bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract A124: Radiomodulation by rosemary extract
Authors: Soyal Dhanraj , Sharma Abhilasha , Singh Inder , Goyal Pradeep 
Published: May 2012

Abstract
A124
Radiomodulation by rosemary extract
Dhanraj Soyal, Abhilasha Sharma, Inder Singh and P.K.Goyal+
Radiation and Cancer Biology Laboratory, Department of Zoology,
Rajasthan University, Jaipur 302004
* E-mail; pkgoyal2002@rediffmail.com
Rosemary (Rosmarinus officinalis, Labiateae) is widely used for its antioxidant activities in many parts of the world. The present study investigates the radioprotective and antioxidative potential of rosemary leaves extract (ROE). Swiss albino mice were administered ROE orally once daily for 5 consecutive days, then exposed to a single dose of 3, 6 and 9 Gy of gamma radiation. lipid peroxidation (LPx), Glutathione (GSH), acid phosphatase estimations in liver were carried out. Radiation-induced increases in the levels of lipid peroxidation (LPO) and acid phosphatase were significantly ameliorated by ROE pre-treatment, and radiation-induced depletion in the level of glutathione (GSH) was significantly inhibited by ROE administration. These alterations were found to be dose dependent. The life-span was increased in the ROE treated irradiated mice in comparison with their respective control mice. Radiation-induced deficits in body and organ weight were significantly reduced or prevented in ROE pretreated mice. The protection afforded by ROE may be attributed to the constituents of the rosemary, which include rosmarinic acid, rosmanol, carnosol which appear to play an important role in free radical scavenging and singlet oxygen quenching. The study does not rule out the possibility of a prophylactic potential of ROE against radiation-induced degenerative changes in liver.
Citation Information: Cancer Prev Res 2008;1(7 Suppl):A124.
Abstract A125: Self reported exposure to pesticides and risk of breast cancer
Authors: Farooq Umar , Joshi Monika , Nookala Vinod , Cheriyath Pramil , Stellman Steven , Graber Nora , Muscat Joshua 
Published: May 2012

Abstract
A125

Background
Several studies have examined the possible role of serum organochlorine pesticide and PCBs levels in the development of breast cancer over the past decade, but there is little data on self-reported residential exposures.

Methods
This was a case control study conducted in New York City and the surrounding area that included 1204 patients (446 cases and 758 controls). Cases were defined as women with newly diagnosed breast cancer or carcinoma in situ, while patients with benign breast diseases and women undergoing non-breast related surgery were included in the control group. All patients were asked a series of questions to determine their pesticide exposure, including the type, location (inside vs. outside), who applied the pesticide, and duration of pesticide use. Logistic regression models were used to estimate unadjusted and adjusted odds ratios (OR) and corresponding 95% confidence intervals (CI).

Results
The most common pests encountered in the residences were ants, carpenter ants and cockroaches. The adjusted odds ratio for self-application of pesticide and professional application for this group of pests was 1.25(95%CI 0.79-1.98) and 1.06(95% CI 0.65-1.73) respectively. The risk did not vary when comparing inside and outside applications, (OR= 1.13(95% CI 0.75-1.72) and 1.22(95% CI 0.60-2.50) respectively. Tests for trend showed no dose-response relationship with each type of application.

Conclusion
Our study did not show an association between self-reported exposure to pesticides and breast cancer risk, which is consistent with the vast majority of studies including our own that showed no increased risk of breast cancer with biological levels of pesticides.
Citation Information: Cancer Prev Res 2008;1(7 Suppl):A125.
Abstract A130: Effect of high-dose estrogen exposure in adolescence on mammographic density in adulthood.
Authors: Jordan Helen , Kavanagh Anne , Gertig Dorota , Hopper John , Venn Alison 
Published: May 2012

Abstract
A130

Background
Since adolescence is an important stage of mammary development, exposure to high-dose estrogens at this time may have long-term effects on breast tissue and therefore mammographic density. It is well-established that women with greater mammographic density for age and BMI are at an increased risk of breast cancer.

Methods
We conducted a retrospective cohort study of women from the Australian Tall Girls Study who were 40 years or older and had been assessed for tall stature during adolescence between 1959 and 1993. Eligible women included 263 who had been treated during adolescence with high-dose estrogens and 254 who had not been treated. Treated women had received one of two types of estrogen: 3mg diethylstilbestrol (DES) daily, or 150 μg ethinyl estradiol (EE).
A mammogram within the previous two years was obtained from 167 treated women (mean age 48.4 yrs) and 142 untreated women (mean age 46.2 yrs). The total area of the breast image and the area of mammographically dense tissue (dense area), and hence non-dense area and percent mammographic density (PMD), were calculated from digitally scanned cranio-caudal mammographic films using a computer thresholding technique. Reproductive history, lifestyle factors, hormone exposure, treatment and anthropometric data were collected from medical records and by telephone interview using a structured questionnaire.

Results
After adjusting for age and BMI, treated women had, on average, 17% lower dense area (p=0.03); adjusted means for treated and untreated women were 24.5 cm2 (95% CI: 21.8, 27.2) and 29.1 cm2 (95% CI: 26.0, 32.4), respectively. There was no difference in adjusted means between treated and untreated women for non-dense area [71.7 cm2 (95% CI: 66.2, 77.7) versus 70.5 cm2 (64.7, 76.9); p=0.78], PMD [ 24.8 % (95% CI: 22.4, 27.4) versus 27.7% (95% CI: 24.8, 30.7); p=0.16], or total area [105.6 cm2 (95%CI: 100.1,111.4) vs 109.3 cm2 (95%CI: 103.1,115.8); p=0.41].

Conclusion
High-dose estrogen treatment for tall stature in adolescence is unlikely to increase risk of breast cancer through mechanisms related to mammographic density.
Citation Information: Cancer Prev Res 2008;1(7 Suppl):A130.
Abstract A7: Identification of novel genetic alterations in GI tumors using whole-genome profiling
Authors: Bashyam Murali , Raman Ratheesh , Viswakalyan Kotapalli , Ramaswamy Pandila , Chaudhary Ajay , Reddy Chandrakant , Gowrishankar Swarnalata , Srinivasulu Mukta , Sastry R , Pattnaik Sujith , Vamsy Mohana 
Published: May 2012

Abstract
A7
In our previous studies, we identified novel pancreatic cancer genes using a combination of array-based comparative genomic hybridization (aCGH) and gene expression microarrays (Neoplasia, 2007 and Kwei and PLOS Genet, 2008). In the current study, we have used a multipronged approach to address two important GI cancers prevalent in India. Colorectal cancer (CRC) is a major health problem worldwide and is usually an age-related disease. A small proportion of patients present at an early age due to familial cancer syndromes. Surprisingly, there appears to be a high proportion of patients in India who present at an early age without a family background and succumb to aggressive metastatic tumors. Using immunohistochemistry, mutation screening and microsatellite instability analysis of more than 150 samples, we show that Wnt signaling, a hallmark of CRC in the West, is not a major feature in a majority of young patients in India unlike older patients. There does not appear to be a significant difference between the two categories of CRC patients in other parameters including gender, lifestyle, diet, tumor location, frequency of microsatellite instability, and Loss of Heterozygosity at the BRCAI locus. In addition, we have identified several novel mutations in the APC gene in Wnt positive tumors. Determination of genome-wide copy number alterations and transcript profiles is expected to delineate the genetic aberrations that may lead to CRC in the young in India.
Squamous cell carcinoma of the esophagus (ESCC) is common in India and Asia but rare in the West, as against esophagus adenocarcinoma which is common in the West but not in India. ESCC is a poorly studied highly aggressive cancer with survival rates below 15% in most populations. We have carried out molecular analysis of about 75 ESCC samples and 26 adenocarcinoma samples using archived as well as fresh resected tumors. Results indicate that unlike the ESCC samples, a significant proportion of adenocarcinoma samples exhibited an activated Wnt signaling pathway. Inactivation of p53 however appeared to be a common event in both Esophagus cancer subtypes. Analysis of copy number alterations using array-based CGH has revealed a recurrent amplification at 10q21 in ESCC samples. The amplification harbored genes that exhibited comparably altered transcript levels, as determined by array-based transcript profiling. We are also carrying out molecular analyses of mixed adeno-squamous tumors of the esophagus; results are expected to reveal whether the squamous and adeno components have an independent origin or vice versa.
Citation Information: Cancer Prev Res 2008;1(7 Suppl):A7.
Abstract A72: HESA-A: Bright prospect for prevention and treatment of malignancies
Authors: ahmadi amrollah 
Published: May 2012

Abstract
A72

Background
Cancer is one of the leading causes of death in the world, particularly in developing countries that represents a tremendous burden on patients, families and societies. More than 70% of all cancer deaths occur in low and middle income countries, where resources available for prevention, diagnosis and treatment of cancer are limited or nonexistent. The effect of different types of drugs on quality of life and survival of end-stage cancer patients has been investigated, however many side effects of these drugs limited their usage. HESA-A is a compound of natural origin, consisting of rare elements and organic materials, which in several animal and cellular studies have shown powerful anticancer effects and less toxicity on normal cells. The aim of the present study was to investigate the efficacy and safety of HESA-A in the prevention and treatment of Osteosarcoma as a lethal malignancy entire the world.

Methods
In an experimental study, 40 rabbits were randomly allocated to one of two groups of administered HESA-A (study group) and placebo (control group) for 10 days. After this time, carcinogen agent was inserted under the periost for Osteosarcoma formation and bone radiography and magnetic resonance imaging were performed after three months. Also, cases were followed for 6 months.

Results
In study group, among 20 rabbits, pathological bone changes were not detected in 16 cases and after 6 months following-up, all cases were alive and no changes in their appetite and weight were observed. Besides, in placebo group, all cases suffered from Osteosarcoma. In the second stage, control cases were divided into two groups (10 rabbits were treated with HESA-A and 10 cases as non-treated group) and followed-up for 6 months. All non-treated cases were died, whereas treated cases were survived and their appetite and weight were improved.

Conclusion
This study proved the preventive and curative effects of HESA-A on Osteosarcoma and create a bright prospect for the future in the treatment of cancers.
Citation Information: Cancer Prev Res 2008;1(7 Suppl):A72.
Abstract A83: Organophosphate pesticides and sex steroid hormones in NHANES III
Authors: Christensen Carol , Rohrmann Sabine , Rifai Nader , Platz Elizabeth 
Published: May 2012

Abstract
A83

Background
Organophosphate pesticides (OP) may perturb hormone balance, and thus may affect men’s health, e.g., prostate cancer. We evaluated whether men from the general population with higher urinary OP metabolites had higher or lower concentrations of sex steroid hormones than men with lower levels.

Methods
Concentrations of 3,5,6-trichloro-2-pyridinol (TCPY), a chlorpyrifos metabolite, and 4-nitrophenol (4-NP), a methyl parathion metabolite, previously were measured in spot urine for 1,338 men ages 20-59 who participated in the Third National Health and Nutrition Examination Survey (NHANES III). We measured serum concentrations of testosterone, estradiol, and sex hormone binding globulin (SHBG) for 1,637 men ≥ 12 years old who participated in the morning session of Phase I of NHANES III. 189 men participated in both sub-studies, forming the study population. Linear regression was used to estimate geometric mean hormone concentration by binary category of creatinine-corrected urinary OP concentration adjusting for age, US region, smoking, race, education, body mass index, and physical activity. We tested for trend across quartiles of TCPY and across 3 categories (&lt; limit of detection (LOD), 2 categories ≥ LOD) of 4-NP by entering a single ordinal term in the model with values at the category medians, the coefficient for which was evaluated by the Wald test.

Results
Mean testosterone (95% confidence interval) was significantly higher in men with higher TCPY (≥ median: 5.55 (4.95, 6.22)) compared with lower (&lt;median: (4.93 (4.43, 5.48)). Although not statistically significant, mean estradiol and SHBG concentrations were also higher comparing higher to lower TCPY. There was no statistically significant difference in mean testosterone (&lt;LOD: 5.44 (4.85, 6.10); ≥LOD: 5.14 (4.54, 5.83)) or estradiol (&lt;LOD: 37.83 (34.88, 41.03); ≥LOD: 35.94 (32.94, 39.21)) between men with 4-NP concentration ≥LOD versus &lt;LOD, although men with higher 4-NP tended to have lower hormone levels. SHBG did not differ by 4-NP category. None of the trends was significant (p&gt;0.10).

Conclusion
This cross-sectional study, the first in a general population of US adult men, suggests positive associations of chlorpyrifos with testosterone, estradiol, SHBG, and inverse associations of methyl parathion with testosterone and estradiol. These findings differ somewhat from those in occupationally-exposed groups. Given that a) our findings are compatible with the hypothesis that OPs influence hormones even at low exposure, b) OPs were available to consumers and commonly used, and c) a prior study observed a higher prostate cancer risk in commercial applicators who used an OP and had a family history of prostate cancer (Am J Epidemiol 2003;157:800-14), future studies are warranted on OPs and men’s health, including prostate cancer.
Funding: Maryland Cigarette Restitution Fund at Johns Hopkins
Citation Information: Cancer Prev Res 2008;1(7 Suppl):A83.
Abstract A85: Incidence rates of exocrine and endocrine pancreatic cancers in the United States
Authors: Zhou Jing , Enewold Lindsey , Zhu Kangmin 
Published: May 2012

Abstract
A85
Pancreatic cancer is the most fatal of all major cancers with an incidence rate that approximates mortality. However, studies describing pancreatic cancer incidence, which may provide insight into its etiology, have been sparse particularly in terms of histology and tumor stage. The purpose of this study was to examine the incidence rates of exocrine and endocrine pancreatic cancers by age at diagnosis, gender, race/ethnicity and stage of the disease using data from the Surveillance, Epidemiology, and End Results (SEER) program of the National Cancer Institute from 1973 to 2005. Based on the data from nine SEER registries, the age-adjusted incidence rates, expressed per 100,000, of exocrine and endocrine pancreatic cancer were higher among males (8.18 and 0.24) than females (6.02 and 0.17), and the rates tend to be higher among Blacks (10.12 and 0.23) than Whites (6.78 and 0.20) and other races (6.01 and 0.16). The incidence rate for exocrine pancreatic cancer was generally stable over the 33 year period, whereas the incidence rate for endocrine pancreatic cancer increased over time. This difference in trend by histology existed across age, gender and racial groups. The increase in endocrine tumors was observed for all stages of disease: localized, regional and distant. However, it was most prominent for localized tumors. Additional analysis showed similar trends for exocrine and endocrine tumors across four racial/ethnic groups (Non-Hispanic White, Hispanic White, Non-Hispanic Black, Asian and Pacific Islander) using data from 1992 to 2005 for thirteen SEER registries. While improvement in diagnosis may have contributed to the rising incidence of endocrine tumors, other factors may also be related.
Citation Information: Cancer Prev Res 2008;1(7 Suppl):A85.
Abstract B1: Genome-wide LOH and copy number alterations show heterogeneity in esophageal squamous cell carcinoma
Authors: Hu Nan , Wang Chaoyu , Ng David , Clifford Robert , Yang Howard , Tang Ze-Zhong , Wang Quan-Hong , Han Xiao-You , Giffen Carol , Goldstein Alisa , Taylor Philip , Lee Maxwell 
Published: May 2012

Abstract
B1

Background
Genomic instability appears to play an important role in most human cancers. To more fully characterize genomic instability and assess its effect on gene expression in esophageal squamous cell carcinoma (ESCC), we examined loss of heterozygosity (LOH), copy number (CN) loss, and CN gain, as well as gene expression, using genome-wide methods in cases from a high-risk region of China.

Methods
Micro-dissected tumor and matched germ-line DNA from 30 ESCC patients from Shanxi Province, PR China who underwent surgical resection were tested using the Affymetrix GeneChip Human Mapping 500K array set and frequencies of LOH and CN alterations were determined. Matched micro-dissected tumor/non-tumor samples were also tested for RNA expression with Affymetric Human Genome U133A 2.0 arrays on a subset of 17 of these patients.

Results
Genomic instability measures varied widely among cases and separated them into two distinct groups: a high frequency instability group (two-thirds of all cases with 1 or more instability measure &gt;10%) and a low frequency instability group (one-third of cases with no instability measures &gt;10%). Genomic instability also varied widely across chromosomal arms, with the highest frequency of LOH on 9p (33% of informative SNPs), of CN loss on 3p (33%), and of CN gain on 3q (48%). Genome-wide LOH measured with the 500K chip produced remarkably similar frequency rankings for chromosome arms as previous less-dense genome-wide scans that used microsatellites or the 10K SNP chip, although absolute frequencies were reduced. Twelve regions with particularly high CN gain were identified, including six on 3q, one on 7q, four on 8q, and one on 11q. The most gene-rich of these CN gain regions was 11q13.1-13.4, where we identified 26 genes with frequent CN gain which also had RNA expression data available. CN gain was significantly correlated with increased RNA expression in over 80% of these genes.

Conclusions
Genomic instability patterns show two heterogeneous groups of ESCC cases; the high-frequency instability group may harbor germ-line variants or acquired somatic mutations in genes that maintain genomic stability. Genome-wide studies from this high-risk population show a consistent pattern of high LOH on selected chromosome arms which are targets in searching for loss-of-function genes involved in ESCC. Our findings demonstrate the potential utility of combining CN and gene expression data to screen for genes involved in esophageal carcinogenesis. Future studies should combine results in tumors with germ-line genotypes to find functional changes, and determine if these changes are associated with genetic susceptibility to ESCC or might serve as early detection markers.
Citation Information: Cancer Prev Res 2008;1(7 Suppl):B1.
Abstract B104: Targeting Nrf2/ARE pathway by inhibition of HDAC in breast cancer prevention
Authors: Zhou Qun , Chaerkady Raghothama , Shaw Patrick , Kensler Thomas , Pandey Akhilesh , Davidson Nancy 
Published: May 2012

Abstract
B104
Cancer chemoprevention may be achieved through induction of phase II detoxifying enzymes, a process mediated by the antioxidant response element (ARE) in the promoter region of these genes. A key transcription factor involved in induction of phase II enzymes is nuclear factor erythoid-2 related factor (Nrf2). Although cellular function of Nrf2-Keap1 pathway in human carcinogenesis has been extensively investigated, majority of these studies focus on the negative regulator Keap1, which is responsible for cytoplasmic retention of the Keap1-Nrf2 complex, thereby preventing Nrf2-mediated gene transcription. Given the critical role of lysine acetylation in regulating diverse cellular pathways, we use clinically relevant histone deacetylase (HDAC) inhibitors to explore novel mechanisms that govern Nrf2/ARE pathway. By a global proteomic survey, we have learned that the HDAC inhibitor, vorinostat, induces lysine acetylation of 73 proteins in MDA-MB-231 human breast cancer cells. These proteins include chromatin-associated proteins, transcriptional factors, transcriptional regulators, chaperone proteins, DNA repair enzymes, structural proteins and kinase mediators. Among these proteins, SQSTM1 is of particular interest as a recent study has confirmed its critical function in activation of the Nrf2/ARE pathway. Our work shows that vorinostat down-regulates Keap1 protein and elevates protein expression of Nrf2 and NQO1. Induction of Nrf2 by vorinostat is mediated through SQSTM1 as depletion of SQSTM1 by siRNA diminishes the effect of vorinostat on Nrf2 and NQO1. These findings suggest that therapeutic HDAC inhibitors may be found to be useful as chemopreventive agents for breast cancer and support work to elucidate the roles of lysine acetylation in the Nrf2/ARE dependent gene transcription as an underlying mechanism. Supported by FAMRI, Department of Defense Era of Hope, and NIH CA88843.
Citation Information: Cancer Prev Res 2008;1(7 Suppl):B104.
Abstract B106: Inhibition of IKKb and NFκB signaling by a novel curcumin analogue
Authors: Kasinski Andrea , Du Yuhong , Thomas Shala , Zhao Jing , Sun Shi-Yong , Khuri Fadlo , Wang Chun-Yu , Shoji Mamoru , Sun Aming , Snyder James , Liotta Dennis , Fu Haian 
Published: May 2012

Abstract
B106
The nuclear factor kappa-B (NF-κB) signaling pathway has been targeted for therapeutic applications in a variety of human diseases such as cancer. A number of naturally occurring substances including curcumin have been investigated for their actions on the NF-κB pathway because of their significant therapeutic potential and safety profile. A synthetic monoketone compound termed EF24 was developed from curcumin and exhibited a potent anticancer activity. Here we report a mechanism by which EF24 potently suppresses the NF-κB signaling pathway in both head and neck cancer and lung cancer cell lines through direct action on the I-κB kinase (IKK). We demonstrate that (i) EF24 induces death of lung, head and neck, breast, ovarian, and cervical cancer cells with a potency about 10 times higher than curcumin does, (ii) EF24 rapidly blocks the nuclear translocation of NF-κB with an IC50 of 1.3 μM compared with curcumin with an IC50 of 13 μM, (iii) EF24 effectively inhibits TNFα-induced I-κB phosphorylation and degradation, suggesting a role of this compound in targeting IKK, and (iv) EF24 indeed directly inhibits the catalytic activity of IKK in an in vitro reconstituted system. This study identifies IKK as an effective target for EF24 and provides a molecular explanation for a superior activity of EF24 over curcumin. The effective inhibition of TNFα-induced NF-κB signaling by EF24 extends the therapeutic application of EF24 to other NF-κB-dependent diseases, including inflammatory diseases such as rheumatoid arthritis.
Citation Information: Cancer Prev Res 2008;1(7 Suppl):B106.