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961.
962.
Molecular pathology and potential therapeutic targets in esophageal basaloid squamous cell carcinoma
Tsuyoshi Saito Hiroyuki Mitomi Takashi Yao 《International journal of clinical and experimental pathology》2015,8(3):2267-2273
Basaloid squamous cell carcinoma (BSCC) is a rare and poorly differentiated variant of typical squamous cell carcinoma. Emerging studies show that genetic alterations are more frequent in BSCC than in conventional SCC, and some of which led to the identification of potential therapeutic targets in esophageal BSCC. Approximately half of the esophageal BSCC cases harbor either an EGFR mutation or amplification, and these occur in a mutually exclusive fashion. Therefore, the application of tyrosine kinase inhibitors may be beneficial to esophageal BSCC patients. This tumor is partly characterized by the activation of the Wnt and Hedgehog (HH) signaling pathways. Wnt signaling is activated by SFRP2 promoter hypermethylation and HH signaling is activated by the frequent mutations in PTCH1. Increasing evidence shows that the Wnt signaling pathway is involved in cross-talk with other developmental pathways, including the HH pathway. Therefore, pharmaceutical therapy targeting both the HH and Wnt pathways would be quite effective in patients with esophageal BSCC with highly malignant potential. In this review, we discuss the pathology, prognostic factors, genetic alterations and potential therapeutic targets in BSCC of esophagus. 相似文献
963.
964.
Jeffrey J. Pouliot Michael Thomson Mi Xie Joseph Horton John Johnson David Krull Amanda Mathis Yoshio Morikawa Derek Parks Richard Peterson Takashi Shimada Elizabeth Thomas Jessica Vamathevan Stephanie Van Horn Zhiping Xiong Robert Hamatake Andrew J. Peat 《Antimicrobial agents and chemotherapy》2015,59(10):6539-6550
The hepatitis C virus (HCV) NS4B protein is an antiviral therapeutic target for which small-molecule inhibitors have not been shown to exhibit in vivo efficacy. We describe here the in vitro and in vivo antiviral activity of GSK8853, an imidazo[1,2-a]pyrimidine inhibitor that binds NS4B protein. GSK8853 was active against multiple HCV genotypes and developed in vitro resistance mutations in both genotype 1a and genotype 1b replicons localized to the region of NS4B encoding amino acids 94 to 105. A 20-day in vitro treatment of replicons with GSK8853 resulted in a 2-log drop in replicon RNA levels, with no resistance mutation breakthrough. Chimeric replicons containing NS4B sequences matching known virus isolates showed similar responses to a compound with genotype 1a sequences but altered efficacy with genotype 1b sequences, likely corresponding to the presence of known resistance polymorphs in those isolates. In vivo efficacy was tested in a humanized-mouse model of HCV infection, and the results showed a 3-log drop in viral RNA loads over a 7-day period. Analysis of the virus remaining at the end of in vivo treatment revealed resistance mutations encoding amino acid changes that had not been identified by in vitro studies, including NS4B N56I and N99H. Our findings provide an in vivo proof of concept for HCV inhibitors targeting NS4B and demonstrate both the promise and potential pitfalls of developing NS4B inhibitors. 相似文献
965.
966.
Takahiro Oike Tatsuya Ohno Katsuyuki Shirai Takashi Inoue Takashi Nakano 《Clinical Case Reports》2015,3(8):710-713
Interstitial pneumonia (IP) sometimes precedes collagen vascular disease (CVD) onset. A patient with bladder cancer and mild IP received pelvic irradiation and experienced unexpectedly severe urinary toxicity followed by polymyositis onset and fatal IP exacerbation. Careful observation for “alarm adverse effects” of radiotherapy in IP patients may help predicting CVD onset. 相似文献
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968.
969.
Koichiro Ina Toshio Hayashi Atsushi Araki Seinosuke Kawashima Hirohito Sone Hiroshi Watanabe Takashi Ohrui Koutaro Yokote Minoru Takemoto Kiyoshi Kubota Mitsuhiko Noda Hiroshi Noto Qun‐Fang Ding Jie Zhang Ze‐Yun Yu Byung‐Koo Yoon Hideki Nomura Masafumi Kuzuya Japan CDM Group 《Geriatrics & Gerontology International》2014,14(4):806-810