bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 1844: Reduced expression of miR-342-3p in prostate cancer.
Authors: Jones Dominique , Anene Divine , Aloway April , Anene Praise , Avila Diana , Gobejishvili Leila , Barve Shirish , McNally Lacey , Kidd LaCreis 
Published: August 2014

Abstract
Patients with bone metastasis of the prostate have a 5-year survival rate of less than 30%. Due to inconsistencies in the presentation, prognosis, and treatment options of metastatic prostate cancer (PCa), biomarkers are urgently needed for personalized treatment of this disease. MicroRNAs (miRNAs) are small, non-coding, single-stranded endogenous RNAs that regulate the expression of multiple messenger RNA targets. Studies have demonstrated that these non-coding RNAs are significantly expressed in lung, breast and prostate cancer tumors. We hypothesize that miRNAs are differentially expressed between non-cancerous and aggressive tumor phenotypes in PCa, e.g. bone-specific metastasis. To test this hypothesis, we evaluated 384 miRNAs in the serum of stage-matched patients with stage I (n = 5), stage III (n = 5), stage IV (n = 5) PCa compared to non-cancerous age and stage-matched controls (n = 5). Total RNA was isolated from 500 μl of serum (Bioserve Biotechnologies, Ltd). The expression profiles of miRNAs were measured using TLDA cards and statistical analyses were performed using Expression Suite Software version 1.0. MiRNAs (miR-106b/17, -302b, -342-3p) were differentially expressed in the serum of PCa patients with (stage I, III, IV) when compared to controls. Mir-342-3p was significantly reduced in expression (P = 0.018-0.028) in all PCa patients relative to non-cancerous controls, after adjusting multiple hypothesis testing. However, other serum miRNAs were differentially expressed for only stage III PCa (P=0.001-0.018). Validation of these differentially expressed miRNAs in large sample sizes will lead to the identification of pre- and metastatic biomarkers. Ultimately, the investigation of these biomarkers will improve personalized treatment of PCa patients.
Citation Format: Dominique Jones, Divine Anene, April Aloway, Praise Anene, Diana Avila, Leila Gobejishvili, Shirish Barve, Lacey McNally, LaCreis Kidd. Reduced expression of miR-342-3p in prostate cancer. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1844. doi:10.1158/1538-7445.AM2013-1844
Abstract 1846: Potential of tumor-suppressive miR-596 targeting LGALS3BP as a therapeutic agent in oral cancer.
Authors: Kozaki Ken-ichi , Endo Hironori , Muramatsu Tomoki , Furuta Mayuko , Uzawa Narikazu , Pimkhaokham Atiphan , Amagasa Teruo , Inazawa Johji 
Published: August 2014

Abstract
The incidence and mortality statistics for oral squamous cell carcinoma (OSCC) were 10th and 12th, respectively, in human cancers diagnosed worldwide in 2008. In this study, to identify novel tumor-suppressive microRNAs (TS-miRNAs) and their direct targets in OSCC, we performed methylation-based screening for 43 miRNAs encoded by 46 miRNA genes located within 500bp downstream of 40 CpG islands and genome-wide gene expression profiling in combination with a prediction database analysis, respectively, in 18 cell lines, resulting in the identification of a novel TS-miRNA miR-596 directly targeting LGALS3BP/Mac-2 BP/90K. DNA hypermethylation of CpG island located 5’-upstream of miR-596 gene was frequently observed in OSCC cell lines (100% of 18 cell lines) and primary OSCC cases (46.2% and 76.3% of 26 Japanese and 38 Thais primary cases) in a tumor-specific manner. The ectopic transfection of double-stranded RNA (dsRNA) mimicking miR-596 or specific siRNA for LGALS3BP significantly induced growth inhibition and apoptosis in cell lines lacking miR-596 expression or overexpressing LGALS3BP, respectively, in a manner associated with a suppression of ERK1/2 phosphorylation. Moreover, we also mention the effect of dsRNA mimicking miR-596 on the growth of an OSCC cell line in vivo. Our findings define a central role for miR-596 in OSCC and suggest the potential of miR-596 as an anti-cancer agent for miRNA replacement therapy in OSCC.
Citation Format: Ken-ichi Kozaki, Hironori Endo, Tomoki Muramatsu, Mayuko Furuta, Narikazu Uzawa, Atiphan Pimkhaokham, Teruo Amagasa, Johji Inazawa. Potential of tumor-suppressive miR-596 targeting LGALS3BP as a therapeutic agent in oral cancer. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1846. doi:10.1158/1538-7445.AM2013-1846
Abstract 1847: Molecular profiles of microRNA in endometrial carcinoma using paraffin-embedded (FFPE) specimens.
Authors: Lee Taek Sang , Jeon Hye-Won , Kim Yong-Beom 
Published: August 2014

Abstract
MicroRNAs (miRNAs) are small non-coding RNAs that regulate
mRNA stability and protein expression at post-transcriptional level.
Certain miRNAs have been demonstrated to act either as oncogenes or tumor suppressors. The specific expression profiles of miRNAs have been found in many human cancers, but the role of miRNAs in endometrioid endometrial cancer (EEC) remains poorly understood. Most miRNA profiling studies have used fresh tissue samples. This study was to provide the candidate miRNAs for further confirming the role of miRNAs in carcinogenesis of EEC and to explore whether FFPE material would be suitable for miRNA profiling. We found the differences in miRNA expression profile using human miRNA microarray in EECs and normal endometrium. Of those, the miR-200a*, miR-200b*, miR-141, miR-182, and miR-205 were greatly enriched. The expressions of these 5 miRNAs were validated using quantitative real time reverse transcription-PCR (qRT-PCR). Then, we performed qRT-PCR profiling of miR expression in 30 microdissected formalin-fixed paraffin-embedded (FFPE) specimens (20 EECs, 10 non-tumor specimens) and reconfirmed the results of differential expression between cancer and normal tissue. We next tested whether specific inhibition of overexpressed microRNAs would alter the chemosensitivity. In in vitro cell viability assay, anti-miR200b* slightly enhanced cisplatin cytotoxicity compared with negative control although it showed marginal statistical significance (p=0.07). This information provided the candidate miRNAs for further confirming the role of miRNAs in carcinogenesis of EEC and potentially serving as a diagnostic or therapeutic tool. FFPE specimens of endometrial tissues are suitable as a source for miRNA microarray profiling.
Citation Format: Taek Sang Lee, Hye-Won Jeon, Yong-Beom Kim. Molecular profiles of microRNA in endometrial carcinoma using paraffin-embedded (FFPE) specimens. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1847. doi:10.1158/1538-7445.AM2013-1847
Abstract 1848: Let-7 brings new insights into chronic myeloid leukemia therapy.
Authors: Yi Bin , Li Xiaobo , Du Wenjun , Piazza Gary A. , Xi Yaguang 
Published: August 2014

Abstract
Human chronic myelogenous leukemia (CML) is a malignancy of pluripotent hematopoietic cells that is caused by the deregulated activity of the tyrosine kinase that is encoded by the chimeric bcr-abl oncogene. Given that CML cells are usually highly resistant to chemotherapy, novel and more efficacious strategies against this disease are urgently needed. MicroRNA (miRNA) is a set of newly discovered 20-22 nucleotides RNA molecules, and they broadly repress their cognate target genes at post-transcriptional/translational level. Up to date, there are approximately 2,000 human miRNA transcripts have been characterized, which are estimated to modulate more than 30% human genes and are widely involved in many essential biological processes including differentiation, proliferation, apoptosis, and also tumorigenesis. In this study, we studied let-7, a miRNA with tumor suppressive signature, for its therapeutic potential in CML. When treating CML K562 and KU812 cell by imatinib, let-7 can be significantly induced. Overexpression of let-7 can sensitize K562 and KU812 cells to imatinib, while knock-down of let-7 can increase the drug resistance of these cells. The mechanistic studies found that let-7 was able to promote apoptosis of CML cells, inhibit the tumor cell proliferation, and lead to a cell cycle arrest in the G0/G1 phase. These results demonstrate that let-7 is a potential target for treating CML by imatinib and/or other anti-cancer druges. The pro-apoptosis and anti-proliferation roles of let-7 in CML cells may provide novel insights into discovery and development novel drugs for conquering this malignant disease.
Citation Format: Bin Yi, Xiaobo Li, Wenjun Du, Gary A. Piazza, Yaguang Xi. Let-7 brings new insights into chronic myeloid leukemia therapy. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1848. doi:10.1158/1538-7445.AM2013-1848
Note: This abstract was not presented at the AACR Annual Meeting 2013 because the presenter was unable to attend.
Abstract 185: Secoisolariciresinol diglucoside (SDG, flaxseed lignan) improves biomarkers of early mammary gland cancer progression in a rat model of breast and ovarian cancer.
Authors: Delman Devora , Kimler Bruce F. , Fabian Carol J. , Petroff Brian K. 
Published: August 2014

Abstract
Breast cancer prevention efforts increasingly are focused on potentially beneficial dietary modifications due to their ease of implementation, wide acceptance and excellent subject compliance. SDG is a bioactive component of flaxseed suggested to have beneficial SERM-like effects in females at high risk for the development of breast cancer. In parallel with a human phase II prevention trial, female Sprague Dawley rats (n=10-12/group) received 0, 1, 10 or 20 mg/kg/day SDG in the feed. Simultaneously, rats were induced to concurrent mammary and ovarian cancer progression in a previously validated model using sustained release 17β-estradiol and local ovarian DMBA treatment starting at 6 weeks of age. Serum was collected at 3 weeks to measure steady state SDG metabolite concentrations. Mammary gland and ovarian tissues were collected at 3 months post-treatment and examined for changes in epithelial cell proliferation (Ki-67, cell counts), histopathology and dysplasia scores as well as a panel of cancer risk and progression biomarker genes. Carcinogen treatment markedly elevated dysplasia scores while SDG decreased dysplasia in a dose-dependent fashion, with an approximately 50% improvement the highest dose. Mammary epithelial cell numbers were increased by carcinogen and this effect was mitigated similarly at all doses of SDG and reflected in reduced Ki-67 expression. Overall, SDG decreased mammary epithelial proliferation and dysplasia resulting from carcinogen treatment. This preclinical benefit occurred at serum concentrations similar to our human pilot study, in which dietary SDG reduced KI-67 expression in mammary epithelial cells, and decreased the proportion of women with RPFNA atypia.
Supported in part by funds from Komen for the Cure grant KG101039.
Citation Format: Devora Delman, Bruce F. Kimler, Carol J. Fabian, Brian K. Petroff. Secoisolariciresinol diglucoside (SDG, flaxseed lignan) improves biomarkers of early mammary gland cancer progression in a rat model of breast and ovarian cancer. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 185. doi:10.1158/1538-7445.AM2013-185
Abstract 1854: Metabolic cross talk between omental derived adipose stromal cells from lean and obese patients with ovarian cancer cells.
Authors: Rizi Bahar Salimian , Nowicka Alexandra , Klopp Ann H. , Nagrath Deepak 
Published: August 2014

Abstract
Advanced-stage ovarian cancers have been shown to be metastatic in peritoneal cavity. Ovarian cancer metastasis is diagnosed primarily in omentum which is a soft fatty pad that extends from stomach and covers the bowel. The location of excess adipose tissue appears to be an important factor which influences the effect of obesity on cancer incidence. For example, increased total body obesity is associated with relative risk of 1.14 of developing ovarian cancer. However, a waist to hip circumference ratio of &gt;0.85 is associated with a much higher 8-fold increased risk of developing ovarian cancer. Individuals with greater waist to hip ratio generally have more visceral adipose including omental adipose. The tumor promoting effects of regional adipose may be attributed, at least in part, to the presence of a population of mesenchymal stem cells (MSC) in adipose tissue. Adipose stem cells or adipose derived stromal cells (ASCs) are a multi-potent population of mesenchymal stem cells, which support cancer progression in many models. These cells are uniquely tumor tropic, migrating into tumor stroma from regional sources where they support formation of tumor stroma elements and promote tumor progression. Here, we use metabolic foot-printing approach to dissect the metabolic networks regulated by ASCs and ACs, as well as their role in imparting drug resistance to tumors by deregulating metabolic pathways in ovarian cancer cells. Importantly, we found that O-ASCs from obese patients differentially induce metabolic reprogramming in cancer cells and that cancer cells induce reciprocal metabolic alterations and phenotypic changes in O-ASCs from lean patients.
Citation Format: Bahar Salimian Rizi, Alexandra Nowicka, Ann H. Klopp, Deepak Nagrath. Metabolic cross talk between omental derived adipose stromal cells from lean and obese patients with ovarian cancer cells. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1854. doi:10.1158/1538-7445.AM2013-1854
Abstract 1860: Metabolomics for the identification of prognostic biomarkers of pancreatic cancer.
Authors: Unger Keith , Kaur Prabhjit , Cheema Amrita K. 
Published: August 2014

Abstract
Introduction: Although the survival outcomes of Pancreatic Ductal Adenocarcinoma (PDAC) continue to be poor, clinical and basic research in this field is disproportionately under-represented as compared to other cancer sites. Currently, there is no blood or fluid test for diagnosis or prognosis of PDAC. Sensitive and specific biomarkers are thus critical for improving clinical outcomes of PDAC. Our goal in this study was to identify molecular features that could be used for disease stratification. The underlying hypothesis was that targeted, quantitative evaluation of molecular fingerprints of PDAC in serum, calculated originally via matched tissue metabolomic profiles using an untargeted approach may have direct clinical applicability.
Approach: We have used mass spectrometry based metabolomics, an emerging field that provides new information on biological perturbations based on changes in multiple endogenous metabolites. These metabolites represent the endpoint of cellular processes and are hence a direct readout of the phenotype or the physiological status. Detection of PDAC using a metabolomics approach is based on the establishment of specific key metabolite signatures in pancreatic tumor tissue derived from patients diagnosed with PDAC. A shortlisted panel of these putative markers was tested for their pre-clinical performance using serum samples from the same patients. This combinatorial approach allowed us to interrogate the PDAC tissue metabolome in a global and unbiased fashion and subsequently test the clinical applicability using a targeted approach in serum samples.
Results: The untargeted metabolomics profiling resulted in the identification of a panel of key metabolites which could help discriminate PDAC tissue profiles from pancreatitis and colo-rectal tumor tissue. Validation of these metabolites in serum is ongoing.
Conclusion: Our results demonstrate the power of metabolomics for developing clinical assays for diagnosis and prognosis of PDAC. Identification of cellular target molecules, associated with pancreas cancer oncogenesis, progression and metastasis is critical for designing new treatment options for advanced stage disease. Developing a specific and sensitive panel of bio-markers offers a pragmatic approach towards increasing overall survival rates; identify molecular targets for therapeutic development, improving treatment strategies and thus clinical outcomes
Supported by American Cancer Society
Citation Format: Keith Unger, Prabhjit Kaur, Amrita K. Cheema. Metabolomics for the identification of prognostic biomarkers of pancreatic cancer. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1860. doi:10.1158/1538-7445.AM2013-1860
Abstract 1864: Mitochondrial bioenergetics of metastatic breast cancer cells in response to decreasing oxygen tension.
Authors: Vayalil Praveen K. , Diers Anne R. , Olivia Claudia R. , Griguer Corinne E. , Darley-Usmar Victor , Hurst Douglas R. , Welch Danny R. , Landar Aimee 
Published: August 2014

Abstract
Solid tumors are characterized by regions of low oxygen tension, which play a central role in tumor progression and resistance to therapy. The major organelle affected by reduced oxygen tension is the mitochondrion, which has to functionally adapt to maintain cellular bioenergetics for the cell survival. In the present study, a novel experimental approach was developed to examine the real-time bioenergetic changes during adaptation to various oxygen tensions ranging from 20% to &lt; 1% oxygen using highly sensitive extracellular flux technology. Oxygen was gradually removed from the culture medium, and bioenergetic changes were measured in normal breast epithelial (MCF10A) and metastatic cancer cell lines (MDA-MB-231 and MCF10CA clones). We found that breast cancer cells, but not MCF10A cells, rapidly responded to low oxygen tension by stabilizing HIF-1α, increasing hypoxia responsive gene expression, and stimulating cellular uptake of glucose, confirming previous observations. In addition, breast cancer cells increased extracellular acidification rate (ECAR) or glycolysis during adaptation to low oxygen tension, and this effect was markedly lower in MCF10A cells. Interestingly, breast cancer cells exhibited a biphasic response in oxygen consumption rate (OCR) as the oxygen tension was reduced gradually from 20% to &lt;1.0%, a response not previously described. This effect is HIF-1α-dependent, as silencing HIF-1α function in cancer cells completely abolished the biphasic response in OCR and increase in ECAR. Moreover, cancer cells demonstrated the ability to restore and maintain its OCR steadily at specific oxygen tension either during deoxygenation or reoxygenation, an effect not observed in HIF-1α silenced cells. Additional studies confirmed that the initial stimulation of OCR is due to increased mitochondrial respiration. In conclusion, our results suggest that HIF-1α provides high degree of bioenergetic flexibility under different oxygen tensions which may confer an adaptive advantage in the ever-changing tumor microenvironment as well as during invasion and metastasis. Moreover, these differences may be useful in screening novel therapeutic agents that target the bioenergetics of cancer cells in response to low oxygen tension.
Citation Format: Praveen K. Vayalil, Anne R. Diers, Claudia R. Olivia, Corinne E. Griguer, Victor Darley-Usmar, Douglas R. Hurst, Danny R. Welch, Aimee Landar. Mitochondrial bioenergetics of metastatic breast cancer cells in response to decreasing oxygen tension. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1864. doi:10.1158/1538-7445.AM2013-1864
Abstract 1878: Acetyl coA carboxylase1 and its role in prostate cancer initiation and progression.
Authors: Davis Amanda L. , Scott Kristen , Chen Yong , Kridel Steven 
Published: August 2014

Abstract
The alteration of cellular metabolic processes is a common event in the initiation and progression of several cancer types. One metabolic hallmark of cancer cells is an increase in de novo lipogenesis. The enzymes responsible for de novo fatty acid synthesis are overexpressed in cancer, suggesting that these enzymes may be appropriate targets in efforts to inhibit or treat disease. Specifically, Acetyl CoA Carboxylase 1 (ACC1), the cytosolic enzyme that catalyzes the rate limiting step of de novo fatty acid synthesis through the ATP and biotin-dependent carboxylation of acetyl-CoA to malonyl-CoA, has received attention as a potential target for cancer treatment. Pharmacological inhibition and siRNA mediated knockdown of ACC1 has been shown to selectively kill prostate cancer cells in vitro by denying cells of adequate amounts of fatty acids needed to proliferate and survive. Although ACC1 has been implicated in cancer, its role has not been examined in a spontaneous model of cancer. To address this issue, we first generated mice with prostate-specific deletion of exon 22 of the Acetyl CoA Carboxylase 1 (ACCL/L) gene by breeding with Probasin-Cre mice. Loss of ACC1 activity did not appear to affect prostate function as survival, prostate weight, histology, and breeding was similar between ACCL/L Cre+ and ACCL/L Cre− mice. To determine the role of ACC1 in prostate cancer, the ACC+/L mice were crossed with PtenL/L; Cre+ mice. To our surprise, ACC1 activity was not required for prostate cancer development or progression in vivo, despite its apparent requirement in vitro. Total prostate weight and individual lobe weight did not differ among ACC+/L; PtenL/L; Cre+ mice, ACCL/L; PtenL/L; Cre+ mice and ACC1+/+; PtenL/L; Cre+ mice. These early studies suggest that ACC1 activity, and perhaps the fatty acid synthesis pathway, may not be required for prostate cancer development. The role of ACC1 in redox modulation, rescue of impaired de novo fatty acid synthesis by circulating and dietary fatty acid, and the potential compensation for ACC1 activity by ACC2 in prostate cancer are possible explanations for this unexpected phenotype. These results could have significant impact on the development and use of anti-cancer therapeutics that target the fatty acid synthesis pathway.
Citation Format: Amanda L. Davis, Kristen Scott, Yong Chen, Steven Kridel. Acetyl coA carboxylase1 and its role in prostate cancer initiation and progression. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1878. doi:10.1158/1538-7445.AM2013-1878