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Diagnostic Value of Combining Tumor and Inflammatory Markers in Lung Cancer.

Ho Il YOON ; Oh Ran KWON ; Kyung Nam KANG ; Yong Sung SHIN ; Ho Sang SHIN ; Eun Hee YEON ; Keon Young KWON ; Ilseon HWANG ; Yun Kyung JEON ; Yongdai KIM ; Chul Woo KIM

Journal of Cancer Prevention.2016;21(4):302-302. doi:10.15430/JCP.2016.21.4.302

In Table 2 and 3, cutoff values of RANTES, ApoA2, TTR, Svcam-1 (and sensitivity and specificity values accordingly) were wrongly marked.

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The Role of Oral Contraceptive Pills on Increased Risk of Breast Cancer in Iranian Populations: A Meta-analysis.

Ali SOROUSH ; Negin FARSHCHIAN ; Saeid KOMASI ; Neda IZADI ; Nasrin AMIRIFARD ; Afshar SHAHMOHAMMADI

Journal of Cancer Prevention.2016;21(4):294-301. doi:10.15430/JCP.2016.21.4.294

BACKGROUND: Cancer is one of the main public health issues in the world. Breast cancer is one of the most common types of cancer among women. It is also the second cause of mortality in women. The association between the use of oral contraceptive pills and breast cancer is controversial and a main issue in public health. Some findings have shown that taking these pills does not have a significant effect in increasing the risk of breast cancer, while others have confirmed the carcinogenic effect of these products. These contradictory findings necessitated this meta-analysis, through of all correlated studies in Iran. METHODS: All published studies were considered from June 2000 until June 2015, using reliable Latin databases like PubMed, Google Scholar, Google search, Scopus, and Science Direct, and Persian database like SID, Irandoc, IranMedex, and Magiran. Finally, 26 papers were selected: 24 studies were case control while two were population based studies. A total of 26 papers with 46,260 participants were assessed since 2001. RESULTS: Overall estimate of OR for the effect of oral contraceptive pills on breast cancer is 1.521 (CI = 1.25–1.85), which shows that the intervention group had more chance (52%) compared to the control group (P = 0.001). Using these pills increased the risk of breast cancer up to 1.52 times. CONCLUSIONS: Because of directly increasing levels of estrogen and the role of estrogen in gaining weight indirectly, oral contraceptive pills can stimulate the occurrence of breast cancer. More studies should be conducted for controlling the period of pill use.
Breast Neoplasms* ; Breast* ; Case-Control Studies ; Estrogens ; Female ; Humans ; Iran ; Mortality ; Public Health ; Sudden Infant Death

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The Evaluation of p53 Polymorphism at Codon 72 and Association With Breast Cancer in Iran: A Systematic Review and Meta-analysis.

Abozar SOLEIMANI ; Yousef RAHMANI ; Negin FARSHCHIAN ; Ali DELPISHEH ; Kivan KHASSI ; Afshar SHAHMOHAMMADI ; Nasrin AMIRIFARD

Journal of Cancer Prevention.2016;21(4):288-293. doi:10.15430/JCP.2016.21.4.288

BACKGROUND: Breast cancer is the most common cancer among women in Iran and the world. Multiple environmental factors and genetic variations such as genetic polymorphisms are of its main causes. p53 gene plays an important role in conserving and sustaining the genome as a tumor suppressing gene. Change and polymorphism at codon 72 of p53 gene are correlated with increased risk of lung, mouth, endometrial, prostate, and colorectal cancers, and could be considered an indicator of susceptibility to breast cancer. METHODS: Twelve studies (1,190 cases and 1,145 control studies with evaluation of three types of Arg/Arg, Arg/Pro, and Pro/Pro genotypes) have been conducted using keywords, such as polymorphism at codon 72, gene p53 polymorphisms, and the relation between polymorphisms and breast cancer, from databases in Iran, including Magiran, Medlibe, Sid, and Iranmedex, as well as Latin databases such as PubMed, Google Scholar, Science Direct, and Scopus. RESULTS: The OR for Arg/Arg is 1.58 (95% CI: 2.45 to 1.01), the OR for Arg/Pro is 0.75 (95% CI: 1.10 to 0.51), and the OR for Pro/Pro is 0.62 (95% CI: 0.93 to 0.42). p53 gene polymorphism at codon 72 is statistically significant in Arg/Arg and Pro/Pro genotypes. CONCLUSIONS: Arg/Arg genotype can be considered as a risk factor for breast cancer, and Pro/Pro genotype can be accounted for as a protective factor against breast cancer.
Breast Neoplasms* ; Breast* ; Codon* ; Colorectal Neoplasms ; Female ; Genes, p53 ; Genes, Tumor Suppressor ; Genetic Variation ; Genome ; Genotype ; Humans ; Iran* ; Lung ; Mouth ; Polymorphism, Genetic ; Prostate ; Protective Factors ; Risk Factors ; Sudden Infant Death

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Expression of Leucine-rich Repeat-containing G-protein Coupled Receptor 5 and CD44: Potential Implications for Gastric Cancer Stem Cell Marker.

Yoon Jin CHOI ; Nayoung KIM ; Hye Seung LEE ; Seon Mee PARK ; Ji Hyun PARK ; Hyuk YOON ; Cheol Min SHIN ; Young Soo PARK ; Jin Wook KIM ; Dong Ho LEE

Journal of Cancer Prevention.2016;21(4):279-287. doi:10.15430/JCP.2016.21.4.279

BACKGROUND: The human leucine-rich repeat-containing G-protein coupled receptor (LGR) 5 and CD44 are one of the candidates for the marker of gastric cancer stem cells. We compared the expressions of two genes among control, dysplasia and cancer groups. METHODS: We compared the mRNA expression of LGR5, CD44 and CD44v8–10 and immunohistochemistry (IHC) of LGR5 and CD44 in gastric antral mucosa of 45 controls, 36 patients with gastric dysplasia, and 39 patients with early gastric cancer. Additionally, IHC of LGR5 in gastric body mucosa was analyzed. Normal mucosa adjacent to dysplastic or cancer lesions was used for the quantitative real-time–PCR and IHC. RESULTS: Immunoreactivity of LGR5 in base of antral mucosa was higher in non-cancerous tissues of cancer than those of control (P = 0.006), whereas the expression of LGR5 mRNA was not different among the three groups. Immunostaining of LGR5 was much stronger in the antrum than in the body of stomach (P < 0.001). Although there was no difference in antral immunointensity of LGR5 according to the severity of intestinal metaplasia, stronger immunostaining was found in the body with an aggravation of intestinal metaplasia (P trend < 0.001). The expression of CD44v8–10 mRNA was higher in cancer patients than control subjects and patients with dysplasia (P = 0.018 and 0.009) while the expression of CD44 mRNA was higher in the control groups than the others. CONCLUSIONS: IHC of LGR5 in crypt base and CD44 may be used for gastric CSC markers. LGR5 expression may be associated with the developing of corporal intestinal metaplasia. The expression of CD44v8–10 mRNA would be more suitable for gastric cancer stem cell marker than CD44 or LGR5 mRNA.
GTP-Binding Proteins* ; Humans ; Immunohistochemistry ; Metaplasia ; Mucous Membrane ; RNA, Messenger ; Stem Cells* ; Stomach ; Stomach Neoplasms*

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The Effect of Sex on the Azoxymethane/Dextran Sulfate Sodium-treated Mice Model of Colon Cancer.

Sun Min LEE ; Nayoung KIM ; Hee Jin SON ; Ji Hyun PARK ; Ryoung Hee NAM ; Min Hee HAM ; Daeun CHOI ; Sung Hwa SOHN ; Eun SHIN ; Young Jae HWANG ; Jihee SUNG ; Dong Ho LEE ; Ha Na LEE

Journal of Cancer Prevention.2016;21(4):271-278. doi:10.15430/JCP.2016.21.4.271

BACKGROUND: The colitis-associated cancer exhibits different characteristics according to sex in the initiation and progression of the tumors. The aim of this study was to investigate the sex-associated difference in the azoxymethane/dextran sulfate sodium (AOM/DSS)-induced colitis-associated cancer model. METHODS: The AOM/DSS ICR mouse model was established to compare male with female, and then the severity of colitis-associated carcinogenesis was examined macroscopically and histologically regarding the number, size, and location of tumors. Subsequently, levels of colonic mucosal cytokine, interleukin (IL)-1β and myeloperoxidase (MPO) were assessed. RESULTS: At the 16th week, the tumor multiplicity and the pro-inflammatory factors differed according to sex. The total tumor number was significantly higher in male (P = 0.020) and the number of large tumors (diameter > 2 mm) was higher in male (P = 0.026). In male, the tumors located more in distal colon (P = 0.001). MPO was significantly higher in AOM/DSS-treated male mice compared to the control group (P = 0.003), whereas the corresponding female group showed no significant change (P = 0.086). Colonic IL-1β level significantly increased in AOM/DSS groups compared to control groups both in male and female (male, P = 0.014; female, P = 0.005). It was higher in male group; however, there was no statistical significance (P = 0.226). CONCLUSIONS: In AOM/DSS murine model, colitis-associated colon tumorigenesis are induced more severely in male mice than female probably by way of inflammatory mediators such as IL-1β and MPO. The sex-related differences at the animal model of colon cancer suggest the importance of approach to disease with sex-specific medicine in human.
Animals ; Carcinogenesis ; Colitis ; Colon* ; Colonic Neoplasms* ; Female ; Humans ; Interleukins ; Male ; Mice* ; Mice, Inbred ICR ; Models, Animal ; Peroxidase ; Sodium

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Iron Supplementation Reverses the Reduction of Hydroxymethylcytosine in Hepatic DNA Associated With Chronic Alcohol Consumption in Rats.

Stephanie A TAMMEN ; Jung Eun PARK ; Phil Kyung SHIN ; Simonetta FRISO ; Jayong CHUNG ; Sang Woon CHOI

Journal of Cancer Prevention.2016;21(4):264-270. doi:10.15430/JCP.2016.21.4.264

BACKGROUND: Alcohol is known to affect two epigenetic phenomena, DNA methylation and DNA hydroxymethylation, and iron is a cofactor of ten-eleven translocation (TET) enzymes that catalyze the conversion from methylcytosine to hydroxymethylcytosine. In the present study we aimed to determine the effects of alcohol on DNA hydroxymethylation and further effects of iron on alcohol associated epigenetic changes. METHODS: Twenty-four male Sprague-Dawley rats were fed either Lieber-DeCarli alcohol diet (36% calories from ethanol) or Lieber-DeCarli control diet along with or without iron supplementation (0.6% carbonyl iron) for 8 weeks. Hepatic non-heme iron concentrations were measured by colorimetric assays. Protein levels of hepatic ferritin and transferrin receptor were determined by Western blotting. Methylcytosine, hydroxymethylcytosine and unmodified cytosine in DNA were simultaneously measured by liquid chromatography/mass spectrometry method. RESULTS: Iron supplementation significantly increased hepatic non-heme iron contents (P < 0.05) but alcohol alone did not. However, both alcohol and iron significantly increased hepatic ferritin levels and decreased hepatic transferrin receptor levels (P < 0.05). Alcohol reduced hepatic DNA hydroxymethylation (0.21% ± 0.04% vs. 0.33% ± 0.04%, P = 0.01) compared to control, while iron supplementation to alcohol diet did not change DNA hydroxymethylation. There was no significant difference in methylcytosine levels, while unmodified cytosine levels were significantly increased in alcohol-fed groups compared to control (95.61% ± 0.08% vs. 95.26% ± 0.12%, P = 0.03), suggesting that alcohol further increases the conversion from hydroxymethylcytosine to unmodified cytosine. CONCLUSIONS: Chronic alcohol consumption alters global DNA hydroxymethylation in the liver but iron supplementation reverses the epigenetic effect of alcohol.
Alcohol Drinking* ; Alcohols ; Animals ; Blotting, Western ; Cytosine ; Diet ; DNA Methylation ; DNA* ; Epigenomics ; Ferritins ; Humans ; Iron* ; Liver ; Male ; Methods ; Rats* ; Rats, Sprague-Dawley ; Receptors, Transferrin ; Spectrum Analysis

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Protective Effect of an Isoflavone, Tectorigenin, Against Oxidative Stress-induced Cell Death via Catalase Activation.

Rui ZHANG ; Mei Jing PIAO ; Min Chang OH ; Jeong Eon PARK ; Kristina SHILNIKOVA ; Yu Jin MOON ; Dong Hyun KIM ; Uhee JUNG ; In Gyu KIM ; Jin Won HYUN

Journal of Cancer Prevention.2016;21(4):257-263. doi:10.15430/JCP.2016.21.4.257

BACKGROUND: Isoflavones are biologically active compounds that occur naturally in a variety of plants, with relatively high levels in soybean. Tectorigenin, an isoflavone, protects against hydrogen peroxide (H2O2)-induced cell damage. However, the underlying mechanism is unknown. METHODS: The MTT assay was performed to determine cell viability. Catalase activity was assessed by determining the amount of enzyme required to degrade 1 μM H2O2. Protein expression of catalase, phospho-extracellular signal-regulated kinase (ERK), IκB-α, and NF-κB were evaluated by Western blot analysis. A mobility shift assay was performed to assess the DNA-binding ability of NF-κB. Transient transfection and a NF-κB luciferase assay were performed to assess transcriptional activity. RESULTS: Tectorigenin reduced H2O2-induced death of Chinese hamster lung fibroblasts (V79-4). In addition, tectorigenin increased the activity and protein expression of catalase. Blockade of catalase activity attenuated the protective effect of tectorigenin against oxidative stress. Furthermore, tectorigenin enhanced phosphorylation of ERK and nuclear expression of NF-κB, while inhibition of ERK and NF-κB attenuated the protective effect of tectorigenin against oxidative stress. CONCLUSIONS: Tectorigenin protects cells against oxidative damage by activating catalase and modulating the ERK and NF-κB signaling pathway.
Animals ; Blotting, Western ; Catalase* ; Cell Death* ; Cell Survival ; Cricetinae ; Cricetulus ; Electrophoretic Mobility Shift Assay ; Extracellular Signal-Regulated MAP Kinases ; Fibroblasts ; Hydrogen Peroxide ; Isoflavones ; Luciferases ; Lung ; NF-kappa B ; Oxidative Stress ; Phosphorylation ; Phosphotransferases ; Soybeans ; Transfection

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Sorbus rufopilosa Extract Exhibits Antioxidant and Anticancer Activities by Inducing Cell Cycle Arrest and Apoptosis in Human Colon Adenocarcinoma HT29 Cells.

You Na OH ; Soojung JIN ; Hyun Jin PARK ; Hyun Ju KWON ; Byung Woo KIM

Journal of Cancer Prevention.2016;21(4):249-256. doi:10.15430/JCP.2016.21.4.249

BACKGROUND: Sorbus rufopilosa, a tsema rowan, is a species of the small ornamental trees in the genus Sorbus and the family Rosaceae found in East Asia. The bioactivities of S. rufopilosa have not yet been fully determined. The objective of this study is to evaluate the antioxidant and anticancer effects of ethanol extract of S. rufopilosa (EESR) and to determine the molecular mechanism of its anticancer activity in human colon carcinoma HT29 cells. METHODS: To examine the antioxidant activity of EESR, 2,2-diphenyl-1-picrylhydrazyl radical scavenging activity assay was performed. Inhibitory effect of EESR on cancer cell growth and proliferation was determined by water-soluble tetrazolium salt assay. To investigate the mechanism of EESR-mediated cytotoxicity, HT29 cells were treated with various concentrations of EESR and the induction of cell cycle arrest and apoptosis was analyzed by flow cytometry, 4,6-diamidino-2-phenylindole staining, and Western blot analysis. RESULTS: EESR showed significant antioxidant activity and inhibitory effect on HT29 cell growth in a dose-dependent manner. EESR induced cell cycle arrest at G2/M phase in a dose-dependent manner by modulating cyclin B, cyclin-dependent kinase 1 (CDK1), and CDK inhibitor p21 expression. EESR-induced apoptosis was associated with the upregulation of p53, a death receptor Fas, and a pro-apoptotic protein Bax and the activation of caspase 3, 8, and 9, resulting in the degradation of PARP. CONCLUSIONS: EESR possessing antioxidant activity efficiently inhibits proliferation of HT29 cells by inducing both cell cycle arrest and apoptosis. EESR may be a possible candidate for the anticancer drug development.
Adenocarcinoma* ; Apoptosis* ; Blotting, Western ; Caspase 3 ; CDC2 Protein Kinase ; Cell Cycle Checkpoints* ; Cell Cycle* ; Colon* ; Cyclin B ; Ethanol ; Far East ; Flow Cytometry ; HT29 Cells* ; Humans* ; Rosacea ; Rosaceae ; Sorbus* ; Trees ; Up-Regulation

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Inducible Mouse Models for Cancer Drug Target Validation.

Joseph H JEONG

Journal of Cancer Prevention.2016;21(4):243-248. doi:10.15430/JCP.2016.21.4.243

Genetically-engineered mouse (GEM) models have provided significant contributions to our understanding of cancer biology and developing anticancer therapeutic strategies. The development of GEM models that faithfully recapitulate histopathological and clinical features of human cancers is one of the most pressing needs to successfully conquer cancer. In particular, doxycycline-inducible transgenic mouse models allow us to regulate (induce or suppress) the expression of a specific gene of interest within a specific tissue in a temporal manner. Leveraging this mouse model system, we can determine whether the transgene expression is required for tumor maintenance, thereby validating the transgene product as a target for anticancer drug development (target validation study). In addition, there is always a risk of tumor recurrence with cancer therapy. By analyzing recurrent tumors derived from fully regressed tumors after turning off transgene expression in tumor-bearing mice, we can gain an insight into the molecular basis of how tumor cells escape from their dependence on the transgene (tumor recurrence study). Results from such studies will ultimately allow us to predict therapeutic responses in clinical settings and develop new therapeutic strategies against recurrent tumors. The aim of this review is to highlight the significance of doxycycline-inducible transgenic mouse models in studying target validation and tumor recurrence.
Animals ; Biology ; Doxycycline ; Drug Delivery Systems ; Humans ; Mice* ; Mice, Transgenic ; Recurrence ; Transgenes ; United Nations

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Identification of Biomarkers for Breast Cancer Using Databases.

Eunhye LEE ; Aree MOON

Journal of Cancer Prevention.2016;21(4):235-242. doi:10.15430/JCP.2016.21.4.235

Breast cancer is one of the major causes of cancer death in women. Many studies have sought to identify specific molecules involved in breast cancer and understand their characteristics. Many biomarkers which are easily measurable, dependable, and inexpensive, with a high sensitivity and specificity have been identified. The rapidly increasing technology development and availability of epigenetic informations play critical roles in cancer. The accumulated data have been collected, stored, and analyzed in various types of databases. It is important to acknowledge useful and available data and retrieve them from databases. Nowadays, many researches utilize the databases, including The Cancer Genome Atlas (TCGA), Gene Expression Omnibus (GEO), Surveillance, Epidemiology and End Results (SEER), and Embase, to find useful informations on biomarkers for breast cancer. This review summarizes the current databases which have been utilized for identification of biomarkers for breast cancer. The information provided by this review would be beneficial to seeking appropriate strategies for diagnosis and treatment of breast cancer.
Biomarkers* ; Breast Neoplasms* ; Breast* ; Diagnosis ; Epidemiology ; Epigenomics ; Female ; Gene Expression ; Genome ; Humans ; Industrial Development ; Sensitivity and Specificity

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