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Search Results: 1 - 10 of 4287 matches for " Takuji Tanaka "
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Development of an Inflammation-Associated Colorectal Cancer Model and Its Application for Research on Carcinogenesis and Chemoprevention
Takuji Tanaka
International Journal of Inflammation , 2012, DOI: 10.1155/2012/658786
Abstract: Chronic inflammation is a well-recognized risk factor for development of human cancer in several tissues, including large bowel. Inflammatory bowel disease, including ulcerative colitis and Crohn’s disease, is a longstanding inflammatory disease of intestine with increased risk for colorectal cancer development. Several molecular events involved in chronic inflammatory process may contribute to multistep carcinogenesis of human colorectal cancer in the inflamed colon. They include overproduction of reactive oxygen and nitrogen species, overproduction and upregulation of productions and enzymes of arachidonic acid biosynthesis pathway and cytokines, and intestinal immune system dysfunction. In this paper, I will describe several methods to induce colorectal neoplasm in the inflamed colon. First, I will introduce a protocol of a novel inflammation-associated colon carcinogenesis in mice. In addition, powerful tumor-promotion/progression activity of dextran sodium sulfate in the large bowel of mice will be described. Finally, chemoprevention of inflammation-associated colon carcinogenesis will be mentioned. 1. Introduction Relationship between inflammation and cancer has been suggested for a long time [1]. Since Marshall and Warren [2], who discovered Helicobacter pylori and reported its infection closely associated with gastric cancer development, won the Nobel Prize in Physiology or Medicine in 2005, there have been an increasing number of reports on PubMed as to the relationship between inflammation and carcinogenesis in a variety of tissues (Table 1) and it has been featured in major journals. Table 1: Inflammation and cancer in various tissues. In terms of the large bowel, it has been found that the risk of colorectal cancer increases in relation to the degrees of inflammation and the disease duration (duration/risk = 10 years/1.6%, 20 years/8.3%, and 30 years/18.4%) in inflammatory bowl diseases (IBDs) such as ulcerative colitis (UC) and Crohn’s disease (CD) (Figure 1) [3]. I have been interested in inflammation-associated colorectal carcinogenesis for a long time, since even younger patients with UC have high risk of colorectal cancer [4]. Figure 1: UC patients are high-risk groups of colorectal cancer (CRC) development. Patients with UC as well as those with colorectal cancer have been increasing in Asian countries including Japan, similarly to Western countries (Figure 2) [5]. Therefore, it is necessary to investigate the mechanisms of colorectal cancer development with the background of inflammation for establishing the countermeasure strategy
Preclinical Cancer Chemoprevention Studies Using Animal Model of Inflammation-Associated Colorectal Carcinogenesis
Takuji Tanaka
Cancers , 2012, DOI: 10.3390/cancers4030673
Abstract: Inflammation is involved in all stages of carcinogenesis. Inflammatory bowel disease, such as ulcerative colitis and Crohn’s disease is a longstanding inflammatory disease of intestine with increased risk for colorectal cancer (CRC). Several molecular events involved in chronic inflammatory process are reported to contribute to multi-step carcinogenesis of CRC in the inflamed colon. They include over-production of free radicals, reactive oxygen and nitrogen species, up-regulation of inflammatory enzymes in arachidonic acid biosynthesis pathway, up-regulation of certain cytokines, and intestinal immune system dysfunction. In this article, firstly I briefly introduce our experimental animal models where colorectal neoplasms rapidly develop in the inflamed colorectum. Secondary, data on preclinical cancer chemoprevention studies of inflammation-associated colon carcinogenesis by morin, bezafibrate, and valproic acid, using this novel inflammation-related colorectal carcinogenesis model is described.
Colorectal carcinogenesis: Review of human and experimental animal studies
Tanaka Takuji
Journal of Carcinogenesis , 2009,
Abstract: This review gives a comprehensive overview of cancer development and links it to the current understanding of tumorigenesis and malignant progression in colorectal cancer. The focus is on human and murine colorectal carcinogenesis and the histogenesis of this malignant disorder. A summary of a model of colitis-associated colon tumorigenesis (an AOM/DSS model) will also be presented. The earliest phases of colorectal oncogenesis occur in the normal mucosa, with a disorder of cell replication. The large majority of colorectal malignancies develop from an adenomatous polyp (adenoma). These can be defined as well-demarcated masses of epithelial dysplasia, with uncontrolled crypt cell proliferation. When neoplastic cells pass through the muscularis mucosa and infiltrate the submucosa, they are malignant. Carcinomas usually originate from pre-existing adenomas, but this does not imply that all polyps undergo malignant changes and does not exclude de novo oncogenesis. Besides adenomas, there are other types of pre-neoplasia, which include hyperplastic polyps, serrated adenomas, flat adenomas and dysplasia that occurs in the inflamed colon in associated with inflammatory bowel disease. Colorectal neoplasms cover a wide range of pre-malignant and malignant lesions, many of which can easily be removed during endoscopy if they are small. Colorectal neoplasms and/or pre-neoplasms can be prevented by interfering with the various steps of oncogenesis, which begins with uncontrolled epithelial cell replication, continues with the formation of adenomas and eventually evolves into malignancy. The knowledge described herein will help to reduce and prevent this malignancy, which is one of the most frequent neoplasms in some Western and developed countries.
Understanding Carcinogenesis for Fighting Oral Cancer
Takuji Tanaka,Rikako Ishigamori
Journal of Oncology , 2011, DOI: 10.1155/2011/603740
Abstract: Oral cancer is one of the major global threats to public health. Oral cancer development is a tobacco-related multistep and multifocal process involving field cancerization and carcinogenesis. The rationale for molecular-targeted prevention of oral cancer is promising. Biomarkers of genomic instability, including aneuploidy and allelic imbalance, are able to measure the cancer risk of oral premalignancies. Understanding of the biology of oral carcinogenesis will give us important advances for detecting high-risk patients, monitoring preventive interventions, assessing cancer risk, and pharmacogenomics. In addition, novel chemopreventive agents based on molecular mechanisms and targets against oral cancers will be derived from research using appropriate animal carcinogenesis models. New approaches, such as interventions with molecular-targeted agents and agent combinations in high-risk oral individuals, are undoubtedly needed to reduce the devastating worldwide consequences of oral malignancy. 1. Introduction Head and neck cancer is the sixth most common human cancer [1], representing 3% of all types of cancer. They are located in the oral cavity in 48% of cases, and 90% of these are oral squamous cell carcinoma [2]. They are sometimes preceded by precancerous lesions, such as leukoplakia and erythroplakia. More than 300,000 new cases worldwide are being diagnosed with oral squamous cell carcinoma annually [3]. Approximately 35,000 new cases are recorded annually in the US [2], 40,000 new cases in the EU, and 10915 new cases in Japan [4]. The most common site for intraoral carcinoma is the tongue, which accounts for around 40% of all cases in the oral cavity proper. Tongue cancers most frequently occur on the posteriorlateral border and ventral surfaces of the tongue. The floor of the mouth is the second most common intraoral location. Less common sites include the gingival, buccal mucosa, labial mucosa, and hard plate. The incidence of oral cancer has significant local variation. In India and other Asian countries, oral and pharyngeal carcinomas comprise up to half of all malignancies, with this particularly high prevalence being attributed to the influence of carcinogens and region-specific epidemiological factors, especially tobacco and betel quid chewing. An increase in oral cancer prevalence among young adults is a cause of special concern. There has been a 60% increase in the number of under 40 years old with tongue cancer over past 30 years. However, few data have been published on the etiology and natural history of this increase [5]. Oral
Protein expression analysis of inflammation-related colon carcinogenesis
Yasui Yumiko,Tanaka Takuji
Journal of Carcinogenesis , 2009,
Abstract: Background: Chronic inflammation is a risk factor for colorectal cancer (CRC) development. The aim of this study was to determine the differences in protein expression between CRC and the surrounding nontumorous colonic tissues in the mice that received azoxymethane (AOM) and dextran sodium sulfate (DSS) using a proteomic analysis. Materials and Methods: Male ICR mice were given a single intraperitoneal injection of AOM (10 mg/kg body weight), followed by 2% (w/v) DSS in their drinking water for seven days, starting one week after the AOM injection. Colonic adenocarcinoma developed after 20 weeks and a proteomics analysis based on two-dimensional gel electrophoresis and ultraflex TOF/TOF mass spectrometry was conducted in the cancerous and nontumorous tissue specimens. Results: The proteomic analysis revealed 21 differentially expressed proteins in the cancerous tissues in comparison to the nontumorous tissues. There were five markedly increased proteins (beta-tropomyosin, tropomyosin 1 alpha isoform b, S100 calcium binding protein A9, and an unknown protein) and 16 markedly decreased proteins (Car1 proteins, selenium-binding protein 1, HMG-CoA synthase, thioredoxin 1, 1 Cys peroxiredoxin protein 2, Fcgbp protein, Cytochrome c oxidase, subunit Va, ETHE1 protein, and 7 unknown proteins). Conclusions: There were 21 differentially expressed proteins in the cancerous tissues of the mice that received AOM and DSS. Their functions include metabolism, the antioxidant system, oxidative stress, mucin production, and inflammation. These findings may provide new insights into the mechanisms of inflammation-related colon carcinogenesis and the establishment of novel therapies and preventative strategies to treat carcinogenesis in the inflamed colon.
Oral Carcinogenesis and Oral Cancer Chemoprevention: A Review
Takuji Tanaka,Mayu Tanaka,Takahiro Tanaka
Pathology Research International , 2011, DOI: 10.4061/2011/431246
Abstract: Oral cancer is one of the major global threats to public health. The development of oral cancer is a tobacco-related multistep and multifocal process involving field cancerization and carcinogenesis. The rationale for molecular-targeted prevention of oral cancer is promising. Biomarkers of genomic instability, including aneuploidy and allelic imbalance, are possible to measure the cancer risk of oral premalignancies. Understanding of the biology of oral carcinogenesis will yield important advances for detecting high-risk patients, monitoring preventive interventions, and assessing cancer risk and pharmacogenomics. In addition, novel chemopreventive agents based on molecular mechanisms and targets against oral cancers will be derived from studies using appropriate animal carcinogenesis models. New approaches, such as molecular-targeted agents and agent combinations in high-risk oral individuals, are undoubtedly needed to reduce the devastating worldwide consequences of oral malignancy. 1. Introduction Head and neck cancer is the sixth most common human cancer [1], representing 3% of all types of cancer. They are located in the oral cavity in 48% of cases, and 90% of these are oral squamous cell carcinoma [2]. They are sometimes preceded by precancerous lesions, such as leukoplakia and erythroplakia. More than 300,000 new cases of oral squamous cell carcinoma are diagnosed annually [3]. Approximately 35,000 new cases are recorded annually in the US [2], 40,000 new cases are recorded in the EU and 10915 new cases in Japan [4]. The most common site for intraoral carcinoma is the tongue, which accounts for around 40% of all cases in the oral cavity proper. Tongue cancers most frequently occur on the posterior-lateral border and ventral surfaces of the tongue. The floor of the mouth is the second most common intraoral location. Less common sites include the gingival, buccal mucosa, labial mucosa, and hard plate. The incidence of oral cancer has significant local variation. Oral and pharyngeal carcinomas account for up to half of all malignancies in India and other Asian countries, and this particularly high prevalence is attributed to the influence of carcinogens and region-specific epidemiological factors, especially tobacco and chewing betel quid. An increase in the prevalence of oral cancer among young adults is a cause of special concern. There has been a 60% increase in the number of under 40 years olds with tongue cancer over past 30 years. However, little has been published on the etiology and natural history of this increase [5]. Oral malignancy,
Cancer chemoprevention through the induction of apoptosis by natural compounds  [PDF]
Toshiya Kuno, Testuya Tsukamoto, Akira Hara, Takuji Tanaka
Journal of Biophysical Chemistry (JBPC) , 2012, DOI: 10.4236/jbpc.2012.32018
Abstract: As cell and tissue homeostasis are mediated by the balance between proliferation and apoptosis, controlling this balance is important for cancer chemoprevention. Cancer chemoprevention can be achieved by the use of natural, synthetic or biologic compounds that reverse, suppress or prevent the development of epithelial malignancies. Natural compounds including flavonoids are able to reduce oxidative stress, which is the most likely mechanism mediating the protective effects against cancer development. In addition, in vitro and in vivo studies have suggested that flavonoids, such as (-)-epigallocatechin-3-gallete (EGCG), quercetin, and curcumin, act by induction of apoptosis. Several natural compounds inhibit cell proliferation and angiogenesis. Certain natural products have been shown to inhibit the activation of nuclear factor kappa B (NF-κB) and Akt signaling pathways, both of which are known to maintain a homeostatic balance between cell survival and apoptosis. Understanding the mechanism of these natural products will contribute to the development of more specific preventive strategies against cancer development. Here we focus on the ability of natural cancer chemopreventive agents to induce apoptosis, and attempt to provide evidence for the preventive and therapeutic effects of natural compounds, EGCG, quercetin, and curcumin, in a succinct manner highlightingκand Akt signaling pathways in vivo.
Use of Liquid-Based Cytology (LBC) and Cell Blocks from Cell Remnants for Cytologic, Immunohistochemical, and Immunocytochemical Diagnosis of Malignancy  [PDF]
Hirofumi Sakamoto, Makiyo Takenaka, Kazuki Ushimaru, Takuji Tanaka
Open Journal of Pathology (OJPathology) , 2012, DOI: 10.4236/ojpathology.2012.23012
Abstract: Great advances in screening have lowered the death rate from cervical cancer in the advanced countries. The major advances in cervical cancer screening include the Papanicolaou (Pap) test and liquid-based cytology (LBC). In this study, we aimed to use cell remnants from LBC specimens from uterine cervix and endometrium, aspirates from breast and thyroid tumors, and liquid samples (ascites, pleural effusion, and urine). Cell blocks made from cell remnants of LBC specimens were immunohistochemically or immunocytochemically stained for several biomarkers including certain tumor markers such together with hematoxylin and eosin staining for accurate diagnosis of malignancies in different samples. The findings from the cell blocks stained with these biomarkers combined with those from Pap stain led to easily diagnosis of the presence or absence of malignancies. Our findings suggest the utility of LBC and cell blocks from cell remnants in cytologic diagnosis in certain specimens.
Esophageal Carcinogenesis  [PDF]
Naoki Watanabe, Masahito Shimizu, Takahiro Kochi, Yohei Shirakami, Takuji Tanaka
Open Journal of Pathology (OJPathology) , 2014, DOI: 10.4236/ojpathology.2014.44021
Abstract: Esophageal cancer is the sixth leading cause of cancer death and remains one of the least survivable cancers. Esophageal cancers show wide variations in incidence in different population, suggesting that environmental or lifestyle risk factors could be controlled to reduce risk of these diseases. There are two major histopathologic types (squamous cell carcinoma and adenocarcinoma) of esophageal epithelial malignancy. Recently, the rate of adenocarcinoma is increasing in developed countries: in the United States, 50% or more is adenocarcinoma and, in about 70%, the increase especially in a white male serves as adenocarcinoma. Esophageal adenocarcinoma develops in the lower esophagus. In contrast, in Japan, the increase in adenocarcinoma is not clear and most (90%) of esophageal cancers are squamous cell carcinoma. Such squamous cell carcinoma occurs onto the middle part esophagus mostly, and 60% or more of the whole esophagus cancer also develops in the middle and upper parts. These differences also influence the treatment results. The scope of this article is to discuss carcinogenesis in the esophagus by giving an overview about its histopathological characteristics and molecular mechanisms.
Cancer Chemoprevention by Citrus Pulp and Juices Containing High Amounts of β-Cryptoxanthin and Hesperidin
Takuji Tanaka,Takahiro Tanaka,Mayu Tanaka,Toshiya Kuno
Journal of Biomedicine and Biotechnology , 2012, DOI: 10.1155/2012/516981
Abstract: β-Cryptoxanthin, a carotenoid, and hesperidin, a flavonoid, possess inhibitory effects on carcinogenesis in several tissues. We recently have prepared a pulp (CHRP) and citrus juices (MJ2 and MJ5) from a satsuma mandarin (Citrus unshiu Mar.) juice (MJ). They contain high amounts of β-cryptoxanthin and hesperidin. We have demonstrated that CHRP and/or MJs inhibit chemically induced rat colon, rat tongue, and mouse lung tumorigenesis. Gavage with CHRP resulted in an increase of activities of detoxifying enzymes in the liver, colon, and tongue rats'. CHRP and MJs were also able to suppress the expression of proinflammatory cytokines and inflammatory enzymes in the target tissues. This paper describes the findings of our in vivo preclinical experiments to develop a strategy for cancer chemoprevention of colon, tongue, and lung neoplasms by use of CHRP and MJs.
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