• Journal of Integrative Natural Science
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• v.5 no.3
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• pp.198-210
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• 2012

Circadian rhythms govern a remarkable variety of metabolic and physiological functions. Accumulating epidemiological and genetic evidence indicates that the disruption of circadian rhythms might be directly linked to cancer. Intriguingly, several molecular gears constituting the clock machinery have been found to establish functional interplays with regulators of the cell cycle, and alterations in clock function could lead to aberrant cellular proliferation. In addition, connections between the circadian clock and cellular metabolism have been identified that are regulated by chromatin remodelling. This suggests that abnormal metabolism in cancer could also be a consequence of a disrupted circadian clock. Therefore, a comprehensive understanding of the molecular links that connect the circadian clock to the cell cycle and metabolism could provide therapeutic benefit against certain human neoplasias.

• Journal of Microbiology and Biotechnology
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• v.12 no.4
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• pp.664-668
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• 2002

Antioxidants either scavenge superoxide and free radicals or stimulate the detoxification mechanisms within cells, resulting in increased detoxification of free radicals formation. Hyperin, isolated from the stem of Uncaria rhynchophylla, prevented oxygen radical formation and inhibited lipid oxidation. The effective concentrations were 31.3 $\mu$M for a radical scavenging assay and 2.2 $\mu$M for a microsome assay. cDNA microarray analysis to determine which genes were modulated by hyperin found that 50 genes were upregulated and 37 genes were downregulated in SNU-668 human gastric cancer cells. Among these genes, thirteen genes that were significantly affected by hyperin were verified by RT-PCR for their effect of genetic reprogramming.

• Biomolecules & Therapeutics
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• v.26 no.1
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• pp.1-3
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• 2018

• BMB Reports
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• v.36 no.1
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• pp.28-34
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• 2003

Breast cancer is the most prevalent cancer among women in Western countries, and its prevalence is also increasing in Asia. The major risk factor for breast cancer can be traced to reproductive events that influence the lifetime levels of hormones. However, a large percentage of breast cancer cases cannot, be explained by these risk factors. The identification of susceptibility factors that predispose individuals to breast cancer (for instance, if they are exposed to particular environmental agents) could possibly give further insight into the etiology of this malignancy and provide targets for the future development of therapeutics. The most interesting candidate genes include those that mediate a range of functions. These include carcinogen metabolism, DNA repair, steroid hormone metabolism, signal transduction, and cell cycle control. We conducted a hospital-based case-control study in South Korea to evaluate the potential modifying role of the genetic polymorphisms of selected low penetrance genes that are involved in carcinogen metabolisms (i.e., CYP1A1, CYP2E1, GSTM1/T1/P1, NAT1/2, etc.), estrogen synthesis and metabolism (i.e., CYP19, CYP17, CYP1B1, COMT, ER-$\alpha$, etc.), DNA repair (i.e., XRCC1/3, ERCC2/4, ATM, AGT, etc.), and signal transduction as well as others (i.e., TGF-$\beta$, IGF-1, TNF-$\beta$, IL-1B, IL-1RN, etc.). We also took into account the potential interaction between these and the known risk factors of breast cancer. The results of selected genes will be presented in this mini-review.

• Journal of Gastric Cancer
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• v.14 no.1
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• pp.1-6
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• 2014

Aerobic glycolysis has been the most important hypothesis in cancer metabolism. It seems to be related to increased bioenergetic and biosynthetic needs in rapidly proliferating cancer cells. To this end, F-18 fluorodeoxyglucose (FDG), a glucose analog, became widely popular for the detection of malignancies combined with positron emission tomography/computed tomography (PET/CT). Although the potential roles of FDG PET/CT in primary tumor detection are not fully established, it seems to have a limited sensitivity in detecting early gastric cancer and mainly signet ring or non-solid types of advanced gastric cancer. In evaluating lymph node metastases, the location of lymph nodes and the degree of FDG uptake in primary tumors appear to be important factors affecting the diagnostic accuracy of PET/CT. In spite of the limited sensitivity, the high specificity of PET/CT for lymph node metastases may play an important role in changing the extent of lymphadenectomy or reducing futile laparotomies. For peritoneal metastases, PET/CT seems to have a poorer sensitivity but a better specificity than CT. The roles of PET/CT in the evaluation of other distant metastases are yet to be known. Studies including primary tumors with low FDG uptake or peritoneal recurrence seem suffer from poorer diagnostic performance for the detection of recurrent gastric cancer. There are only a few reports using FDG PET/CT to predict response to neoadjuvant or adjuvant chemotherapy. A complete metabolic response seems to be predictive of more favorable prognosis.

• Journal of Gastric Cancer
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• v.13 no.2
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• pp.106-110
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• 2013

Purpose: We designed our study to evaluate the hypothesis that gastric cancer is correlated with iodine deficiency or thyroid dysfunction. Materials and Methods: We investigated the total body iodine reserve, thyroid function status and autoimmune disorder in 40 recently diagnosed gastric adenocarcinoma cases versus 80 healthy controls. The participants came from a region with high gastric cancer rate but sufficient iodine supply due to salt iodination. The investigation included urine iodine level, thyroid gland clinical and ultrasonographic examination, and thyroid function tests. Results: Goiter was detected more frequently in the case group (P=0.001); such a finding, however, was not true for lower than normal urine iodine levels. The free T3 mean level was significantly lower in the case group compared to the control group (P=0.005). Conclusions: The higher prevalence of goiter rather than low levels of urinary iodine in gastric adenocarcinoma cases suggests that goiter, perhaps due to protracted but currently adjusted iodine deficiency, is more likely to be associated with gastric adenocarcinoma compared to the existing iodine deficiency itself.

• Asian Pacific Journal of Cancer Prevention
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• v.17 no.2
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• pp.661-665
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• 2016

Background: Stomach cancer is the fifth most common cancer and the third leading cause of death among cancers throughout the world. Therefore, stomach cancer outcomes can affect health systems at the national and international levels. Although stomach cancer mortality and incidence rates have decreased in developed countries, these indicators have a raising trend in East Asian developing countries, particularity in Iran. In this study, we aimed to determine the time trend of age-standardized rates of stomach cancer in different districts of Iran from 2000 to 2010. Materials and Methods: Cases of cancer were registered using a pathology-based system during 2000-2007 and with a population-based system since 2008 in Iran. In this study, we collected information about the incidence of stomach cancer during a 10 year period for 31 provinces and 376 districts, with a total of 49,917 cases. We employed two statistical approaches (a random effects and a random effects Markov model) for modeling the incidence of stomach cancer in different districts of Iran during the studied period. Results: The random effects model showed that the incidence rate of stomach cancer among males and females had an increasing trend and it increased by 2.38 and 0.87 persons every year, respectively. However, after adjusting for previous responses, the random effects Markov model showed an increasing rate of 1.53 and 0.75 for males and females, respectively. Conclusions: This study revealed that there are significant differences between different areas of Iran in terms of age-standardized incidence rates of stomach cancer. Our study suggests that a random effects Markov model can adjust for effects of previous responses.

• Nutritional Sciences
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• v.6 no.3
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• pp.160-166
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• 2003

To examine the evidence that wheat bran is protective against breast cancer development and that its main mechanism of action is by modulating estrogen metabolism. This review explores the role of different experimental factors on the anticancer effects of wheat bran and the relationship of changes to estrogen metabolism by wheat bran on breast cancer risk The timing of the experimental diets in relation to carcinogen administration, the length of feeding of the experimental diets, and the level of dietary fat had an impact on the effectiveness of different doses of wheat bran in reducing breast carcinogenesis. Wheat bran supplementation resulted in significant reductions in human plasma estrogen levels but not in that of animals tested. The change in excretory metabolism of estrogen by wheat bran feeding in animals was not related to any of the tumor indices measured. The protective effect of wheat bran in breast carcinogenesis is greatest at the promotional phase and when supplemented in a high fat diet. Doses of wheat bran in the 9-12% range in diet have been consistently protective. The inconsistency observed with higher doses of wheat bran may be dependent on the animal model used. Although wheat bran's inhibitory effects on tumor growth may involve changes to estrogen metabolism, the fiber and phytochemical components of wheat bran may also act through estrogen-independent mechanisms. For a better understanding of the effect of wheat bran on breast carcinogenesis, studies comparing the effects of different wheat bran components both alone and in combination need to be performed.

• Biomolecules & Therapeutics
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• v.26 no.1
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• pp.10-18
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• 2018

Tumors are dynamic metabolic systems which highly augmented metabolic fluxes and nutrient needs to support cellular proliferation and physiological function. For many years, a central hallmark of tumor metabolism has emphasized a uniformly elevated aerobic glycolysis as a critical feature of tumorigenecity. This led to extensive efforts of targeting glycolysis in human cancers. However, clinical attempts to target glycolysis and glucose metabolism have proven to be challenging. Recent advancements revealing a high degree of metabolic heterogeneity and plasticity embedded among various human cancers may paint a new picture of metabolic targeting for cancer therapies with a renewed interest in glucose metabolism. In this review, we will discuss diverse oncogenic and molecular alterations that drive distinct and heterogeneous glucose metabolism in cancers. We will also discuss a new perspective on how aberrantly altered glycolysis in response to oncogenic signaling is further influenced and remodeled by dynamic metabolic interaction with surrounding tumor-associated stromal cells.

• Toxicological Research
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• v.31 no.4
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• pp.323-330
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• 2015

Cancer is a disease characterized by uncontrolled growth. Metabolic demands to sustain rapid proliferation must be compelling since aerobic glycolysis is the first as well as the most commonly shared characteristic of cancer. During the last decade, the significance of metabolic reprogramming of cancer has been at the center of attention. Nonetheless, despite all the knowledge gained on cancer biology, the field is not able to reach agreement on the issue of mitochondria: Are damaged mitochondria the cause for aerobic glycolysis in cancer? Warburg proposed the damaged mitochondria theory over 80 years ago; the field has been testing the theory equally long. In this review, we will discuss alterations in metabolic fluxes of cancer cells, and provide an opinion on the damaged mitochondria theory.