility among multiple loci in organisms belonging to genetically diverging populations. Laboratory C57BL/6J mice, which predominantly originated from Mus musculus domesticus, and a MSM/Ms strain derived from Japanese wild mice (M. m. molossinus, genetically close to M. m. musculus) are reproductively isolated. Their [F.sub.1] hybrids are fertile, but successive intercrosses result in sterility. A consomic strain, C57BL/6J-[ChrX.sup.MSM] which carries the X chromosome of MSM/Ms in the C57BL/6J background, shows male sterility, suggesting a genetic incompatibility of the MSM/Ms X chromosome and other C57BL/6J chromosome(s). In this study, we conducted genomewide linkage analysis and subsequent QTL analysis using the sperm shape anomaly that is the major cause of the sterility of the C57BL/6J-[ChrX.sup.MSM] males. These analyses successfully detected significant QTL on chromosomes 1 and 11 that interact with the X chromosome. The introduction of MSM/Ms chromosomes 1 and 11 into the C57BL/6J-[ChrX.sup.MSM] background failed to restore the sperm-head shape, but did partially restore fertility. This result suggests that this genetic interaction may play a crucial role in the reproductive isolation between the two strains. A detailed analysis of the male sterility by intracytoplasmic sperm injection and zona-free in vitro fertilization demonstrated that the C57BL/6J-[ChrX.sup.MSM] spermatozoa have a defect in penetration through the zona pellucida of eggs.

Published
2007

36. Abstract of Poster Presentation

Author

Uchida, Hiroshi, Maruyama, Tetsuo, Sugiura, Jkuko, Kajitani, Takashi, Arase, Touru, Ono, Masanori, Nagashima, Takashi, Masuda, Hirotaka, Asada, Hironori, Yoshimura, Yasunori, Saito, Soichiro, Ghosh, Mila, Morita, Keiko, Miwa, Masanao, Hirano, Takashi, Todoroki, Takeshi, Kanao, Kento, Ohya, Mototsugu, Murai, Masaru, Ohnuki, Junko, Khor, Lee Wee, Kamiyama, Naoya, Tomioka, Nobumoto, Nakagawa, Takahito, Takahashi, Masato, Todo, Satoru, Kusakabe, Moriaki, Aotsuka, Satoshi, Inoue, Jun, Matsuba, Kyouichi, Hashimoto, Hisashi, Isonishi, Seiji, Yasuda, Makoto, Ishikawa, Hiroshi, Ueda, Masatsugu, Terai, Yoshito, Yamaguchi, Hiroyuki, Ueki, Minoru, Uchinokura, Shunro, Miyata, Shiro, Fukushima, Tsuyoshi, Itoh, Hiroshi, Nakano, Shinichi, Wakisaka, Shinichiro, Kataoka, Hiroaki, Ohi, Satoshi, Tabei, Isao, Hirabayashi, Tetsuya, Ninomiya, Kozou, Ichikawa, Ayumi, Ogata, Tomomi, Tachibana, Toshiyuki, Sato, Kahei, Yanaga, Katsuhiko, Tamagawa, Tomoharu, Iguchi, Megumi, Tokieda, Yuko, Ishiwata, Isamu, Ono, Isao, Kiguchi, Kazushige, Ishiwata, Chieko, Ishiwata, Emiko, Soma, Masayuki, Nakamura, Hiroko, Mizuno, Jinji, Fueta, Youichi, Kamakura, Hirokazu, Murayama, Yoshinobu, Omata, Sadao, Akaishi, Kazuyuki, Inui, Hiroaki, Mizuno, Jinii, Ostrovidov, Serge, Sakai, Yasuyuki, Fujii, Teruo, Watanabe, Natsumi, Hirayma, Kazuhiro, Kuriki, Eiko, Kobayashi, Mamoru, Yakuwa, Takushi, Okamoto, Naoki, Sato, Yorino, Tanaka, Fumi, Kazami, Ai, Hasegawa, Hisataka, Tanaka, Naoki, Araki, Yasuyuki, Yoshizawa, Midori, Araki, Yasuhisa, Sakaguchi, Eriko, Tomita, Kouichi, Ninomiya, Kozo, Ishida, Yuichi, Tachibana, Toshiaki, Tsuboi, Kumiko, Ishikawa, Mayumi, Ueshiba, Hajime, Kitahara, Shinzo, Yoshino, Gen, Tamagawa, Tomoharu, Ishiwata, Samu, Miharada, Kenichi, Sudo, Kazuhiro, Nakamura, Yukio, Li, Qiang, Ryu, Takashi, Azuma, Keiichi, Hosaka, Naoki, Ikehara, Susumu, Kawamoto, Keiji, Ono, Masanori, Hamatani, Toshio, Okano, Hideyuki, Matsuzaki, Yumi, Yamamoto, Matsuo, Sakoda, Kenji, Negishi, Yoichi, Sekiya, Hideki, Sakiyama, Yusuke, Suzuki, Kazunari, Yano, Tomoya, Fukawa, Yukiko, Node, Koichi, Izumi, Yuichi, Kobayashi, Makoto, Takagi, Takamasa, Takahashi, Noriko, Mitsui, Masashi, Murayama, Reiichiro, Moritaka, Shunichiro, Tsurumi, Ayuko, Hayashi, Iyou, Hayashi, Yukie, Okamatsu, Yoshimasa, Miharada, Ken-ichi, Hiroyama, Takashi, Fujioka, Tsuyoshi, Nagasawa, Toshiro, Suzuki, Nao, Orikawa, Kimiko, Tamada, Yutaka, Suzuki, Atsushi, Susumu, Nobuyuki, Tsukazaki, Katsumi, Mukai, Makio, Kojima-Aikawa, Kyoko, Ishida, Isao, Aoki, Daisuke, Kobayashi, Yoichi, Takahashi, Noriyuki, Ohara, Tatsuru, Okuda, Yoshiko, Sato, Sojiro, Ishizuka, Bunpei, Sato, Akinori, Ito, Keiichi, Ooya, Mototsugu, Asano, Takako, Sumitomo, Makoto, Horiguchi, Yutaka, Asano, Tomohiko, Hayakawa, Masamichi, Sasaki, Naoki, Kita, Tsunekazu, Okamoto, Sanshiro, Takano, Masashi, Kudoh, Kazuya, Furuya, Kenichi, Kikuchi, Yoshihiro, Nariai, Koichi, Yoshikawa, Tetsuya, Mitsunaga, Makoto, Sumi, Makoto, Yumoto, Yoko, Mabashi, Yasuo, Namiki, Yoshihisa, Tsubota, Akihito, Fujise, Kiyotaka, Takahashi, Hiroshi, Harada, Hideki, Suzu, Shinya, Ito, Takaaki, Okada, Seiji, Suzuki, Nagazumi, Ueda, Kazu, Yamada, Kyosuke, Tanaka, Tadao, Kondo, Kan, Shimada, Yutaka, Nakagami, Yoshihiro, Aoyagi, Teiichiro, Gondo, Tatsuo, Sakamoto, Noboru, Ohno, Yoshio, Koga, Shouji, Namiki, Kazunori, Yoshioka, Kunihiko, Ohori, Makoto, Hatano, Tadashi, Tachibana, Masaaki, Kobayashi, Yoichi, Watanabe, Mari, Wada, Yasuna, and Mizuhara, Hiroshi

Published
2005
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38. Abstracts of Workshop

Author

Takechi, Teiji, Koizumi, Katsuhisa, Azuma, Atsushi, Fukushima, Masakazu, Kobayashi, Katsutoshi, Oda, Shinya, Yanaga, Katsuhiko, Mullenders, Leon, Karran, Peter, Ueda, Masatsugu, Terai, Yoshito, Ueki, Minoru, Sakamoto, Masaru, Kondo, Aako, Miyake, Kiyohiko, Koyamatsu, Yauko, Akiya, Tsukasa, Nakano, Makoto, Iwabuchi, Hiroshi, Muroya, Tetsuya, Tenjin, Yoshio, Ochiai, Kazunori, Tanaka, Tadao, Ymada, Kyosuke, Ueda, Kazu, Misawa, Akihiko, Okamoto, Aikou, Kimura, Eizo, and Yasuda, Makoto

Published
2004
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50. A rat model for LGI1-related epilepsies

Author

Baulac, Stéphanie, Ishida, Saeko, Mashimo, Tomoji, Boillot, Morgane, Fumoto, Naohiro, Kuwamura, Mitsuru, Ohno, Yukihiro, Takizawa, Akiko, Aoto, Toshihiro, Ueda, Masatsugu, Ikeda, Akio, LeGuern, Eric, Takahashi, Ryosuke, and Serikawa, Tadao

Published
2012
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