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| 1 | Familial pancreatic cancer: Concept, management and issues显示文摘Familial pancreatic cancer (FPC) is broadly defined as two first-degree-relatives with pancreatic cancer (PC) and accounts for 4%-10% of PC. Several genetic syndromes, including Peutz-Jeghers syndrome, hereditary pancreatitis, hereditary breast-ovarian cancer syndrome(HBOC), Lynch syndrome, and familial adenomatous polyposis (FAP), also have increased risks of PC, but the narrowest definition of FPC excludes these known syndromes. When compared with other familial tumors, proven genetic alterations are limited to a small proportion (<20%) and the familial aggregation is usually modest. However, an ethnic deviation (Ashkenazi Jewish>Caucasian) and a younger onset are common also in FPC. In European countries, 'anticipation' is reported in FPC families, as with other hereditary syndromes; a trend toward younger age and worse prognosis is recognized in the late years. The resected pancreases of FPC kindred often show multiple pancreatic intraepithelial neoplasia (Pan IN) foci, with various K-ras mutations, similar to colorectal polyposis seen in the FAP patients. As with HBOC patients, a patient who is a BRCA mutation carrier with unresectable pancreatic cancer (accounting for 0%-19% of FPC patients) demonstrated better outcome following platinum and Poly (ADP-ribose) polymerase inhibitor treatment. Western countries have established FPC registries since the 1990 s and several surveillance projects for highrisk individuals are now ongoing to detect early PCs. Improvement in lifestyle habits, including non-smoking, is recommended for individuals at risk. In Japan, the FPC study group was initiated in 2013 and the Japanese FPC registry was established in 2014 by the Japan Pancreas Society. | Hiroyuki Matsubayashi Kyoichi Takaori Chigusa Morizane Hiroyuki Maguchi Masamichi Mizuma Hideaki Takahashi Keita Wada Hiroko Hosoi Shinichi Yachida Masami Suzuki Risa Usui Toru Furukawa Junji Furuse Takamitsu Sato Makoto Ueno Yoshimi Kiyozumi Susumu Hijioka Nobumasa Mizuno Takeshi Terashima Masaki Mizumoto Yuzo Kodama Masako Torishima Takahisa Kawaguchi Reiko Ashida Masayuki Kitano Keiji Hanada Masayuki Furukawa Ken Kawabe Yoshiyuki Majima Toru Shimosegawa | 2017 | World Journal of Gastroenterology2017，23，6： | 5 |
| 2 | PI3K-Akt inactivation induced CHOP expression in endoplasmic reticulum-stressed cells显示文摘 | Kanae Hyoda Toru Hosoi Naohiro Horie Yasunobu Okuma Koichiro Ozawa Yasuyuki Nomura | 2005 | Biochemical and Biophysical Research Communications2005，，1： | 1 |
| 3 | Akt up- and down-regulation in response to endoplasmic reticulum stress显示文摘 | Toru Hosoi Kanae Hyoda Yasunobu Okuma Yasuyuki Nomura Koichiro Ozawa | 2007 | Brain Research2007，，： | 1 |
| 4 | Edaravone protects against hypoxia/ischemia-induced endoplasmic reticulum dysfunction显示文摘 | Xin Qi Yasunobu Okuma Toru Hosoi and Yasuyuki Nomum | 2004 | J Pharmacoi Exp Ther2004，3，： | 1 |
| 5 | Neuroprotective Effects of 4-phenylbutyric Acid and Its Derivatives: Possible Therapeutics for Neurodegenerative Diseases显示文摘 | Seisuke Mimori Toru Hosoi Masayuki Kaneko Koichiro Ozawa Tetsuto Kanzaki Akinori Nishi Yasuyuki Nomura | 2017 | Journal of Health Science2017，5，1： | 0 |
| 6 | Geldanamycin induces CHOP expression through a 4-(2-aminoethyl)-benzenesulfonyl fluoride-responsive serine protease显示文摘Dear Editor:Geldanamycin is a benzoquinone ansamycin,which wasoriginally described as a tyrosine kinase inhibitor.How-ever,subsequent studies have revealed that geldanamycinbinds to and inhibits heat-shock protein 90(Hsp90)activity[1].Hsp90 is a molecular chaperone involved in the con-formational maturation of proteins such as mutated p53,Raf-1,Akt,Bcr-Ab1,and ErbB2.It is suggested that agentsinhibiting Hsp90 have anti-cancer properties,although theprecise molecular mechanisms underlying the anti-cancereffects of geldanamycin are not well understood.Increasing evidence has suggested that diabetes andneurodegenerative disorders such as Parkinson's andAlzheimer's diseases are related to the disruption ofendoplasmic reticulum(ER)function.In response to ERstress,unfolded proteins accumulate and aggregate in theER,which will trigger many rescuer responses,includingthe unfolded protein response(UPR)and ER-associateddegradation.Interestingly,geldanamycin has been shownto upregulate ER chaperones and the expression of CHOP[2].Moreover,Hsp90 associates with PERK and IRE1α,ER-resident trans-membrane protein kinases involved inER stress response[3].These observations suggest | Toru Hosoi Kanae Hyoda Yasunobu Okuma Yasuyuki Nomura Koichiro Ozawa | 2007 | Cell Research2007，17，2： | 0 |
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