bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 4131: Serum miRNA profiles of patients with oral cancer and pre-cancer
Authors: MacLellan Sara A. , Lawson James , Baik Jonathan , Guillaud Martial , Poh Catherine F. , Garnis Cathie 
Published: August 2012

Abstract
Oral cancer is one of the most commonly diagnosed cancers worldwide. Those diagnosed with this disease are often diagnosed at late stage with poor 5-year survival rate and/or suffer from a high rate of local recurrence or second primary tumor. Novel approaches for early detection for treatment stratification are needed to improve these statistics. MicroRNAs (miRNAs), a group of small, non-coding RNAs, can be isolated from blood serum samples and have shown the potential to be used as a non-invasive detection method in several cancer types. The purpose of this study is to examine the expression profiles of circulating miRNAs in the serum of patients with high-risk oral lesions (HRLs; oral cancer/carcinoma in situ) and to explore their utility as potential oral cancer biomarkers. Methods: Serum samples were collected from 33 patients with HRL (17 oral cancer and 16 carcinoma in situ) undergoing intent-to-cure surgical treatment and from a demographically matched (for age, sex, and smoking status) normal control group (N=15). RNA was extracted from serum samples using a modified miRNeasy (Qiagen) protocol. The miRCURY LNA™ Universal RT miRNA PCR system was used to profile all serum samples. The system allowed for the profiling of 742 miRNAs plus required controls within a single experiment. Statistical tests were carried out using Statistica 64 and Microsoft Excel. Results: Using analysis of variance, we detected 37 miRNAs that showed a significant differential expression between the three groups (oral squamous cell carcinoma, carcinoma in situ, and controls). Among these 37 miRNAs, miR-223, miR-342-3p, miR-423-5p, and miR-451 were the most differentially expressed. Conclusions: By examining circulating miRNA expression profiles, we have identified potential biomarkers that can be obtained from a simple blood test. The differential expression of serum miRNAs between disease stages suggests the possible utility of these miRNAs as biomarkers for the early detection of oral cancer and its progression. Blood samples are easily collected from patients, and combining serum miRNA profiles with other screening techniques could greatly improve the sensitivity in oral cancer detection. Early detection to facilitate treatment decision making for those with oral cancer or premalignant disease would have a great impact on disease survival.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 4131. doi:1538-7445.AM2012-4131
Abstract 4134: miR1288 in colorectal cancers: Altered expression and its clinicopathological significance
Authors: Gopalan Vinod , Salajegheh Ali , Smith Robert A. , Lam Alfred K-Y 
Published: August 2012

Abstract
Introduction: MicroRNA-1288 (miR-1288) is a non-coding RNA located in 17p11.2 and not been studied solely in cancer. We aim to examine the miR-1288 expression in a large cohort of patients with colorectal carcinoma, adenoma and non-neoplastic colorectal tissues. The implications of miR-1288 expression and clinicopathological features were also studied. Methods: Tissues from 102 patients with surgical resection of colorectum (82 adenocarcinomas, 10 adenomas and 10 non-neoplastic tissues), two colon cancer cell lines (SW480 and SW48) and one normal colonic epithelial cell line (FHC) were recruited. miRNA was extracted from all these samples and were converted in to cDNA. Quantitative real-time polymerase chain reaction (qRT-PCR) was performed for the detection of miR-1288 expression. The results were correlated with the clinical and pathological data. Results: miR-1288 expression was decreased in majority of colorectal adenocarcinoma when compared to colorectal adenoma and non-neoplastic tissues. Reduced or absence expression of miR-1288 was noted in 78% (n=64) of the cancers. The colon cancer cell lines showed reduced expression of miR-1288 compared to normal colonic epithelial cell line. Distal colorectal cancers showed higher expression levels of miR-1288 than proximal cancers (p= 0.007). The expression levels of miR-1288 were significantly altered in different levels of cancer invasion (T staging) (p= 0.023). Conclusions: Altered expression pattern of miR-1288 in colorectal cancers compare to non-neoplastic tissues was identified. Also, differential regulation of miR-1288 was found to be related to location and pathological staging of colorectal cancers.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 4134. doi:1538-7445.AM2012-4134
Abstract 4135: Plasma miRNAs as potential predictive/prognostic biomarker for ovarian cancer
Authors: Chen Kexin 
Published: August 2012

Abstract
Background: Ovarian cancer is the fifth leading cause of cancer death in women worldwide. While the survival rates of women with early stage ovarian cancer are high, most cases are diagnosed late. Due to asymptomatic development and few screening options, almost 70% of women present at late stages of carcinogenesis. Sensitive, non-invasive biomarkers that can facilitate disease detection, staging and prediction of therapeutic outcome are highly desirable to improve survival rate and help to determine optimized treatment for ovarian cancer. The small non-coding RNAs, microRNAs (miRNAs), have recently been identified as critical regulators for various diseases including cancer and may represent a novel class of cancer biomarkers. The purpose of this study was to identify and validate circulating microRNAs in human plasma for use as such biomarkers in ovarian cancer. Methods/ Principle findings: We scan the circulating plasma miRNAs by Taqman Low Density Array, then identify and validated 30 markers in plasma samples among 70 cases and 70 controls by real-time PCR assay. Promising associations were evaluated in a second stage, comprising 150 cases and 150 controls. We found that compared with normal, there are 9 miRNAs (miR-205, miR-200a, miR-184, miR-34a*, miR-141, miR-483-5p, miR-193b*, let-7e*, miR-363*) expressed higher in ovarian cancer group, while the miR-98 and let-7f have the lower levels in ovarian cancer. Compared with early stage cases (stage I), there is only miR-483-5p expressed higher in advanced stages (stage II-IV). Receiver operating characteristic (ROC) analysis was used to evaluate the sensitivity and specificity of candidate plasma microRNA markers. We observed that combination of these identified miRNAs and CA-125, a widely used marker for ovarian cancer, further improved the accuracy of detection. Furthermore, our analysis showed that high levels of plasma miR-483-5p or low levels of let-7f predicted poor prognosis of ovarian cancer patients, consistent with the expression of miRNAs in ovarian cancer tissues. Conclusions/Significance: We propose that plasma miRNAs (miR-205, miR-200a, miR-184, miR-34a*, miR-141, miR-483-5p, miR-193b*, let-7e*, miR-363*) are potential biomarkers that complements CA-125 in detecting ovarian cancer; miR-483-5p and let-7f may predict the prognosis of ovarian cancer. It may provide new avenues for the detection, diagnosis, and therapy of this deadly disease.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 4135. doi:1538-7445.AM2012-4135
Abstract 4138: miRNA-362-3p is associated with recurrence of colorectal cancer and targets E2F1, USF2 and PTPN1
Authors: Tobiasen Heidi , Christensen Lise Lotte , Holm Anja , Schepeler Troels , Thorsen Kasper , Rasmussen Mads H. , Birkenkamp-Demtroeder Karin , Sieber Oliver M. , Gibbs Peter , Lamy Philippe , Laurberg Søren , Øster Bodil , Hansen Kristian Q. , Hagemann-Madsen Rikke , Byskov Kristina , Ørntoft Torben F. , Andersen Claus L. 
Published: August 2012

Abstract
Colorectal cancer (CRC) is one of the leading causes of cancer death in Western countries. A significant number of CRC patients undergoing curative-intented surgery subsequently develop recurrence and die from the disease. MicroRNAs (miRNAs) are aberrantly expressed in cancers and appear to have both diagnostic and prognostic significance. In this study we identified novel miRNAs associated with recurrence of CRC. TaqMan® Human MicroRNA Array Set v2.0 was used to profile the expression of 667 miRNAs in 14 normal colon mucosas and 46 microsatellite stable CRC tumors. Four miRNAs (miR-362-3p, miR-570, miR-148a* and miR-944) were expressed at a lower level in the tumors from patients with recurrence (p &lt; 0.015) compared to tumors from patients with no recurrence. A significant association of low expression with reduced disease free survival was confirmed for miR-362-3p in a second independent cohort of 43 CRC patients using single TaqMan® microRNA assays. In vitro functional analysis showed that over-expression of miR-362-3p in colon cancer cell lines (HCT116, LS174T, and DLD1) reduced cell viability and proliferation mainly due to cell cycle arrest. E2F1, USF2 and PTPN1 were identified as potential miR-362-3p targets by mRNA profiling of HCT116 cells over-expressing miR-362-3p. Subsequently, these genes were confirmed as direct targets by Luciferase reporter assays. In vitro knock-down confirmed that these targets are important players in the miR-362-3p target network. We conclude that miR-362-3p may be a novel prognostic marker in CRC and hypothesize that augmented expression of miR-362-3p may prevent the development of distant metastasis by targeting E2F1, USF2 and PTPN1.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 4138. doi:1538-7445.AM2012-4138
Abstract 4149: Pathway-based serum microRNA profiling and late-stage non-small cell lung cancer survival
Authors: Wang Yan , Lippman Scott M. , Minna John D. , Roth Jack A. , Wu Xifeng 
Published: August 2012

Abstract
Non-small cell lung cancer (NSCLC) is one of the leading causes of cancer mortality in the world. Nearly half of NSCLC patients are diagnosed with late-stage (stage III or stage IV) disease with an overall 5-year survival rate of less than 15%. Deregulation of microRNAs (miRNAs) is involved in cancer development, progression, and prognosis. Circulating miRNAs have been suggested as promising biomarkers for early detection, diagnosis, and prognosis of cancer. This ongoing study is to utilize a pathway-based approach to screen and validate serum miRNA profiles as predictors of survival using a large patient cohort of 348 late-stage NSCLC patients. In the testing set, pre-treatment serum miRNA profiles of four good- (survival time &gt; 24 months) and four poor-survival (survival time &lt; 6 months) patients were compared by Taqman miRNA microarray. 145 highly expressed serum miRNAs were identified from initial screening and 37 of them were mapped onto the 3′UTRs of a panel of 23 genes in TGF-β signaling pathway using computer-assisted miRNA target prediction program. All 37 miRNA candidates were subject to large-scale single-probe quantitative reverse transcriptase polymerase chain reaction (qRT-PCR). The expression level of serum miR-30d, which targets TGFBR2 and was a previously reported serum marker for early-stage lung cancer survival, was significantly higher in the poor-survival group than the good-survival group (P = 0.0208) in our study population of late-stage lung cancer. The level of serum miR-93-3p that targets SMAD7 was significantly higher in the poor-survival group than the good-survival group (P = 9x10−6). The 2-year overall survival rate in patients with high serum miR-93-3p expression was significantly lower than that in those with low expression with an adjusted HR of 1.59 (95% CI, 1.24 - 2.03) (P = 2x10−4). In contrast, serum level of let-7g, that targets SMAD2, TGFBR1 and the activin A receptor family was significantly lower in the poor-survival group than in the good-survival group (P = 7x10−4), and patients with high serum let-7g expression was associated with a significantly better two-year survival (HR=0.48, 95% CI, 0.37 - 0.62, P = 1x10−8). Our results suggest that serum miR-30d, miR-93-3p and let-7g may become valuable biomarkers for survival in late-stage NSCLC patients.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 4149. doi:1538-7445.AM2012-4149
Abstract 415: Human embryonic stem cell-derived endothelial cells as cellular delivery vehicles for targeting therapy of metastatic breast cancer
Authors: Su Weijun , Wang Lina , Zhou Manqian , Tong Lingling , Xiang Rong , Li Zongjin 
Published: August 2012

Abstract
Recent reports revealed that endothelial progenitor cells (EPCs) isolated from bone marrow, cord blood or embryos have been experimentally utilized to deliver therapeutic agents for cancer treatment. Their potential in cancer therapy highlights the need for a consistent and renewable source of endothelial cells for clinical applications. Moreover, one of the most critical issues for ensuring success of endothelial therapy is the development of technologies for non-invasive monitoring of the distribution of transplanted cells and kinetic of tumor progression or regression. We generated human embryonic stem cell-derived endothelial cells (hESC-ECs) from H9 cell line. The hESC-ECs resemble adult endothelial cells HUVEC in endothelial markers and angiogenesis potential. In vitro study revealed the paracrine effects of hESC-ECs on tumor cells using conditioned medium (EC-CM). After treated with EC-CM, human breast cancer cells MDA-MB-231 proliferated slower and exhibited a higher apoptosis rate in low-serum condition, and the migration ability was impaired. Furthermore, we introduced a multitude of non-invasive, quantitative, functional imaging techniques with reporter gene methods to probe breast cancer model processes, and to track the hESC-ECs for targeting therapy in vivo by firefly luciferase (Fluc)/renilla luciferase (Rluc) imaging. We transduced hESC-ECs with triple fusion (TF) reporter gene containing the herpes simplex virus truncated thymidine kinase (HSV-ttk), renilla luciferase (Rluc) and RFP (RL-RFP-HSV-ttk). The NOD/SCID mice breast cancer metastasis model was established by tail vein injection of 1.5×106 MDA-MB-231 cells, which carry a reporter system encoding the gene of Fluc and GFP. Bioluminescence imaging (BLI) revealed that hESC-ECs can be sequenced in tumor sites for more than 72 hours. When given pro-drug ganciclovir (GCV), targeting HSV-ttk gene, the MDA-MB-231 tumor was inhibited by the indication of Fluc imaging. And immunofluorescence staining also confirmed that hESC-EC can exclusively home to tumor lesions instead of normal lung tissue. Taken together, our results revealed that hESC-ECs can specifically target tumor sites and kill nearby tumor cells by bystander effect when GCV is given. These finds suggest that hESC-ECs are attractive targeting vehicles for cancer therapy, and molecular imaging in small animals is an invaluable part of cancer diagnosis, prediction of tumor response to available therapies and monitoring response to therapy as well as developing drugs prior to clinical translation.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 415. doi:1538-7445.AM2012-415
Abstract 4161: Rab25 cooperates with RIN1 to suppress p21 Ras
Authors: Cheng Jiming , Ayyagari Vijayalakshmi , Rao Krishna 
Published: August 2012

Abstract
Introduction: Our previous work has shown that the loss of Rab25 occurs in estrogen receptor (ER) and progesterone receptor (PR) negative breast cancer cell lines and human tumor samples and seems to correlate with an active Ras pathway. Loss of Rab25 cooperates with mutant Ras to promote tumorigenesis. RIN1 is a protein inhibitor of Ras, and our current works confirms that Rab25 binds to RIN1 and cooperates to inhibit Ras. Rab25 also has multiple effects on microRNAs. Materials and Methods: Cell culture -RAO-1-4 cell lines was grown in DFCI-1 medium. Immunoprecipitation- Protein extracts from RAO-1, RAO-2, and RAO-3/Rab25 were tested for RIN1expression. Immunoprecipitated extracts were then assayed by western blot for RAB25 expression. Chemiluminescence Assay- Cell extract from MDA-MB-231 cells with shRIN1 was used. These cells contained no Rab25 as well. Recombinant RIN1 and recombinant Rab25 were tested in various combinations for ras inhibition using the Active Motif kit. MicroRNA assay- RNA was extracted from RAO-2, RAO-4, and RAO-4/Rab25 and sent to Phalanx Biotech for microRNA profiling. Results: 1. Rab25 binds to RIN1 in a ternary complex with Ras. 2. Rab25 coopeates with RIN1 in an additive manner to inhibit Ras. 3. Rab25 expression impacts several microRNAs including 29b, 100, 138, 146a, 205, 524-5p, 762, 1246, 1260b, 1307, 1826, 3172, 3175, and 3178. Conclusions: 1. Rab25 is a tumor modulator. It can regulate tumor growth and angiogenesis through inhibition of ras in cooperation with RIN1. 2. Our data previous indicated that Rab25 could localize to the nucleus, and it appears to effect the expression of several microRNAs.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 4161. doi:1538-7445.AM2012-4161
Abstract 4177: Synergistic role of ecdysoneless with oncogenic Ras in transformation of human mammary epithelial cells
Authors: Bele Aditya , Gurumurthy Channabasavaiah Basavaraju , Zhao Xiangshan , Wang Jun , Mirza Sameer , Mohibi Shakur , Band Hamid , Band Vimla 
Published: August 2012

Abstract
Precisely regulated cell proliferation is essential for embryonic development as well as homeostasis in adult organs and tissues, whereas uncontrolled cell proliferation is a hallmark of cancer. Thus, elucidating how the cell cycle machinery is controlled is an important area of research in cancer cell biology. A large body of evidence has established a basic paradigm of the control of cell cycle progression involving the Retinoblastoma (Rb) protein family in conjunction with the E2F family of transcription factors. During G0/G1, interaction of hypo-phosphorylated Rb proteins with E2Fs prevents the transcription of E2F target genes. Cyclin-CDK complexes generated during cell cycle progression hyper-phosphorylate Rb, leading to release of Rb from E2Fs; this allows E2F target gene transcription and cell cycle progression. We previously identified the mammalian ortholog of Drosophila ecdysoneless (Ecd) protein as a novel and essential regulator of Rb-E2F-dependent cell cycle progression. Loss of Ecd retards the separation of Rb from E2F, arrests cells at G1/S boundary and prevents cell cycle progression. Consistent with role of Ecd in cell cycle, our recent studies show Ecd is overexpressed in breast cancer cell lines as well as in ductal carcinoma in situ and infiltrating ductal carcinomas of the breast. To understand the mechanism of Ecd overexpression and its correlation with oncogenesis, we overexpressed either Ecd alone, 61L-HRas alone or both genes together in hTERT-immortalized hMECs. These transfectants were then examined for their oncogenic properties. We observed while vector infected cells do not exhibit anchorage independence, all three transfectants showed anchorage independent proliferation, particularly Ecd+Ras showed a dramatic increase in anchorage independence in comparison with either Ecd or H-Ras. Similarly, other oncogenic traits such as proliferation on matrigel, invasion and migration were dramatically increased when both genes were expressed in comparison with individual genes. Considering the known oncogenic role of Ras in human cancer and the known role of Ecd in cell cycle, these data are highly significant and present a novel synergistic pathway for mammary cell transformation. We are currently defining the molecular mechanism of this synergistic oncogenic effect. In addition, we are generating Ecd overexpressed transgenic mice to examine the role of Ecd in oncogenesis in in vivo models.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 4177. doi:1538-7445.AM2012-4177
Abstract 4185: Identifying transcriptional start sites of human microRNAs based on high-throughput sequencing data
Authors: Tsou Ann-Ping , Chien Chia-Hung , Chiang-Hsieh Pei-Yun , Tsai Wei-Chih , Huang Hsien-Da 
Published: August 2012

Abstract
MicroRNAs (miRNAs) are critical small non-coding RNAs that regulate gene expression by hybridizing to the 3′-untranslated regions (3′ UTR) of target mRNAs, subsequently controlling diverse biological processes at posttranscriptional level. How miRNA genes are regulated receives considerable attention because it directly affects miRNA-mediated gene regulatory networks. Although numerous prediction models were developed for identifying miRNA promoters or transcriptional start sites (TSSs), most of them lack experimental validation and are inadequate to elucidate relationships between miRNA genes and transcription factors (TFs). Here, we integrate three experimental datasets, including Cap analysis of gene expression (CAGE) tags, TSS Seq libraries, and H3K4me3 chromatin signature derived from high-throughput sequencing analysis of gene initiation, to provide direct evidence of miRNA TSSs, thus establishing an experimental-based resource of human miRNA TSSs, named miRStart. Moreover, a machine learning based Support Vector Machine (SVM) model is developed to systematically identify representative TSSs for each miRNA gene. Finally, to demonstrate the effectiveness of the proposed resource, an important human intergenic miRNA, hsa-miR-122, is selected to experimentally validate putative TSS owing to its high expression in a normal liver. In conclusion, this work successfully identify 847 human miRNA TSSs (292 of them are clustered to 70 TSSs of miRNA clusters) based on the utilization of high-throughput sequencing data from TSS-relevant experiments, and establish a valuable resource for biologists in advanced research in miRNA-mediated regulatory networks.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 4185. doi:1538-7445.AM2012-4185