bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract A50: Black raspberry treatment in FAP patients shows re-expression of methylation-silenced genes
Authors: Stoner Kristen M. , Seguin Claire M. , Huang Yi-Wen , Huang Tim , Yang Guang-Yu , Hasson Henrietta , Burke Carol A. , Sardo Christine , Stoner Gary D. , Wang Li-Shu 
Published: May 2012

Abstract
In a clinical trial, we found that freeze-dried black raspberry (BRB) powder reduced the number of rectal polyps in patients with familial adenomatous polyposis (FAP). The present study was undertaken to determine if the berries influenced the growth and apoptosis of cells in rectal polyps. In addition, because the p16 tumor suppressor gene is inactivated by methylation in greater than 60 percent of colon tumors, we examined the levels of both p16 and of DNA methyltransferase 1 (DNMT1) expression in normal and polyp specimens. DNMT1 has been shown to be overly expressed in cultured human colon cancer cell lines and this correlated with silencing of the p16 gene. Polyps and normal tissues were obtained from FAP patients before and after 36 weeks of berry treatment. Immunohistochemical staining for Ki-67 and c-MYC showed that cell proliferation was significantly reduced by berry treatment in both normal rectum and in rectal polyps. TUNEL staining for apoptosis was observed to increase significantly in both normal rectum and in rectal polyps. There was a significant decrease in DNMT1 expression and an increase in p16 expression in berry-treated normal and polyp specimens. These results suggest that nine months of black raspberry treatment resulted in reduced cell proliferation, increased apoptosis and p16 gene expression and decreased DNMT1 expression in both normal and polyp specimens taken from FAP patients. The p16/DNMT1 data suggest that black raspberries may act as a demethylating agent and should be further evaluated for their effects on the methylation status of other candidate tumor suppressor genes in colonic polyps and tumors. This research was supported by NCI grant CA103180 and USDA grant 38903-03560.
Citation Information: Cancer Prev Res 2010;3(1 Suppl):A50.
Abstract A52: Characterization of Indian honey and its anticancerous activity against colon cancer
Authors: Mandal Mahitosh , Jaganathan Saravana Kumar 
Published: May 2012

Abstract
Four multifloral honey types from different Indian origin (named as Samples A, B, C and D) were analyzed for their phenolic acids using high performance liquid chromatography (HPLC). HPLC-Mass Spectroscopy analysis revealed that dihydroxy benzoic acid, caffeic acid, ferulic acid and cinnamic acid were the major phenolic acid constituents of the tested honey. The total antioxidant potential and free radical scavenging ability varied among the honey samples and exhibited a significant correlation with their phenolic content. Further the honey samples were studied for rheology and thermal properties. Controlled shear rate viscometry indicated the Newtonian behavior (a drop in the viscosity as the temperature increases) in the honey samples. Differential Scanning Calorimetry (DSC) analysis revealed the inflection transition temperature (Tg) of the honey samples ranged between - 51.40 °C to −30.64 °C. Thiazolyl blue tetrazolium bromide (MTT) assay revealed that the honey samples containing higher phenolic content showed significant antiproliferative effect against colon cancer cells. From the abovesaid experiments, Sample C among the four was found to be better based on its phenolic, antioxidant and antiproliferative effects and chosen for further studies. Honey induced the apoptotic signal via initial depletion of intracellular non protein thiols, consequently reducing the mitochondrial membrane potential (MMP) and increased the reactive oxygen species (ROS) generation. P53 up-regulation and modulation of pro and antiapoptotic proteins were observed in the honey induced apoptosis. The work was extended further to study the constituents of honey that induced apoptosis. For this, we screened the antiproliferative effect of some reported phenolic constituents namely p-coumaric acid, caffeic acid, gallic acid and eugenol in colon cancer cells. We had selected eugenol based on their better antiproliferative nature and elucidated the mechanism. Eugenol treatment resulted in reduction of intracellular non-protein thiols and increase in the earlier lipid layer break. Further events like dissipation of mitochondrial membrane potential and generation of ROS were accompanied in the eugenol-induced apoptosis. Finally we had studied the anticancer activity of honey samples (Samples B and C) and eugenol against Ehrlich ascites carcinoma. We found that Sample C remarkably inhibited the tumor growth by 40 % compared to Sample B (12.17 %) against Ehrlich ascites carcinoma when given 25% v/v intraperitoneally (i/p). We had found eugenol with a dose of 100 mg/Kg showed nearly 29% tumor inhibition.
Citation Information: Cancer Prev Res 2010;3(1 Suppl):A52.
Abstract A64: Chemopreventive potential of Bauhinia variegata against DMBA-induced skin papillomagenesis in Swiss albino mice
Authors: Singh Manju , Kale Raosaheb K. 
Published: May 2012

Abstract
The present study is an attempt to evaluate the cancer chemopreventive potential of Bauhinia variegata bark against DMBA-induced skin papillomagenesis in mice. We investigated chemopreventive effect of three different doses (2%, 4% and 6% w/w) of test diets of bark of B. variegata during DMBA-induced skin papillomagenesis in mice and tumor cell proliferation and apoptosis. Its effect was also studied in a short-term animal protocol on carcinogen metabolizing enzymes in liver.
DMBA and croton oil was used to induce and promote skin papillomagenesis, respectively. Skin papillomagenesis study was done by using three different doses of B. variegata before, during and after the DMBA treatment to mice till termination of the experiment (120 days). In addition, the expression of proliferation [proliferating cell nuclear antigen (PCNA), glutathione-S-transferse (GST-π) and apoptosis were analyzed in the skin tumors by immunohistochemistry. For biochemical studies, mice were given with the same doses of B. variegata in the test diet for two weeks. The specific activities/levels of phase-I and phase-II enzymes, antioxidant enzymes, lactate dehydrogenase, glutathione content, and peroxidative damage were determined in the liver of the mice.
Results showed a significant reduction in the skin tumors in B. variegata treated animals, as compared to the control group of animals. The tumor incidence in case of control group of animals was 100% whereas it was 90%, 70% and 99% in groups treated with 2%, 4% and 6% test diets, respectively. Tumor multiplicity in control group was 12±3.9 whereas it was reduced to 8±3.7, 3±2.9 and 4±2.4 by the lower, intermediate and higher dose of B. variegata treatment. The dietary administration of three different doses of B. variegata significantly decreased the expression of PCNA, GST-π, Bcl-2 and VEGF and on the other hand significantly increased the expression of Bax and total Caspase 3 as compared to DMBA and croton oil treated group of animals. The effect of 2 weeks of dietary feeding of B. variegata inhibited phase I, activated phase II and antioxidant enzymes in the mouse liver. The content of reduced glutathione was significantly elevated whereas the peroxidative damage and specific activity of lactate dehydrogenase exhibited a significant reduction with all the doses of test diets, respectively.
All these findings were indicative of that Bauhinia variegata has chemopreventive potential against DMBA-induced skin carcinogenesis. It would be of interest to investigate for active cancer chemopreventive agents in Bauhinia variegata for its future implication in cancer prevention and control.
Citation Information: Cancer Prev Res 2010;3(1 Suppl):A64.
Abstract A70: Kava as a lung cancer chemopreventive agent
Authors: Xing Chengguo , Johnson Thomas , Hermanson David , Kassie Fekadu , Upadhyaya Pramod , O'Sullivan Michael , Hecht Stephen 
Published: May 2012

Abstract
Lung cancer is a serious malignancy with high incidence and death. Chemoprevention is a complementary approach to smoking cessation to help control lung cancer. Recently, we reported that kava inhibits 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) plus benzo(a)pyrene (BaP)-induced lung tumorigenesis in A/J mice. In the present study, we examined the dose-dependent lung tumor inhibitory activities of kava and attempted to identify the active constituent(s). Carcinogen-treated mice, dosed eight times with a mixture of NNK plus BaP (2 µmol each) administered by gavage, had 12.2 ± 5.7 lung adenomas per mouse after 26 weeks. Carcinogen-treated mice given diets containing kava at dosages of 1.25, 2.5, 5, and 10 mg/g had 8.4 ± 3.5, 6.6 ± 3.5, 4.3 ± 2.4, and 3.8 ± 2.3 lung adenomas per mouse, corresponding to reductions of 31%, 46%, 64%, and 69%, respectively. All reductions were significant (P &lt; 0.05). Flavokawains A, B, and C from kava demonstrated either no or much weaker chemopreventive efficacies, suggesting that they are unlikely to be responsible for the chemopreventive activity of kava. Western blot analyses of lung adenoma tissues and lung cancer cells reveal that kava modulates the NF-kB signaling pathway, a potential mechanism responsible for kava-induced lung cancer chemoprevention.
Citation Information: Cancer Prev Res 2010;3(1 Suppl):A70.
Abstract A75: Bioactive tanshinones in Salvia miltiorrhiza for prostate cancer chemoprevention
Authors: Gong Yi , Li Yanli , Zhou Jin-Rong 
Published: May 2012

Abstract
Prostate cancer is the second-leading cause of cancer death in American men. Current therapeutic approaches have made significant progression in the control of prostate cancer progression. On the other hand, conventional therapeutics have variable efficacies and are usually associated with metastatic recurrence and/or high cytotoxicity. Therefore the search for effective chemopreventive agents with minimal side effects has remained one of the top priorities in prostate cancer research. Some Chinese herbal medicines have been used for centuries, thus certain Chinese medicines with active anti-cancer ingredients may be effective candidates for the prevention and/or treatment of prostate cancer. Danshen (Salvia miltiorrhiza) has been widely adopted in the traditional Chinese medicinal preparations for treatment of cerebrovascular disorders with minimal side effects. We thus evaluated the effects of several major Danshen components, tanshinones IIA (T2A), tanshinone I (T1) and cryptotanshinone (CT) on the growth of prostate cancer cells and identified the potential molecular targets that were responsive to and might be responsible for the treatments. CT, T2A and T1 significantly inhibited the growth of prostate cancer cells with the IC50s at a few Ms associated with cell cycle arrests and apoptosis induction in vitro, whereas their growth inhibition effects on normal prostate epithelial cells were dramatically reduced by 5–10 folds. T1 showed the most potent activity among the three compounds, but the combination of CT and T2A showed synergistic effects against prostate cancer cell growth. The pilot animal study verified that T1 inhibited the growth of DU145 tumors in a dose-dependent manner. By using the real time PCR arrays for epigenetic markers, we identified Aurora A kinase gene as a potential molecular target of tanshinones. Aurora A gene and protein were up-regulated in prostate cancer cell lines when compared with that in the normal cells, and the tanshinone treatments significantly down-regulated its expression. These results demonstrated potent anti-prostate cancer activities of tanshinones and identified Aurora A as a potential molecular target of tanshinones actions. Further in vivo studies of the chemopreventive effects of tanshinones and the CT and T2A combination on prostate cancer development and/or progression are warranted.
Citation Information: Cancer Prev Res 2010;3(1 Suppl):A75.
Abstract A8: Cytogenetic evaluation of human individual radiation sensitivity with the purpose of primary prevention of radiogenic cancer
Authors: Ryabchenko Natalia 
Published: May 2012

Abstract
Background: Rising of cancer incidences in population of Ukraine is connected with the increasing of cancerogenic loading where ionizing radiation has been recognized as a strong cancer causing agent. Today variations in radiation sensitivity between individuals are shown to be genetically determined and connected with the effectiveness of cell signaling system function after exposure to damaging agents. Recent reports have suggested that elevated chromosome aberration yields observed following radiation exposure of peripheral lymphocytes in G2 phase of cell cycle caused by the impaired DNA repair and hereditary predisposition to cancer. The goal of the presented study was to evaluate chromosomal sensitivity of lymphocytes of healthy individuals on the basis of the modified G2-test.
Materials and Methods: Test-system of human peripheral blood lymphocytes (PBL) of 110 healthy donors with the next metaphase analysis of chromosomal aberrations (chromatid breaks) was used. Test -irradiation of cell cultures was carried out at 1,5 Gy in the late G2-stage. Cells were analyzed in the first mitosis.
Results: The obtained cytogenetic data has revealed high interindividual variability in the levels of radiation induced chromatid breaks (CV = 24%). It was shown that distribution of the examined cytogenetic parameter in the group did not correspond to normal distribution and had bimodal character. Application of variation statistics' methods has revealed existence of two subgroups of donors - with “normal” and “increased” (11,6 % of the group) radiation sensitivity of lymphocytes on chromosomal level.
Taking into account correlations of high radiation-induced genome instability of human somatic cells with cancer predisposition it is competent to relate these individuals with the group of increased radiogenic cancer risk. Application of cytogenetic examinations on the basis of G2-assay is recommended for the formation of groups with the increased radiogenic cancer risk and promotes the efficiency of primary cancer prevention in the cohorts of occupationally exposed individuals.
Citation Information: Cancer Prev Res 2010;3(1 Suppl):A8.
Abstract A90: Reducing colorectal cancer risk among Chinese Americans
Authors: Gor Beverly J. , Forman Michele R. , Hoang TruongSon V. , Hernandez Mike , Jones Lovell A. 
Published: May 2012

Abstract
Colorectal cancer rates are increasing among Chinese Americans, and this trend seems to be reflected among Chinese Americans in Texas. Data from the Texas Cancer Registry indicates that colorectal cancer is among the top three most frequently reported cancers among Chinese Americans. Case control studies among Chinese Americans in other parts of the U.S. suggest that risk factors for colorectal cancer may include high body mass index, inadequate physical activity, low fruit and vegetable consumption, high saturated fat consumption, longer exposure to high fat diet, low fiber diet and tobacco use. The Asian American Health Needs Assessment (AsANA) study collected self reported risk factor data from over 400 Chinese and 400 Vietnamese randomly selected households in the Greater Houston area. The data showed that among Chinese Americans in Houston, 62% reported no leisure time physical activity, 19% were obese, and that as years in the US increased, the percent of Chinese with less than 5 servings of fruits and vegetables a day increased from 41% to almost 80%. Approximately 34% of Chinese adult males smoked cigarettes as compared to the Texas rate of 20%. The AsANA data also showed that only 25% of the Chinese respondents 50 years and older had had colorectal cancer screening as compared to 53% of Texas adults. Research is needed to identify cultural and access barriers to early detection and screening for colorectal cancer among Chinese Americans in Texas. In addition, culturally tailored educational programs and lifestyle interventions should be developed to educate this population on how to modify behaviors to reduce colorectal cancer risk.
Citation Information: Cancer Prev Res 2010;3(1 Suppl):A90.
Abstract A92: Racial and ethnic distribution of mammography outcomes before age 40
Authors: Kapp Julie M. , Walker Rod , Haneuse Sebastien , Buist Diana S.M. , Yankaskas Bonnie C. 
Published: May 2012

Abstract
Purpose: The probability of a woman developing invasive breast cancer &lt; age 40 is low (&lt;1%). For in situ or invasive cancer, the incidence rate per 100,000 woman-years for African American (AA) and white women, respectively, is 16.8 and 15.1 (Brinton et al, 2008). Yet, 34% of non-Hispanic AA women, 30% of non-Hispanic white women, and 22% of Hispanic women ages 30–39 reported ever having a mammogram from a national population-based sample (Kapp et al, 2009). We describe first mammograms in younger women to investigate racial/ethnic differences (AA, Asian, Hispanic, white) in mammography outcomes.
Methods: Data are pooled from the National Cancer Institute's Breast Cancer Surveillance Consortium, a collaborative network of mammography registries created for the purpose of studying performance and outcomes in community practice. We included women ages 18–39, with no prior history of breast cancer, with a first mammogram (screening or diagnostic) between 1996 and 2005. We determined whether a cancer diagnosis (DCIS or invasive) was made within the 12 months following each mammogram and, using standard definitions, classified each mammogram as a true positive (TP), false positive (FP), true negative (TN) or false negative (FN).
Results: Our sample included 73,353 screening mammograms and 26,262 diagnostic mammograms. Our FP results for screening mammograms reflected modest variability across race/ethnicity (10.4–14.1%). AA woman had a TP to total screening mammogram ratio of 1 in 363, compared to 1 in 623 for white women, while the ratio of a FP to total screening mammograms was similar across all racial/ethnic groups (1 in 7–10). Among diagnostic mammograms, the FP variability was greater, ranging from 8.7% for white women to 18.2% for Asian women with an absolute risk difference of a TP of &lt;1% among all racial/ethnic groups.
Conclusions: While the FP rates may vary moderately by race/ethnicity, their impact may vary substantially. Average risk AA women have greater odds than white women of reporting multiple mammograms &lt; age 40 (Kapp et al, 2009); yet ≥40 are less likely to receive adequate mammography screening (Smith-Bindman et al, 2006). Could early mammography testing adversely impact future mammography use? This deserves further study.
Citation Information: Cancer Prev Res 2010;3(1 Suppl):A92.
Abstract A94: Prostate cancer mortality: An evaluation of increasing trend of racial disparity and other factors
Authors: Chen Fan , Eni-Ikeh Nkechi , Bina William 
Published: May 2012

Abstract
Objectives: To understand the increasing trend of racial disparity of prostate cancer in the last three decades and to evaluate the potential impact of social-economic status, early diagnosis, cancer cell differentiation and marital status.
Method: Both prostate cancer incidence and mortality rates as well as case marital status in SEER 9 registration sites were estimated for the period 1973–2006. To stabilize estimation and adjust for social-economic status, we collapsed SEER sites and states, and merged the 200 counties into 20 county groups based on similarity in poverty rates (percentage of population below poverty line).
Results: [1]. The incidence of prostate cancer from 1973 to 2006 increased 74% and 87% for blacks and whites, respectively. During the same time, the mortality rate declined 5% and 25% for blacks and whites, respectively. [2] The incidence rate ratio of black/whites is relatively stable, ranging from 1.4–1.8, but the mortality rate ratio of black/white increased 27%, from 1.85 to 2.34. Regression showed the R2 for the increasing trend of this ratio is 0.91. [3] When we compare the ratio of mortality over incidence, they were 0.40 and 0.35 for blacks and whites in 1973, and declined to 0.22 and 0.14 in 2006, respectively, indicating the survival rate increased for both, but the magnitude of improvement is much larger in whites than in blacks. [4] When we stratified the counties to 20 county groups, we found that there is no trend for incidence or mortality rates associated with the poverty rate increases. [5] There is also no trend of early diagnosis associated with poverty increases in whites or blacks for ages less than 65 or more than 65. Neither regression has R2 larger than 0.06. [6] Among the 20 county groups, only two showed the percent of early diagnosis in blacks lower than in whites with p&lt;0.05. [7] Among the 20 county groups, four showed that a larger percentage of poor differentiated prostate cancer in blacks than in whites, the differences are statistically significant at =0.05 level. [8] The percent of white married cases are 77% and 72% for ages 30–64 and 65 or over, respectively, but the percentage in black counterparts are only 58% and 55%.
Conclusion: The results indicated that [1] The racial mortality disparity increased at 2% per year during 1973 to 2006. This is due to the larger decline of mortality in whites than in blacks. [2] This study does not support the relationship of disparity with social-economic status, early diagnosis or poor differentiation of cancer cells. [3] The percent of married white cases are 33% and 30% higher than that of black counterparts for ages 30–64 years old and 65 and over, respectively. Because married cases showed better survival rates as reported by previous research, the racial disparity may be partly explained by the remarkable difference in married status of prostate cancer cases.
Citation Information: Cancer Prev Res 2010;3(1 Suppl):A94.