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Takao Endo

Bio: Takao Endo is an academic researcher from Sapporo Medical University. The author has contributed to research in topics: Regulation of gene expression & DNA methylation. The author has an hindex of 8, co-authored 9 publications receiving 1725 citations.

Papers
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Journal ArticleDOI
TL;DR: The results of clinical tests in colonoscopy and esophagoscopy indicated that NBI will be useful as a supporting method for observation of the endoscopic findings of early cancer.
Abstract: This study was performed to examine the usefulness of medical endoscopic imaging utilizing narrow-band illumination. The contrast between the vascular pattern and the adjacent mucosa of the underside of the human tongue was measured using five narrow-band illuminations and three broadband illuminations. The results demon- strate that the pathological features of a vascular pattern are depen- dent on the center wavelength and the bandwidth of illumination. By utilizing narrow-band illumination of 415630 nm, the contrast of the capillary pattern in the superficial layer was markedly improved. This is an important benefit that is difficult to obtain with ordinary broad- band illumination. The appearances of capillary patterns on color im- ages were evaluated for three sets of filters. The narrow, band imaging (NBI) filter set (415630 nm, 445630 nm, 500630 nm) was selected to achieve the preferred appearance of the vascular patterns for clini- cal tests. The results of clinical tests in colonoscopy and esophagos- copy indicated that NBI will be useful as a supporting method for observation of the endoscopic findings of early cancer. © 2004 Society of

858 citations

Journal ArticleDOI
TL;DR: A new illumination method for a medical endoscope: narrow band imaging (NBI), in which the spectral bandwidth of the filtered light is narrowed, which has been shown that NBI can enhance the capillary pattern and the crypt pattern on the mucosa.
Abstract: We propose a new illumination method for a medical endoscope: narrow band imaging (NBI), in which the spectral bandwidth of the filtered light is narrowed. To confirm how the spectral specifications of the filtered light influence a reproduced image, an experiment was conducted observing the endoscopic images of the back mucosa of a human tongue. In addition, the effect of NBI on endoscopic images was investigated through preliminary clinical tests in colonoscopy and upper gastrointestinal endoscopy. It has been shown that NBI can enhance the capillary pattern and the crypt pattern on the mucosa. These patterns are useful features for diagnosing an early cancer.

287 citations

Journal ArticleDOI
TL;DR: Magnifying endoscopy by NBI is more useful than conventional magnifying endoscopeopy for the diagnosis of Barrett’s esophagus and the relationship between the endoscopic and histopathologic diagnoses was more accurate by N BI endoscopes than by conventional endoscope.
Abstract: A newly developed endoscope lighting system called a narrow-band imaging system emphasizes certain histological features such as capillary and crypt patterns. The usefulness of NBI for the diagnosis of Barrett’s esophagus (BE) was evaluated. Eleven patients with previously diagnosed BE were enrolled in this study. Magnifying endoscopy was performed by an experienced endoscopist, using both a conventional system and an NBI system. All images were recorded by video and by a digital still image filing system. Differences in images were evaluated by another experienced endoscopist. The quality of images for the visualization of the esophagogastric junction, capillary vessels, and columnar-lined esophagus (CLE) was judged as: optimal (score of 4), diagnostic (3), suboptimal (2), or nondiagnostic (1). In contrast to the low rate of visualization of the esophagogastric junction by conventional endoscopy, visualization of this area endoscopy was better by NBI. Net-like blood vessels were more clearly seen on images obtained by NBI endoscopy. Visualization of the CLE was better by NBI endoscopy than by conventional endoscopy. In contrast to conventional endoscopy, NBI endoscopy captured the optimal view of Barrett’s epithelium. The relationship between the endoscopic and histopathologic diagnoses was more accurate by NBI endoscopy than by conventional endoscopy. Magnifying endoscopy by NBI is more useful than conventional magnifying endoscopy for the diagnosis of BE.

198 citations

Journal Article
TL;DR: By affecting mitotic checkpoint function, CHFR inactivation likely plays a key role in tumorigenesis in gastric cancer, and the aberrant methylation of CHFR appears to be a good molecular marker with which to predict the sensitivity of gastric cancers to microtubule inhibitors.
Abstract: Mitotic checkpoints prevent errors in chromosome segregation that can lead to neoplasia. Therefore, it is notable that gastric cancers often show impaired checkpoint function. In the present study, we examined the functional consequences of epigenetic inactivation of the mitotic checkpoint gene CHFR in gastric cancers. CHFR expression was silenced by DNA methylation of the 5' region of the gene in 20% of the gastric cancer cell lines tested and in 39% of primary gastric cancers; expression could be restored by treatment with 5-aza-2'-deoxycytidine, a methyltransferase inhibitor. In addition, histones H3 and H4 were found to be deacetylated in cell lines showing aberrant methylation, indicating a role for histone deacetylation in the methylation-dependent gene silencing. Cells not expressing CHFR showed impaired checkpoint function, which led to nuclear localization of cyclin B1 after treatment with docetaxel or paclitaxel, two microtubule inhibitors. Apparently, the absence of CHFR is associated with sensitivity of cells to mitotic stress caused by microtubule inhibition, and restoration of CHFR expression by 5-aza-2'-deoxycytidine or adenoviral gene transfer restored the checkpoint. By affecting mitotic checkpoint function, CHFR inactivation likely plays a key role in tumorigenesis in gastric cancer. Moreover, the aberrant methylation of CHFR appears to be a good molecular marker with which to predict the sensitivity of gastric cancers to microtubule inhibitors.

160 citations

Journal Article
TL;DR: In this paper, the expression and DNA methylation status of BNIP3 gene in a panel of colorectal and gastric cancer cell lines were examined, and it was found that methylation of the 5' CpG island was closely correlated with silencing the gene.
Abstract: BNIP3 protein is a proapoptotic member of the Bcl-2 family that is expressed in hypoxic regions of tumors. To examine its role in the progression of gastrointestinal cancer, we examined the expression and DNA methylation status of BNIP3 gene in a panel of colorectal and gastric cancer cell lines. BNIP3 was not expressed in 14 of the 24 cell lines tested, and its absence was not caused by gene mutation or by altered expression of hypoxia inducible factor-1, a key transcription factor that regulates BNIP3 expression. On the other hand, methylation of the 5' CpG island of BNIP3 was closely correlated with silencing the gene. Moreover, treating methylated cells with the methyltransferase inhibitor 5-aza-2'-deoxycytidine restored hypoxia-induced expression of BNIP3 mRNA and protein, which in turn led to cell death. Aberrant methylation of BNIP3 was also detected in 66% of primary colorectal and 49% of primary gastric cancers, but not in normal tissue samples collected from areas adjacent to the tumors. Apparently, epigenetic alteration of BNIP3 is a frequent and cancer-specific event, which suggests that inactivation of BNIP3 likely plays a key role in the progression of some gastrointestinal cancers and that it may be a useful molecular target for therapy.

147 citations


Cited by
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Journal ArticleDOI
TL;DR: Once MMP has been induced, it causes the release of catabolic hydrolases and activators of such enzymes (including those of caspases) from mitochondria, meaning that mitochondria coordinate the late stage of cellular demise.
Abstract: Irrespective of the morphological features of end-stage cell death (that may be apoptotic, necrotic, autophagic, or mitotic), mitochondrial membrane permeabilization (MMP) is frequently the decisive event that delimits the frontier between survival and death. Thus mitochondrial membranes constitute the battleground on which opposing signals combat to seal the cell's fate. Local players that determine the propensity to MMP include the pro- and antiapoptotic members of the Bcl-2 family, proteins from the mitochondrialpermeability transition pore complex, as well as a plethora of interacting partners including mitochondrial lipids. Intermediate metabolites, redox processes, sphingolipids, ion gradients, transcription factors, as well as kinases and phosphatases link lethal and vital signals emanating from distinct subcellular compartments to mitochondria. Thus mitochondria integrate a variety of proapoptotic signals. Once MMP has been induced, it causes the release of catabolic hydrolases and activators of such enzymes (including those of caspases) from mitochondria. These catabolic enzymes as well as the cessation of the bioenergetic and redox functions of mitochondria finally lead to cell death, meaning that mitochondria coordinate the late stage of cellular demise. Pathological cell death induced by ischemia/reperfusion, intoxication with xenobiotics, neurodegenerative diseases, or viral infection also relies on MMP as a critical event. The inhibition of MMP constitutes an important strategy for the pharmaceutical prevention of unwarranted cell death. Conversely, induction of MMP in tumor cells constitutes the goal of anticancer chemotherapy.

3,340 citations

Journal ArticleDOI
TL;DR: Novel aspects of the new definition include a patient-centered approach that is independent of endoscopic findings, subclassification of the disease into discrete syndrome, and the recognition of laryngitis, cough, asthma, and dental erosions as possible GERD syndromes.

3,328 citations

Journal ArticleDOI
TL;DR: A model in which the atypical BH3 domains of hypoxia-induced BNIP3/BNIP3L have been designed to induce autophagy by disrupting the Bcl-2-Beclin1 complex without inducing cell death is proposed.
Abstract: While hypoxia-inducible factor (HIF) is a major actor in the cell survival response to hypoxia, HIF also is associated with cell death. Several studies implicate the HIF-induced putative BH3-only proapoptotic genes bnip3 and bnip3l in hypoxia-mediated cell death. We, like others, do not support this assertion. Here, we clearly demonstrate that the hypoxic microenvironment contributes to survival rather than cell death by inducing autophagy. The ablation of Beclin1, a major actor of autophagy, enhances cell death under hypoxic conditions. In addition, the ablation of BNIP3 and/or BNIP3L triggers cell death, and BNIP3 and BNIP3L are crucial for hypoxia-induced autophagy. First, while the small interfering RNA-mediated ablation of either BNIP3 or BNIP3L has little effect on autophagy, the combined silencing of these two HIF targets suppresses hypoxia-mediated autophagy. Second, the ectopic expression of both BNIP3 and BNIP3L in normoxia activates autophagy. Third, 20-mer BH3 peptides of BNIP3 or BNIP3L are sufficient in initiating autophagy in normoxia. Herein, we propose a model in which the atypical BH3 domains of hypoxia-induced BNIP3/BNIP3L have been designed to induce autophagy by disrupting the Bcl-2-Beclin1 complex without inducing cell death. Hypoxia-induced autophagy via BNIP3 and BNIP3L is clearly a survival mechanism that promotes tumor progression.

1,259 citations

Journal ArticleDOI
TL;DR: The data indicate that Bnip3 regulates the apoptotic balance as an autophagy receptor that induces removal of both mitochondria and ER and that this process significantly reduced both mitophagy and ERphagy.

566 citations