bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 4681: Urothelial gene expression signatures aid bladder cancer detection
Authors: Rosser Charles , Sun Yijun , Urquidi Virginia , Goodison Steve 
Published: February 2011

Abstract
Bladder cancer is the fifth most commonly diagnosed malignancy in the United States and one of the most prevalent worldwide. It harbors a probability of recurrence of &gt;50%, thus rigorous, long-term surveillance of patients is advocated, so improvements in non-invasive urinalysis assessment strategies would benefit patients. We applied gene expression microarray analysis to exfoliated urothelia recovered from bladder washes obtained prospectively from 102 patients with subsequently confirmed presence or absence of bladder cancer. Data from microarrays containing 56,000 targets was subjected to a panel of statistical analyses to identify bladder cancer-associated gene signatures. Hierarchical clustering and supervised learning algorithms were used to classify samples on the basis of tumor burden. A differentially expressed set of 323 gene probes was associated with the presence of bladder cancer (P&lt;0.01). Supervised machine learning and a cross-validation approach were used to build a 55-gene molecular classifier that was able to classify patients with and without bladder cancer with an overall accuracy of &gt;75%. Our results show that it is possible to achieve the detection of bladder cancer using molecular signatures present in exfoliated tumor urothelia. Further investigation and validation of the cancer-associated profiles may reveal important biomarkers for the non-invasive detection and surveillance of bladder cancer.
Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 4681.
Abstract 470: The homing of prostate cancer to bone in vivo is modulated by Zoledronic acid
Authors: Reeves Kim J. , van der Pluijm Gabri , Cecchini Marco G. , Eaton Colby L. , Hamdy Freddie C. , Brown Nicola J. 
Published: February 2011

Abstract
Cancer metastasis to the skeleton is a major problem with prostate cancer and requires the development of specialised approaches to treatment. Zoledronic acid, a bone resorptive agent, is currently the only bisphosphonate with proven benefit in prostate cancer. However, there is minimal research investigating whether Zoledronic acid modulates the early mechanisms involved in metastasis. The aim of this study is to determine whether different treatment regimes using Zoledronic acid modulate the early events in tumour/bone interactions.
Metatarsals from newborn mice (1-3 day old) are engrafted into a Dorsal Skinfold Chamber (DSC) implanted on a SCID mouse (5-6 weeks old). Prostate (PC3-GFP) cancer cells (1 × 105) are then injected via the heart (i.c) to simulate micrometastatic spread (n=20/group). Animals are treated with either i) weekly s.c injection of Zoledronic acid (25µg/kg/inection=100μg/kg in total) or saline or ii) single s.c injection of Zoledronic acid (100μg/kg) or saline for the 4 week study duration. The groups are further subdivided, so half of the animals receive treatment either before or after injection of tumour cells. Recordings of the chamber tissue and metatarsal are made at 48hr intervals for the duration of the experiment for the presence of PC3-GFP cells within the metatarsal. At the end of the study, tissue is harvested and processed for microCT, multi-photon analysis and histology.TreatmentNumber of PC3-GFP cells homing to metatarsalDay 3Day 9Day 15 Weekly treatment before PC3-GFP cells1.1 ± 0.1*1.3 ± 0.2*2.1 ± 0.3*Weekly treatment after PC3-GFP cells3.2 ± 0.5*3.4 ± 0.8*4.4 ± 0.7*Single treatment before PC3-GFP cells1.7 ± 0.3*8.9 ± 0.9*13.6 ± 0.8Control3.2 ± 0.714.7 ± 1.015.9 ± 1.4
Table 1. Number of PC3-GFP cells present in metatarsal after i.c. injection (*p&lt;0.05 compared to control).
Treatment with Zoledronic acid reduces tumour cell homing to bone. Weekly treatment of Zoledronic acid prior to prostate cancer cell administration reduces homing to bone to a greater extent than the other treatment regimes test.
Funded by Sixth European Framework Programme (PROMET).
Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 470.
Abstract 4700: Acrolein-deoxyguanosine DNA adduct formation and lung cancer
Authors: Hu Yu , Rom William , Pass Harvey I. , Spivack Simon D , Tang Moon-shong 
Published: February 2011

Abstract
Cigarette smoke (CS) contains 1,000-10,000 fold more acrolein (Acr) and crotonaldehyde (Crot) than polycyclic aromatic hydrocarbons (PAHs). These aldehydes can induce propanoldeoxyguanosine (propanol-dG) DNA adducts formation in cultured normal human lung epithelial cells. Previously, we have found that the distribution of Acr-dG in the p53 gene coincides with the lung cancer p53 mutational spectrum of cigarette smokers, and that Acr-dG induces similar level of G to T transversion and G to A transition mutations as in lung cancer of cigarette smokers. Hence, we have proposed that Acr is a major etiological agent of CS related lung cancer. We developed a 32P-postlabelling method in combination with 2D TLC/HPLC method to quantify propanol-dG formation in human lung tissue. To date we have determined Acr-dG and Crot-dG in the lung tissue of cigarette smokers (n=27) and nonsmokers (n=25) with lung cancer. We found that 1) both α- and γ-Acr-dG are formed in lung tissues of smokers and nonsmokers, and the level of these two types of adduct in lung tissue varies from 10-4,510, and 0-1,900 fmole/μmole, respectively; and 2) smokers appear to have a higher level of γ-Acr-dG than nonsmokers although the differences have not reached statistical significance (p=0.1854); 3) the level of Crot-dG in smokers is significant higher than that in nonsmokers (p=0.0279). These results indicate a substantial amount of Acr-dG and Crot-dG formed in lung tissue of lung cancer.
Key words: α, β-unsaturated aldehydes, cigarette smoking, DNA adducts, lung cancer.
Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 4700.
Abstract 4707: Clonal expansions as a biomarker of preneoplastic processes in ulcerative colitis
Authors: Salk Jesse J. , Salipante Stephen J. , Risques Rosa Ana , Crispin David A. , Li Lin , Bronner Mary P. , Rabinovitch Peter S. , Horwitz Marshall S. , Loeb Lawerence A. , Brentnall Teresa A. 
Published: February 2011

Abstract
Chronic inflammation predisposes to a variety of human cancers. Affected tissues slowly accumulate mutations, some of which affect growth regulation and drive successive waves of clonal evolution whereas a far greater number are functionally neutral and serve only to passively mark expanding clones. Ulcerative colitis (UC) is an inflammatory bowel disease in which up to 10% of patients eventually develop colon cancer. We have recently reported on mapping of mutations in non-coding polyguanine tracts in patients with UC to delineate the extent of clonal expansions associated with carcinogenesis. We genotyped colon biopsies for length altering mutations at 28 different polyguanine markers. In eight UC patients without neoplasia, blinded genotyping detected only two mutations in a single individual from among 37 total biopsies. In contrast, in eleven UC patients with neoplasia elsewhere in the colon, blinded genotyping identified 63 mutations in 51 nondysplastic biopsies, and every patient possessed at least one mutant clone. As a biomarker of cancer progression the presence of one or more clones was 100% sensitive and 88% specific. A subset of clones were large and extended over many square centimeters of colon. Of these, some occurred as isolated populations in non-dysplastic tissue, considerably distant from neoplastic lesions. Other large clones included regions of cancer, suggesting that the tumor arose within a pre-existing clonal field. This preliminary work indicated that neutral mutations in polyguanine tracts serve as a powerful tool for identifying clonally expanded populations, and suggested that these clones may be clinically useful for distinguishing a subset of UC patients who are at greatest risk for developing cancer. Here we provide updated results of a new and larger case-control study and discuss ongoing efforts to streamline clone detection using other types of neutral genetic markers and next-generation sequencing.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 4707.
Abstract 4712: Characterization of estrogen quinone-derived protein adducts and their identification in human serum albumin
Authors: Lin Po-Hsiung , Wang Tzu-Wen , Wei Tzu-Han , Yang Tsung-Chou , Chen Dar-Ren 
Published: February 2011

Abstract
Both estrogen-2,3-quinone (E2-2,3-Q) and estrogen-3,4-quinone (E2-3,4-Q) are reactive metabolites of estrogen that are thought to be responsible for the estrogen-induced genotoxicity. The aim of this study was to establish a methodology to analyze estrogen quinone-derived protein adducts and to measure the background levels of these adducts in human serum albumin (Alb) derived from female blood donors in Taiwan. The methodology, which employs trifluoroacetic acid anhydride and methanesulfonic acid to selectively cleave cysteinyl adducts, had previously been applied to measure naphthalene adducts in blood proteins. Results from in vitro experiments confirmed that the production of estrogen quinone-derived adducts on serum albumin increased with increased concentration of estrogen quinones (0-100 nM). The average formation of estrogen quinone-derived cysteinyl adducts per unit concentration of estrogen quinones was estimated to be 13.0, 48.2, and 36.1 (pmol/g Alb)/(nM) for E2-2,3-Q-1-S-Alb, E2-2,3-Q-4-S-Alb, and E2-3,4-Q-2-S-Alb, respectively. Time-course experiments indicated that both E2-2,3-Q- and E2-3,4-Q-derived adducts rapidly reached maximum values at 10 min mark and remained constant thereafter. Additionally, with 2,3,7,8-tetrachlorodibenzo-p-dioxin pretreatment (10 nM for 72 h), production of estrogen quinone-derived protein adducts was also detected in human MCF-7 breast cancer cells exposed to estrogen (1 μM for 9 h). Co-treatment of Ro 41-0960, a catechol-o-methyl transferase inhibitor, further enhanced the production of estrogen quinone-derived adducts in all cases. When we investigated the levels of estrogen quinone-derived adducts in human serum Alb derived from female blood donors in Taiwan, cysteinyl adducts of E2-2,3-Q-4-S-Alb and E2-3,4-Q-2-S-Alb were detected in all subjects (n=10). The median levels of E2-2,3-Q-4-S-Alb and E2-3,4-Q-2-S-Alb in human subjects were estimated to be 398 (range 240-807) and 39.0 (range 0.3-101) (pmol/g), respectively. We noticed that levels of E2-2,3-Q-4-S-Alb were significantly correlated with those of E2-3,4-Q-2-S-Alb (correlation coefficient r = 0.684, p&lt;0.05). (This work was supported by the National Science Council, Taiwan, through grants NSC95-2314-B-005-001, and NSC97-2314-B-005-001).
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 4712.
Abstract 4715: Genetic susceptibility to radiation-associated colon and rectum cancers among atomic-bomb survivors with special reference to the CD14 gene
Authors: Hayashi Tomonori , Morishita Yukari , Nagamura Hiroko , Maki Mayumi , Kusunoki Yoichiro , Yoshida Kengo , Imai Kazue , Cologne John B. , Nakachi Kei 
Published: February 2011

Abstract
Past epidemiology studies reported that atomic-bomb (A-bomb) radiation exposure enhanced risk of colon cancer, but not rectum cancer, among the survivors. The reason for this different sensitivity to radiation remains to be elucidated. Colorectal cancer is a multi-factorial disease, the onset of which is attributed to both environmental and genetic factors, with animal experiments showing that intestinal bacterial toxins accelerate carcinogenesis. It was recently reported that single nucleotide polymorphisms (SNPs) identified in the promoter region of CD14, encoding a receptor for the lipopolysaccharide component of the outer membrane of Gram-negative bacteria, regulate CD14 gene expression and thereby affect susceptibility to inflammatory diseases such as atopic dermatitis, coronary artery disease, and hepatic diseases. This study investigated relationship between a novel CD14 gene polymorphism and the development of radiation-associated colon and rectum cancers among an A-bomb survivor cohort, in terms of a case-cohort study. On the basis of this T/G polymorphism, we determined CD14 genotypes with 210 colorectal cancer cases and with a subcohort of 2,160 individuals who were randomly selected from the cohort. Our results showed that the individuals exposed to A-bomb radiation (≥5 mGy) were at an increased risk of colon cancer, but not rectum cancer, with relative risk (RR) of 1.19/Gy (95%CI: 1.04-1.36). When we divided the study subjects into three groups for radiation dose and into two groups for CD14 genotypes, significantly high risk of colon cancer was found with RR of 2.40 (95%CI: 1.37-4.23) for the combined category of CD14-T/T homozygote and the highest dose (≥0.7Gy), compared with the baseline category (CD14-T/G or G/G and no dose). These results suggest that CD14-related inflammatory response might be involved in the development of radiation-associated colon cancer, not rectum cancer, among A-bomb survivors, and that the CD14 genotyping might be involved in individual risk of colon cancer together with radiation dose. To find a functional significance of this polymorphism, we are currently working on ELISA-based assay to measure serum levels of soluble CD14 among healthy individuals in relation to the CD14 genotyping.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 4715.
Abstract 4718: Inherited variants in relapse-associated genes and risk of ovarian cancer
Authors: Peedicayil Abraham , Vierkant Robert A. , Hartmann Lynn C. , Fridley Brooke L. , Fredericksen Zachary S. , White Kristin L. , Elliott Elaine A. , Phelan Catherine M. , Tsai Ya-Yu , Berchuck Andrew , Iversen Edwin S. , Couch Fergus J. , Peethambaram Prema P. , Larson Melissa C. , Kalli Kimberly R. , Kosel Matthew L. , Shridhar Vijayalakshmi , Rider David N. , Liebow Mark , Cunningham Julie M. , Schildkraut Joellen M. , Sellers Thomas A. , Goode Ellen L. 
Published: February 2011

Abstract
Background: We previously identified a panel of genes associated with outcome of ovarian cancer. The purpose of the current study was to assess whether variants in these genes correlated with ovarian cancer risk.
Methods and Findings: Women with and without invasive ovarian cancer (749 cases, 1,041 controls) were genotyped at 136 single nucleotide polymorphisms (SNPs) within 13 candidate genes. Risk was estimated for each SNP and for overall variation within each gene.
At the gene-level, variation within MSL1 (male-specific lethal-1 homolog) was associated with risk of serous cancer (p=0.03); haplotypes within PRPF31 (PRP31 pre-mRNA processing factor 31 homolog) were associated with risk of invasive disease (p=0.03). MSL1 rs7211770 was associated with decreased risk of serous disease (OR 0.81, 95% CI 0.66-0.98; p=0.03). SNPs in MFSD7, BTN3A3, ZNF200, PTPRS, and CCND1A were inversely associated with risk (p&lt;0.05), and there was increased risk at HEXIM1 rs1053578 (p=0.04, OR 1.40, 95% CI 1.02-1.91).
Conclusions: Tumor studies can reveal novel genes worthy of follow-up for cancer susceptibility. Here, we found that inherited markers in the gene encoding MSL1, part of a complex that modifies the histone H4, may decrease risk of invasive serous ovarian cancer.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 4718.
Abstract 472: Murine models mimicking different colorectal cancer liver metastasis phenotypes
Authors: Garcia-Albeniz Xabier , Nadal Cristina , Gomis Roger 
Published: February 2011

Abstract
Introduction
Mechanisms responsible of liver metastasis (LiM) in colorectal cancer (CRC) are largely unknown. Efficient and reliable in vivo and in vitro experimental approaches mimicking clinical scenarios to identify genes responsible of LiM in CRC should be the first step to identify effective targets with clinical relevance. The objective was to develop an animal model of CRC LiM
Experimental procedures
The following human CRC cell lines Colo 205, SW480, SW620, KM12C and KM12L4A and the murine cell line Colo 26 were selected to test the feasibility of the metastatic in vivo model. Each cell line was GTP/luciferase-labelled and injected in a cohort of 6 female balb-c nude mice (Charles River). Two million cells where injected via intrasplenic injection, and splenectomy was performed one minute thereafter. Mice were followed with a Xenogen IVIS system. LiM were disgregated, cells were selected by cell sorting and re-injected with the aim of enriching their metastatic phenotype. .
Results
The cell lines Colo 205 and SW480 did not give rise to any liver metastasis. The rest of the cell lines tested produced liver metastasis with very different patterns. After injection of Colo26, there was not any signal clearance in the liver, followed by a massive infiltration in less than 5 days in every mice. SW620, KM12C and KM12L4A injection was followed by a clearance of the signal in the liver area and recovering of the signal occurred when metastasis developed. SW620 produced metastasis in 40% of the mice after 60 days of follow up. The pattern of metastasis of SW620 was as single spots, recapitulating a very frequent phenotype in patients. KM12C and KM12L4A produced multiple spots in 50% of the mice after 35 days of follow up. Disgregation and re-injection of SW620, KM12C and KM12L4A metastatic cells resulted into an enriched metastatic phenotype, with higher number of metastasis, shorter time to metastasis development and higher percentage of mice developing metastasis.
Conclusion
We provide different animal models that mimic different clinical scenarios. Enrichment of metastatic phenotype is feasible by re-injecting metastatic cells.
Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 472.
Abstract 4720: Genome-wide copy number variation and breast cancer risk: Preliminary report
Authors: Lee Kyoung-Mu , Park Miey , Moon Sang-Hoon , Kim Hyung-Chol , Lee Ji-Young , Li Lian , Park Sue K. , Han Wonshik , Noh Dong-Young , Yoo Keun-Young , Ahn Sei-Hyun , Han Bokki , Kang Daehee 
Published: February 2011

Abstract
Background: DNA copy number variation (CNV) is a common phenomenon in human genome and some CNVs have been associated with susceptibility or resistance to disease. It has been suggested that gene copy number can be elevated in cancer cells. To evaluate potential role of CNV in breast cancer development, we conducted genome-wide association study of CNV in Seoul Breast Cancer Study.
Methods: Cases were diagnosed with breast cancer and underwent curative surgery at two teaching hospitals located in Seoul, Korea, between 2001 and 2007 (n=2,386). Control subjects were selected from multi-center based cohort study in 2007 (n=2,386). The Affymetrix SNP assay 6.0 array, which includes 946,000 probes for the detection of copy number variation, was used. Nexus Copy Number version 4.1 was used for detecting CNVs (significance threshold=10−6; minimum number of probes per segment=4), and statistical analysis. After quality control step (i.e., robust variance sample QC), total 2,315 cases and 2,039 controls were compared for the difference of each CNV. In this study, we selected the CNVs that were different between cases and controls by at least 5% (P adjusted for multiple comparison &lt;0.01). Adjacent CNVs were grouped into CNV regions ranging 10 kb to 300 kb.
Results: Between case and controls, thirteen CNV regions including chr115q11.2, chr3q26.1, chr6q16.3, chr17q31.1 were significantly different for copy number. We note that those regions include genes such as UGT2B17 (UDP glucuronosyltransferase 2 family, polypeptide B18), OR4C11 (olfactory receptor, family 4, subfamily C, member 11), LRRC37A2 (leucine rich repeat containing 37, member A2), ARL17P1 (ADP-ribosylation factor-like 17 pseudogene 1), LOC644974, and the others. We are planning validation study for the regions by quantitative PCR to verify the association with breast cancer risk found in this study.
Conclusion: Our results suggest that common CNVs may be associated with breast cancer in Korean women. However, further variation study is essential to support our observation and underlying biological mechanisms for the associations needs to be elucidated.
Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 4720.