Prevention of Colorectal Cancer by Targeting Obesity-Related Disorders and Inflammation.

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Annotation Summary

Term Occurence Count Dictionary
obesity 22 endocrinologydiseases
Insulin 1 endocrinologydiseasesdrugs
captopril 2 endocrinologydiseasesdrugs
diabetes mellitus 1 endocrinologydiseases
hyperinsulinemia 2 endocrinologydiseases
hyperlipidemia 1 endocrinologydiseases
metabolic syndrome 1 endocrinologydiseases
metformin 3 endocrinologydiseasesdrugs

Graph of close proximity drug and disease terms (within 200 characters).

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Select Drug Character Offset Drug Term Instance
Insulin 11976 experimental evidence has indicated that obesity is related to the incidence of CRC [[8],[9],[10],[50]]. Insulin resistance and hyperinsulinemia, metabolic disorders associated with obesity, are considered important
captopril 19617 obesity-related CRC model [[25]]. The employed agents were an angiotensin-converting enzyme inhibitor, captopril , and an angiotensin-II type 1 receptor blocker, telmisartan, both of which have the ability to inhibit
captopril 19891 development of colorectal lesions, ACF and BCAC, was significantly inhibited by the treatment with either captopril or telmisartan. These agents markedly decreased the expression levels of TNF-α in the colonic mucosa,
metformin 16919 trials examining the effects of non-steroidal anti-inflammatory drugs such as celecoxib, aspirin, and metformin on the development of CRC or its precursor lesion adenomatous polyp in patients, where these agents
metformin 24379 [[75]]Metformin (250 mg/day)Sporadic colorectal polyps151 subjects (72 in the placebo and 79 in the metformin group)One yearThe prevalence of total polyps and adenomas in the metformin group was significantly lower;
metformin 24454 the placebo and 79 in the metformin group)One yearThe prevalence of total polyps and adenomas in the metformin group was significantly lower; (total polyps) risk ratio 0.67 (95% CI: 0.47–0.97), (adenomas) risk
Select Disease Character Offset Disease Term Instance
diabetes mellitus 2989 and experimental evidence has indicated that obesity and related metabolic abnormalities, especially diabetes mellitus , are associated with the development of various malignancies, including CRC [[8],[9]]. Several pathophysiological
hyperinsulinemia 11999 indicated that obesity is related to the incidence of CRC [[8],[9],[10],[50]]. Insulin resistance and hyperinsulinemia , metabolic disorders associated with obesity, are considered important risk factors for CRC development
hyperinsulinemia 13781 types metabolic disorders [[66]]. Hirose et al. [[67]] have shown that db/db mice have hyperlipidemia, hyperinsulinemia , and hyperleptinemia, and are susceptible to the colonic carcinogen AOM. We used a db/db mouse and investigated
hyperlipidemia 13765 investigating various types metabolic disorders [[66]]. Hirose et al. [[67]] have shown that db/db mice have hyperlipidemia , hyperinsulinemia, and hyperleptinemia, and are susceptible to the colonic carcinogen AOM. We used a
metabolic syndrome 19178 the renin-angiotensin system (RAS) has been shown to contribute to high blood pressure, obesity, and metabolic syndrome [[85]]. RAS has been demonstrated to be frequently up-regulated in malignancies attributed to systemic
obesity 950 discover agents that help in the prevention of this disease. Chronic inflammation in colonic mucosa and obesity , and its related metabolic abnormalities, are considered to increase the risk of colorectal cancer.
obesity 1306 functional foods, various phytochemicals, including tea catechins, which have anti-inflammatory and anti- obesity properties, and medicinal agents that ameliorate metabolic disorders, might also be beneficial in the
obesity 1547 cancer. In this review article, we summarize the strategies for preventing colorectal cancer by targeting obesity -related disorders and inflammation through nutraceutical and pharmaceutical approaches, and discuss
obesity 2933 the recent years worldwide [[7]]. Recent epidemiological and experimental evidence has indicated that obesity and related metabolic abnormalities, especially diabetes mellitus, are associated with the development
obesity 3155 malignancies, including CRC [[8],[9]]. Several pathophysiological mechanisms of interaction between obesity and CRC have been studied, including insulin resistance, adipocytokine imbalances, alterations in the
obesity 3725 the beneficial effects of green tea catechins (GTCs) on improving the metabolic abnormalities such as obesity , thus preventing the development of malignancies [[13],[14],[15],[16]]. Another plant-derived substance,
obesity 4799 The current review summarizes the most promising strategies for the prevention of CRC by targeting obesity -related disorders and inflammation through nutritional and/or pharmaceutical approaches with several
obesity 5017 phytochemicals and medicinal drugs described above, because these agents have been closely studied in obesity -associated CRC models. In addition, this review article also further discusses the mechanisms of several
obesity 9723 lipid rafts. Among RTKs, IGF-1R is thought to be one of the most critical targets for the inhibition of obesity -related carcinogenesis by tea catechins, although the direct alteration of catechins on IGF-1R needs
obesity 11912 of cancer in the inflamed colon. Recent epidemiological and experimental evidence has indicated that obesity is related to the incidence of CRC [[8],[9],[10],[50]]. Insulin resistance and hyperinsulinemia, metabolic
obesity 12053 CRC [[8],[9],[10],[50]]. Insulin resistance and hyperinsulinemia, metabolic disorders associated with obesity , are considered important risk factors for CRC development [[51]]. It is reported that insulin and its
obesity 12949 resistance, inflammation, and oxidative stress can be considered as important factors in the development of obesity -related CRC [[60],[61]]. This imbalance is usually caused by enhanced fat storage, increased levels
obesity 13401 correlation between the circulating leptin levels and CRC development [[65]]. These findings suggest that obesity -associated abnormalities cooperatively increase the risk of CRC in obese individuals.A genetically-modified
obesity 13591 individuals.A genetically-modified C57BLKS/J-+Leprdb/+Leprdb (db/db) mouse exhibiting the characteristics of obesity and type 2 diabetes was recognized as a useful model for investigating various types metabolic disorders
obesity 15262 pigment in the rhizome of the spice turmeric with known anti-inflammatory properties [[72],[73]], on obesity -related carcinogenesis. Kubota et al. [[18]] have demonstrated that the administration of curcumin successfully
obesity 17407 chronic inflammation and oxidative stress, leading to the prevention of colonic tumorigenesis in an obesity -related colon cancer model [[23]]. In addition, our research group also demonstrated that histamine
obesity 19022 levels of leptin, TNF-α, and IL-6 [[27]].Hypertension and dyslipidemia are thought to be involved in obesity -related diseases [[9],[84]]. The activation of the renin-angiotensin system (RAS) has been shown to
obesity 19165 activation of the renin-angiotensin system (RAS) has been shown to contribute to high blood pressure, obesity , and metabolic syndrome [[85]]. RAS has been demonstrated to be frequently up-regulated in malignancies
obesity 19514 the effects of anti-hypertensive agents on the prevention of colorectal premalignant lesions in an obesity -related CRC model [[25]]. The employed agents were an angiotensin-converting enzyme inhibitor, captopril,
obesity 20288 findings discussed above suggest that both lipid-lowering and anti-hypertensive agents can suppress obesity -associated colorectal carcinogenesis by improving hyperleptinemia and dyslipidemia, and by attenuating
obesity 20546 Therefore, the pharmaceutical approach appears to be one of the potential strategies for the prevention of obesity -related CRC because these drugs are in clinical use and have known pharmacological effects against the
obesity 20657 obesity-related CRC because these drugs are in clinical use and have known pharmacological effects against the obesity -related metabolic disorders, in addition to their cancer chemopreventive effects.5. Concluding RemarksIn

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