bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract B22: Molecular oncogenesis of NANOG in castration-resistant prostate cancer
Authors: Jeter Collene R. , Lu Yue , Liu Bigang , Gaddis Sally , Liang Shoudan , Tang Dean G. 
Published: January 2014

Abstract
Regardless of the cell-of-origin, self-renewing tumor cells may be a driving force in cancer progression to lethal disease. An important outstanding question in the field of oncology is by what molecular mechanisms do tumor cells acquire stem cell (SC) biological properties? The embryonic stem cell pluripotency molecule NANOG appears to be among the important SC-related self-renewal genes underlying molecular oncogenesis. We have previously reported that NANOG attenuation inhibited prostate cancer cell clonogenic growth and in vivo tumorigenicity. Subsequently, we have found that NANOG overexpression in LNCaP prostate cancer cells promoted clonogenicity and tumor development particularly in androgen-deprived conditions. Furthermore, NANOG knockdown in relatively undifferentiated PSA- prostate cancer cells significantly reduced tumor regeneration in castrated hosts implicating NANOG in the emergence of castration-resistant prostate cancer (CRPC). To understand the molecular underpinnings of NANOG-mediated CRPC, we have performed ChIP-Seq analysis of NANOG occupancy in LNCaP cells overexpressing NANOGP8 or NANOG1. These non-biased and global studies have revealed downstream genes and signaling pathways that may potentially be regulated by NANOG in cancer cells and shed light on the NANOG castration-resistance phenotype. ∼60% of the promoter occupied sites are shared between NANOGP8 and NANOG1, representing 806 genes. Among these are many developmental-associated genes, chromatin remodeling and epigenetic regulators and molecules implicated in prostate cancer. In addition, motif analysis of NANOG occupied regions has revealed a novel candidate NANOG-interacting protein in prostate cancer cells. Integration of ChIP-Seq data with RNA-Seq is currently underway and integrative analysis is anticipated to further discriminate the direct and indirect molecular architecture responding to NANOG expression in prostate cancer.
Citation Format: Collene R. Jeter, Yue Lu, Bigang Liu, Sally Gaddis, Shoudan Liang, Dean G. Tang. Molecular oncogenesis of NANOG in castration-resistant prostate cancer. [abstract]. In: Proceedings of the Eleventh Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2012 Oct 16-19; Anaheim, CA. Philadelphia (PA): AACR; Cancer Prev Res 2012;5(11 Suppl):Abstract nr B22.
Abstract B36: Transcriptional targeting of tumor cells with AAV vectors carrying diphtheria toxin A fragment
Authors: Chen Haifeng 
Published: January 2014

Abstract
Suicide gene therapy is an attractive way of combating cancers. Diphtheria toxin (DT) has been widely studied for its application to kill cancer cells. Due to DT's extreme toxicity issue, viral vectors carrying DT are very difficult to produce since producer cells are killed before viral vectors can be produced. In this study adeno-associated viral (AAV) vectors carrying DT fragment A (DT-A) was generated at high titers in insect cells by inserting a mammalian intron to abolish the toxin expression. When these toxin carrying AAV vectors were introduced into mammalian cells, the intron was spliced out and the toxin expressed and killed the mammalian cells. Since they can direct gene expression in tumor cells but not in normal cells, tumor-specific promoters were cloned to direct the expression of the DT-A gene and AAV vectors were prepared. These vectors carrying DT-A under control of surviving or CXCR4 promoter specifically killed tumor cell lines HepG2, Hep3B, and BE (2)-M17, but not the normal human lung cell line WI38. The results in this study indicate that this novel way of targeting tumor cells with AAV vectors carrying DT-A should provide a new tool for the development of toxin-based suicide gene therapy drugs.
Citation Format: Haifeng Chen. Transcriptional targeting of tumor cells with AAV vectors carrying diphtheria toxin A fragment. [abstract]. In: Proceedings of the Eleventh Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2012 Oct 16-19; Anaheim, CA. Philadelphia (PA): AACR; Cancer Prev Res 2012;5(11 Suppl):Abstract nr B36.
Abstract B38: Iodine supplement exerts antineoplastic adjuvancy, chemoresistance inhibition and cardioprotection in mammary cancer treatment with anthracyclines
Authors: Aceves Carmen , Alfaro-Hernandez Yunuen , Delgado Guadalupe 
Published: January 2014

Abstract
Mortality for mammary cancer (MC) has decreased in the past decade, owing principally to early detection and the use of neoadjuvant chemotherapy. Of several preparations that cause regression of MC, Doxorubicin (DOX) is the most active, first-line monotherapeutic. Nevertheless, its use has been limited due to the rapid development of chemoresistance and cardiotoxicity caused by free radicals. In previous studies we have shown that supplementation with moderately high doses of molecular iodine (I2) has a powerful antineoplastic effect in methylnitrosourea (MNU)-induced MC models. These studies also showed a consistent antioxidant effect of I2 in normal and tumoral tissues. In the present study we analyzed the effect of I2 in combination with DOX treatment. Female Sprague Dawley rats with MNU-induced MC were treated with the therapeutic DOX dose (16 mg/kg) and with two lower doses (8 and 4 mg/kg) with and without 0.05% I2 in drinking water. In a first, short-term experiment, iodine treatment began 2 days before a single DOX injection (ip), and the animals were analyzed after 7 days. In a second experiment, animals received two injections (days zero and 14) of 4 mg/kg DOX without or with long-term I2 treatment throughout the 56 days of observation. The results showed that at every DOX dose, short-term I2 treatment induced synergic antineoplastic effects (decreasing tumor size and PCNA signal) with significant protection against body weight loss and cardiotoxicity (CK-MB enzyme and cardiac lipoperoxidation). With long-term I2 treatment, mammary tumors became more sensitive to 4 mg/kg DOX, decreasing chemoresistance markers (Bcl2 and survivin) and increasing peroxisome proliferator-activated receptor type gamma expression, indicating a specific interaction of I2 with these receptors.
The authors thank Felipe Ortóz for his technical assistance and Leonor Casanova for academic supports. Supported in part by PAPIIT/UNAM 201210 and CONACYT 78955.
Citation Format: Carmen Aceves, Yunuen Alfaro-Hernandez, Guadalupe Delgado. Iodine supplement exerts antineoplastic adjuvancy, chemoresistance inhibition and cardioprotection in mammary cancer treatment with anthracyclines. [abstract]. In: Proceedings of the Eleventh Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2012 Oct 16-19; Anaheim, CA. Philadelphia (PA): AACR; Cancer Prev Res 2012;5(11 Suppl):Abstract nr B38.
Abstract B43: Dose-response on the chemopreventive effects of sarcophine-diol on UVB-induced skin tumor development in SKH-1 hairless mice.
Authors: Guillermo Ruth F. , Zhang Xiaoying , Kaushik Radhey S. , Zeman David , Ahmed Safwat A. , Khalifa Sherief , Fahmy Hesham , Dwivedi Chandradhar 
Published: January 2014

Abstract
Sarcophine-diol (SD) is a lactone ring-opened analogue of sarcophine. It has shown chemopreventive effects on chemically-induced skin tumor development in female CD-1 mice, as well as in a UVB-induced skin tumor development model in hairless SKH-1 mice at a dose of 30 μg SD applied topically and 180 mJ/cm2 UVB. The objective of this study was to determine the dose-response on the chemopreventive effects of SD on SKH-1 hairless mice when exposed to a UVB radiation dose of 30 mJ/cm2. This UVB dose better represents chronic human skin exposure to sunlight leading to skin cancer than previous studies applying much higher UVB doses. Carcinogenesis was initiated and promoted by UVB radiation. Female hairless SKH-1 mice were divided into 5 groups. The control group was topically treated with 200 μL of acetone (vehicle), and the SD treatment groups were topically treated with SD (30 μg, 45 μg, and 60 μg dissolved in 200 μL of acetone) 1 hour before UVB radiation (30 mJ/cm2). The last group of animals received 60 μg SD/200 μl acetone without UVB exposure. These treatments were continued for 27 weeks. Tumor multiplicity and tumor volumes were recorded on a weekly basis for 27 weeks. Weight gain and any signs of toxicity were closely monitored as well. Histological characteristics and the proliferating cell nuclear antigen (PCNA) were evaluated in the mice skin collected at the end of the experiment.
The dose-response study proved a modest increase in chemopreventive effects with the increase in SD dose, reflected in reduced tumor multiplicities and tumor volumes. SD also reduced the number of cells positively stained with PCNA proliferation marker in mice skin. The study also showed that SD applications without UVB exposure had no effect on the structure of mice skin. The results from this study suggest that broader range doses of SD are necessary to improve the chemopreventive effects.
Citation Format: Ruth F. Guillermo, Xiaoying Zhang, Radhey S. Kaushik, David Zeman, Safwat A. Ahmed, Sherief Khalifa, Hesham Fahmy, Chandradhar Dwivedi. Dose-response on the chemo-preventive effects of sarcophine-diol on UVB-induced skin tumor development in SKH-1 hairless mice. [abstract]. In: Proceedings of the Eleventh Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2012 Oct 16-19; Anaheim, CA. Philadelphia (PA): AACR; Cancer Prev Res 2012;5(11 Suppl):Abstract nr B43.
Abstract B53: Triterpene Fraction of Cucumis trigonus - A Novel Microtubule Inhibitor and Antitumor Agent, Induce Cell Death in Cancer Cells.
Authors: Patel Viralkumar Laxmanbhai , Wadhwani Ashish D. , P. Vijayan 
Published: January 2014

Abstract
Taxol-based combination chemotherapy remains the predominant treatment for cancer. However, taxane related drug resistance and neurotoxicity have promoted us to develop substitute treatment strategies. Kinesis spindle protein which is crucial for bipolar spindal formation and duplicate chromosome separation in early phase of mitosis, has emerged as an attractive target for cancer chemotherapy. The Aim of study was to investigate the mechanism of inhibition of kinesis spindle protein that plays an essential role in establishing mitotic spindle bipolarity, by the novel small molecular inhibitor.
Antiproliferative activity of triterpene fraction of cucumis trigonus(TF25CT) in cancer cell line was accessed by cell viability assay (MTT and SRB). TF25CT showed dose dependent inhibition of cell proliferation of cancer cells. The antiproliferative effect of TF25CT was also associated with induction of apoptosis as well as morphology changes and DNA fragment. The morphology of Apoptosis nuclei was quantified using Hoechst stating and PI fragmentation. The degree of DNA fragmentation was analyzed by using agarose gel electrophoresis. The observations indicate that induced apoptotic- liked in morphological changes such as cell shrinkage and blebbing. Suppression of microtubule dynamics is responsible for the ability of TF25CT to inhibit the mitotic progression and cell proliferation using fluorescent microscope, we examined the effect of TF25CT on dynamics of individual microtubule in two living human cancer cell line. Taken together the kinesis protein inhibitor represents an imported compound for further investigate as novel anticancer therapeutics.
Citation Format: Viralkumar Laxmanbhai Patel, Ashish D. Wadhwani, Vijayan P. Triterpene fraction of Cucumis trigonus, a novel microtubule inhibitor and antitumor agent, induces cell death in cancer cells. [abstract]. In: Proceedings of the Eleventh Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2012 Oct 16-19; Anaheim, CA. Philadelphia (PA): AACR; Cancer Prev Res 2012;5(11 Suppl):Abstract nr B53.
Abstract B57: STAT3 as a cancer prevention target in colorectal cancer cells
Authors: Lin Li , Yu Wenying , Xiao Hui , Wang Wenlong , Zhao Chongqiang , Lu Jiagao , Li Chenglong , Lin Jiayuh 
Published: January 2014

Abstract
Colorectal cancer is the third most frequently occurring cancer in both men and women and is the second leading cause of cancer deaths in the United States. Despite advances in the treatment of this cancer, the five-year averaged survival rate for all stages has only increased to 66% and more than 49,000 deaths of colon cancer in the United States in 2011. Hence, novel therapeutic approaches of more effective treatments are much needed for colon cancer. Constitutive activation of Signal Transducers and Activators of Transcription 3 (STAT3) signaling is frequently detected in human cancer including colon cancer, and has emerged as an attractive molecular target for cancer prevention and therapy. We tested the efficacy of inhibiting persistent STAT3 signaling by a dietary agent, Ursolic acid from basil and a novel STAT3-selective inhibitor, LY5 in human colon cancer cell lines. Our data demonstrated that Ursolic acid is able to inhibit STAT3 phosphorylation, and induce apoptosis in HCT116 and SW480 human colon cancer cell lines. These results were confirmed by LY5, a novel STAT3-selective small molecular inhibitor, which also inhibits STAT3 phosphorylation and induces apoptosis in HCT116 and SW480 colon cancer cell lines. In addition, LY5 inhibits IL-6 mediated induction of STAT3 phosphorylation in DLD-1 human colon cancer cells. We also found Ursolic acid decrease cell viability and inhibit the tumorsphere formation of ALDH+/CD133+ colon cancer stem cells. Furthermore, administration daily of Ursolic acid suppressed the HCT116 tumor growth in mice in vivo. In summary, our results suggest that STAT3 is target for colon cancer prevention and inhibition of persistently activated STAT3 using dietary agents or inhibitors may offer an effective prevention approach for colorectal carcinoma.
Citation Format: Li Lin, Wenying Yu, Hui Xiao, Wenlong Wang, Chongqiang Zhao, Jiagao Lu, Chenglong Li, Jiayuh Lin. STAT3 as a cancer prevention target in colorectal cancer cells. [abstract]. In: Proceedings of the Eleventh Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2012 Oct 16-19; Anaheim, CA. Philadelphia (PA): AACR; Cancer Prev Res 2012;5(11 Suppl):Abstract nr B57.
Abstract B70: Design of the SHAPE-2 trial; Effects of equivalent weight loss, with and without exercise, on postmenopausal breast cancer risk
Authors: Gemert Willemijn AM van , Peeters Petra HM , Schuit Jantine A. , Monninkhof Evelyn M. 
Published: January 2014

Abstract
Background: Physical inactivity and overweight are two modifiable risk factors for breast cancer. These factors probably act through sex hormone-related pathways. The results of dietary intervention studies (mostly uncontrolled) suggest that diet-induced weight loss reduces postmenopausal sex hormone levels. The question remains if the beneficial effect of physical activity on breast cancer risk is fully explained by the accompanied weight loss. Three out of four exercise intervention studies showed that physical activity mainly influences hormone levels when concordant loss of body fat is achieved. One intervention study, however, suggests an effect of exercise on sex hormones independent of changes in adiposity.
Therefore, we set out to study the effect of weight loss mainly driven by exercise compared to equivalent diet induced weight loss only on sex hormone levels.
Methods/Design: We designed a three-armed, single blind, two-centre trial in 250 sedentary, postmenopausal women who are overweight/obese (BMI 25-35 kg/m2). Women are randomly allocated to a (1) Diet induced weight loss group, (2) Exercise induced weight loss group or (3) a stable weight Control group. The aim of both intervention groups is to loose an equivalent amount of 5-6 kg body weight in 10 to 14-week timeframe. The Diet-group will therefore follow an energy restricted diet. The Exercise-group will participate in a 16-week endurance and strength training programme (4 hours/week) combined with a slight caloric intake restriction. Measurements include blood sampling, questionnaires, anthropometrics, maximal exercise test, total body DEXA-scan (body (fat) composition) and MRI (abdominal fat). The main outcomes are endogenous serum levels of estradiol, estrone, testosterone and sex hormone binding globulin (SHBG).
Discussion: This study will give insight in the possible attributable effect, and the underlying mechanisms, of physical activity on endogenous sex hormone levels, directly and/or mediated by changes in body(fat) composition, in postmenopausal women.
Eventually this may lead to the design of more specific guidelines on lifestyle interventions and physical activity for prevention of breast cancer.
Citation Format: Willemijn AM van Gemert, Petra HM Peeters, Jantine A. Schuit, Evelyn M. Monninkhof. Design of the SHAPE-2 trial: Effects of equivalent weight loss, with and without exercise, on postmenopausal breast cancer risk. [abstract]. In: Proceedings of the Eleventh Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2012 Oct 16-19; Anaheim, CA. Philadelphia (PA): AACR; Cancer Prev Res 2012;5(11 Suppl):Abstract nr B70.
Abstract B84: The association between germline genetic variants in the PI3K pathway and PI3K mutations in breast tumors.
Authors: Brewster Abenaa M. , Bondy Melissa , Do Kim-anh , Sahin Aysegul , Hale Katherine , Wei Caimiao , Mills Gordon , Thompson Patricia 
Published: January 2014

Abstract
Background: Gene mutations in the PI3K pathway in breast tumors are associated with resistance to tamoxifen and poorer prognosis. Differences in host susceptibility to developing breast cancers with PI3K pathway mutations may explain the heterogeneity in response to tamoxifen for chemoprevention and breast cancer outcomes. The objective of the study was to evaluate the association between host germline single nucleotide polymorphisms (SNPs) and activation of the PI3K pathway in breast tumors.
Methods: We extracted tumor and germline DNA from 386 women with stages I-II breast cancer treated at the MD Anderson Cancer Center. Nine PI3K mutation sites were evaluated using the Sequenom assay and 57 tagging single nucleotide polymorphisms (SNPs) of candidate genes in the PI3K pathway were genotyped using the Illumina Golden Gate Platform.
Results: 36 patients (10%) had at least one mutation in the PI3K pathway. There was no association between PI3K mutation status by age at diagnosis or ethnicity. In univariate analysis, there was a statistically significant association between PI3K gene mutation status and 3 tagging SNPs in the genes, PTEN (rs123421, rs1234213) and IGF-1 (rs2033178).
Conclusion: PI3K mutations are rare in breast tumors but represent a druggable target for prevention and treatment. Host genetics may play a role in contributing to tumor biology and serve to identify individuals at risk for tumors with PI3K pathway activation and tamoxifen resistance.
Citation Format: Abenaa M. Brewster, Melissa Bondy, Kim-anh Do, Aysegul Sahin, Katherine Hale, Caimiao Wei, Gordon Mills, Patricia Thompson. The association between germline genetic variants in the PI3K pathway and PI3K mutations in breast tumors. [abstract]. In: Proceedings of the Eleventh Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2012 Oct 16-19; Anaheim, CA. Philadelphia (PA): AACR; Cancer Prev Res 2012;5(11 Suppl):Abstract nr B84.
Abstract B94: Hay fever and asthma as markers of atopic immune response and risk of colorectal cancer in three large cohort studies
Authors: Jacobs Eric J. , Gapstur Susan M. , Newton Christina C. , Turner Michelle C. , Campbell Peter T. 
Published: January 2014

Abstract
Background: In a previous analysis of the Cancer Prevention Study II (CPS-II) cohort that included follow-up from 1982-2000, having both hay fever and asthma was associated with lower colorectal cancer mortality. The combination of these allergy-related conditions may be a marker for allergy-related immune responses that could inhibit the development or progression of colorectal cancer.
Methods: We examined the association between having both hay fever and asthma and colorectal cancer mortality among 1,023,191 participants in Cancer Prevention Study I (CPS-I) followed-up from 1959-1972, and 1,102,092 participants in CPS-II, now followed-up from 1982 through 2008. We also examined associations with colorectal cancer incidence among 174,917 participants in the CPS-II Nutrition Cohort, a subgroup of CPS-II followed from 1992-2007. During follow-up, there were 5,644 colorectal cancer deaths in CPS-I, 13,558 colorectal cancer deaths in CPS-II, and 3,365 incident colorectal cancers in the CPS-II Nutrition Cohort. Cox proportional hazards regression models were used to calculate multivariable-adjusted relative risks (RRs).
Results: RRs for colorectal mortality associated with having both asthma and hay fever, compared to neither condition, were 0.90 (95% confidence interval (CI): 0.74-1.09) in CPS-I, 0.79 (95% CI: 0.69-0.91) in CPS-II, and 0.83 (95% CI: 0.74-0.92) when results from both cohorts were combined using a fixed-effects meta-analysis. The RR for colorectal cancer incidence in the CPS-II Nutrition Cohort was 0.90 (95% CI: 0.71-1.14).
Conclusion: These results are consistent with an association between having both hay fever and asthma and modestly lower colorectal cancer mortality.
Citation Format: Eric J. Jacobs, Susan M. Gapstur, Christina C. Newton, Michelle C. Turner, Peter T. Campbell. Hay fever and asthma as markers of atopic immune response and risk of colorectal cancer in three large cohort studies. [abstract]. In: Proceedings of the Eleventh Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2012 Oct 16-19; Anaheim, CA. Philadelphia (PA): AACR; Cancer Prev Res 2012;5(11 Suppl):Abstract nr B94.
Abstract B99: Colon cancer treatment: Are there racial disparities in an equal-access healthcare system?
Authors: Andaya Abegail , Enewold Lindsey , Zahm Shelia H. , Shriver Craig D. , Warren Joan , Stojadinovic Alexander , McGlynn Katherine , Zhu Kangmin 
Published: January 2014

Abstract
Purpose: Accessibility to medical care may be the most important factor influencing differences in colon cancer treatment among whites and blacks. This study assessed whether racial disparities in colon cancer surgery and chemotherapy existed in an equal access healthcare system. Additionally, we sought to examine whether racial differences varied by tumor stage.
Methods: Patients included 2,570 non-Hispanic whites and non-Hispanic blacks with colon cancer diagnosed from 1998 to 2007. Logistic regression was used to assess the associations between race and the receipt of colon cancer surgery or chemotherapy, while controlling for available potential confounders, both overall and stratified by tumor stage.
Results: Univariate analysis revealed that there were no racial differences in surgery but that non-Hispanic blacks were more likely to receive chemotherapy than non-Hispanic whites. However, after multivariate adjustment, the odds of receiving colon cancer surgery and chemotherapy were similar between the two racial groups and did not vary by tumor stage.
Conclusion: When access to medical care is equal, racial disparities in the receipt of colon cancer surgery and chemotherapy were not apparent. Thus, it is possible that equal access to care is the driving force behind racial disparities in cancer treatment in the general population.
Citation Format: Abegail Andaya, Lindsey Enewold, Shelia H. Zahm, Craig D. Shriver, Joan Warren, Alexander Stojadinovic, Katherine McGlynn, Kangmin Zhu. Colon cancer treatment: Are there racial disparities in an equal-access healthcare system? [abstract]. In: Proceedings of the Eleventh Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2012 Oct 16-19; Anaheim, CA. Philadelphia (PA): AACR; Cancer Prev Res 2012;5(11 Suppl):Abstract nr B99.