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Genda Takuya Ichida Takafumi Tanaka Eiji Mochida Satoshi Ueno Yoshiyuki Terai Shuji Inui Ayano Ueda Yoshihide Ohdan Hideki Egawa Hiroto Umeshita Koji Furukawa Hiroyuki Inomata Yukihiro 《Journal of gastroenterology》2022,57(7):495-504
Journal of Gastroenterology - Following liver transplantation (LT), allograft liver failure can be developed by various causes and requires re-LT. Hence, this study aimed to clarify the... 相似文献
83.
Iwakawa Hidehiro Takigawa Masateru Goya Masahiko Iwata Toyoto Martin Claire A. Anzai Tatsuhiko Takahashi Kunihiko Amemiya Miki Yamamoto Tasuku Sekigawa Masahiro Shirai Yasuhiro Tao Susumu Hayashi Tatsuya Takahashi Yoshihide Watanabe Hiroyuki Sasano Tetsuo 《Journal of interventional cardiac electrophysiology》2022,63(1):185-195
Journal of Interventional Cardiac Electrophysiology - Clinical implication of local impedance (LI) for radiofrequency (RF) ablation has not been fully established. This study aimed to investigate... 相似文献
84.
Kuroda J Kamitsuji Y Kimura S Ashihara E Kawata E Nakagawa Y Takeuichi M Murotani Y Yokota A Tanaka R Andreeff M Taniwaki M Maekawa T 《International journal of hematology》2008,87(5):507-515
Since a variety of cell intrinsic and extrinsic molecular abnormalities cooperatively promote tumor formation in multiple myeloma (MM), therapeutic approaches that concomitantly target more than one molecule are increasingly attractive. We herein demonstrate the anti-myeloma effect of a cephalotaxus alkaloid, homoharringtonine (HHT), an inhibitor of protein synthesis, through the induction of apoptosis. HHT significantly reduced Mcl-1, a crucial protein involved in myeloma cell survival, in all three myeloma cell lines examined, whereas certain BH3-only proteins, such as Bim, Bik, and Puma, remained unchanged following HHT treatment, and their expression levels depended on the cell type. HHT also reduced the levels of c-FLIP(L/S), activated caspase-8, and induced active truncated-Bid. Thus, HHT-induced apoptosis appears to be mediated via both intrinsic and extrinsic apoptosis pathways, and the resultant imbalance between BH3-only proteins and Mcl-1 may be pivotal for apoptosis by HHT. In addition, HHT treatment resulted in reduced levels of beta-catenin and XIAP proteins, which also contribute to disease progression and resistance to chemotherapy in MM. In combination, HHT enhanced the effects of melphalan, bortezomib, and ABT-737. These results suggest that HHT could constitute an attractive option for MM treatment though its ability to simultaneously target multiple tumor-promoting molecules. 相似文献
85.
Expression of p57/Kip2 protein in pancreatic adenocarcinoma 总被引:14,自引:0,他引:14
INTRODUCTION: Evaluation of the biologic character of carcinomas requires understanding of cell cycle regulators. AIMS: To investigate p57 expression in human pancreatic adenocarcinoma and cyst adenoma. METHODOLOGY: We examined the expression of p57(Kip2), a member of the Cip/Kip family, in 45 pancreatic adenocarcinomas, 7 cystadenomas, and 7 chronic pancreatitis cases. RESULTS: The p57 labeling index (LI) in duct epithelia in chronic pancreatitis averaged 32.8+/-8.3 and was significantly higher than in normal duct epithelia (18.8+/-6.6; p = 0.0011). For the carcinoma, the LI averaged 46.0+/-20.9, which was significantly higher than that for normal duct epithelia (p < 0.0001) and cystadenoma (16.0 11.2; p = 0.0007). However, it was significantly reduced in cases with stage IV disease (p = 0.0351), lymph node metastasis (p = 0.0003), larger size (p = 0.0094), capsular invasion (p = 0.0462), lymphatic invasion (p = 0.0351), and cell proliferating activity (p = 0.0002). In multivariate analysis, p57 LI in pancreatic adenocarcinoma was independently linked to high proliferating activity (p = 0.0230). CONCLUSION: These results suggest that p57 plays a role in the hyperplastic change of the ducts in chronic pancreatitis and that pS7 overexpression contributes to the downregulation of cell proliferation, and its decreased expression contributes to the progression of pancreatic adenocarcinoma. 相似文献
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Yoshihide Ueda Kenji Kurihara Tsuyoshi Kondoh Toyotake Okanoue Tsutomu Chiba 《Journal of gastroenterology》1998,33(1):125-128
We report a patient, a 23-year-old man, who had clinical and laboratory findings suggestive of insulinoma. Although imaging
studies did not reveal any tumors in the pancreas, distal pancreatectomy was performed because the possibility of small insulinoma
could not be completely excluded. Grossly, the surgically removed pancreas did not reveal any tumors. Microscopically, the
pancreas exhibited islet cell hyperplasia and nesidioblastosis. To our knowledge, this is the first authentic reported case
of islet-cell hyperplasia occurring in a Japanese adult.
Received Mar. 4, 1997; accepted May 23, 1997 相似文献
89.
Tahara H Imanishi Y Yamada T Tsujimoto Y Tabata T Inoue T Inaba M Morii H Nishizawa Y 《The Journal of clinical endocrinology and metabolism》2000,85(11):4113-4117
The molecular pathway of autonomous growth of the parathyroid glands in uremic patients is poorly understood. Loss of heterozygosity at the recently identified multiple endocrine neoplasia type 1 (MEN1) gene locus on chromosome 11q13 has been found in a subset of parathyroid glands from patients with refractory hyperparathyroidism. To clarify the role of the MEN1 gene in parathyroid tumorigenesis, we analyzed 81 parathyroid glands from 22 Japanese uremic patients for allelic loss on chromosomal arm 11q13 DNA using 3 flanking markers (PYGM, D11S4946, and D11S449) and for mutations of the MEN1-coding exons by PCR-based single strand conformation polymorphism analysis and sequencing. Allelic loss on 11q13 was observed in 6 glands (7%), and 1 of 6 demonstrated a previously unrecognized somatic frameshift deletion (331delG) of the MEN1 gene. This mutation would probably result in a nonfunctional menin protein, consistent with a tumor suppressor mechanism. Clinical and pathological characteristics of hyperparathyroidism were unrelated to the presence or absence of loss of heterozygosity on 11q13 and MEN1 gene mutations. These observations indicate that somatic inactivation of the MEN1 gene contributes to the pathogenesis of uremia-associated parathyroid tumors, but its role in this disease appears to be very limited. 相似文献
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