bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 4660: The National Cancer Human Biobank: CaHUB
Authors: Sawyer Sherilyn J. , Myers Kimberly , Anthony Dickherber , Benkesser Rachel , Fombonne Benjamin , Litwack David , Thomas Mary , Lockhart Nicole , Rogers Joyce , Vaught Jim , Compton Carolyn 
Published: June 2012

Abstract
The Cancer Human Biobank (caHUB) is the first centralized and public biorepository for human biospecimens in the United States. Established by the National Cancer Institute (NCI) Office of Biorepositories and Biospecimen Research (OBBR), caHUB builds upon the foundation of evidence-based biospecimen resource management practices established by the OBBR Biospecimen Research Network (BRN) and the NCI Best Practices for Biospecimen Resources. The mission of the caHUB is to ensure an adequate and continuous supply of high-quality, highly annotated human biospecimens and provide unique biobanking services for the cancer research community. With a goal of fostering collaboration, communication, education, and the public trust, caHUB will be established as a public-private partnership, working with the broader cancer community, including basic and clinical researchers, advocacy organizations, and pharmaceutical and biotechnology companies.
caHUB is a unique centralized biospecimen resource. In response to input from the scientific community, caHUB is focused on providing biospecimens and data collected according to the highest technical and ethical standards, developing biospecimen reference samples that serve as benchmarks for specimen integrity and molecular type, conducting research that supports evidence-based biospecimen best practices, and creating opportunities for collaboration and information exchange across the research enterprise. Through caHUB, the NCI seeks to address the shortage of highly-annotated research biospecimens collected under rigorous standards too costly for private organizations to pursue but required to address difficulties in validation of human biospecimen research results for scientific and regulatory purposes.
caHUB is actively seeking the involvement of the cancer research community and supports engagement through three models of collaboration: 1) as customers seeking access to caHUB‘s Biospecimen Collections and Services; 2) as collaborative research partners who require caHUB to assist with specimen collections and analysis; and 3) as partners interested in information exchange with or financial support of this public initiative. For all interested parties, more information is available at http://cahub.cancer.gov.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 4660. doi:10.1158/1538-7445.AM2011-4660
Abstract 4661: Analysis of DNA adducts: Development of a high-performance analytical platform to meet challenges in human health
Authors: Schmitz Oliver Johannes , Deibel Eduard , Ebersbach Ina 
Published: June 2012

Abstract
The outstanding selectivity and sensitivity of the atmospheric pressure laser ionization (APLI), which is a two-photon ionization process, in combination with a mass spectrometric detection, is demonstrated for the analysis of DNA adducts.
Preparative HPLC with a HILIC-phase and a fraction sampler was used to separate the polar 4-hydroxy-1-(3-pyridyl)-butanone (HPB) and 4-hydroxy-1-(3-pyridyl)-butanol (Diol), which will be formed after acid hydrolysis of the POB- and PHB-DNA adducts. The adducts eluted in the fractions to be analyzed were collected, concentrated to dryness and dissolved in dichloromethane. Then 4-(dimethylamino)pyridine as a base, N,N′-dicyclohexylcarbodiimide as an activator and anthracene-9-yl-methoxyacetic acid as an ionization marker, in analogy to a fluorescence marker, were added, and after several hours at 35 °C the sample was injected into an HPLC-APLI-TOF(MS). With this novel method, only aromatic compounds are ionizable; because the ionization marker of the DNA adducts carries an aromatic group, this allows ionization by the two-photon process.
For the first time we have used a new strategy to analyse DNA adducts by HPLC-APLI-TOF(MS) after derivatization with an ionization marker. To demonstrate the utilizability of this method, we analyzed POB and PHB adducts, which are formed by metabolic activation pathways from 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) and N′-nitrosonornicotine (NNN).
In summary, we have demonstrated that the derivatization strategy significantly increases the analytical applicability of APLI-MS and shows new methods for the important DNA adduct analysis.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 4661. doi:10.1158/1538-7445.AM2011-4661
Abstract 4669: Genetic variations in telomere pathway genes and ovarian cancer risk, survival and treatment response
Authors: Wang Yan , Lu Karen H. , Lin Jie , Huang Maosheng , Wu Xifeng , Liang Dong 
Published: June 2012

Abstract
Telomere dysfunction has been associated with genomic instability and cancer development. Genetic variations in telomere pathway genes may lead to telomere dysfunction and affect cancer risk and outcome. In this retrospective study, we evaluated the associations between common genetic variations in telomere pathway genes and ovarian cancer risk, survival and treatment response in a population of 417 cases and 417 controls. 472 single nucleotide polymorphisms (SNPs) were selected from 42 genes potentially influencing telomere length, telomerase activity, and telomere-associated protein complex. Twenty SNPs were associated with overall ovarian cancer risk at P &lt; 0.01. Two synonymous SNPs from the TEP1 gene, rs938887 and rs2228026, exhibited the strongest association with odds ratios (ORs) of 3.88 (95% CI, 1.42-10.59) and 3.28 (95% CI, 1.72-6.29), respectively. Seven SNPs were associated with overall survival of ovarian cancer at P &lt; 0.01, and five of them presented higher-order gene-gene interactions as suggested by survival tree analysis. Survival tree analysis categorized patients into low, medium and high risk groups with progressively decreased medium survival time based on distinct genotype combinations. In the analysis of response to chemotherapy, 15 SNPs reached a significance level of P ≤ 0.01. SNP rs7826180 in the intronic region of PINX1 gene was shown to substantially increase the risk of poor response with an OR of 6.77 (95% CI, 1.68-27.27). There were significant gene-dosage effects as evidenced by the increased risk of cancer, risk of death, and risk of poor response with the increasing number of unfavorable genotypes. Our results suggest that common genetic variations in telomere pathway genes are significantly associated with ovarian cancer risk, survival, and treatment response. With further validation, these results may contribute to improve personalized risk assessment, prognosis, and treatment of ovarian cancer.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 4669. doi:10.1158/1538-7445.AM2011-4669
Abstract 4676: Survival of gastric cancer differs by ethnicity: A population-based experience from British Columbia, Canada
Authors: Bashash Morteza , Hislop T Greg , Shah Amil , Le Nhu , Brooks-Wilson Angela , Bajdik Chris 
Published: June 2012

Abstract
Introduction: Prognostic factors can be classified into three broad groups: i) tumor-related, ii) host-related, and iii) environment-related (health care, treatment, lifestyle) factors. The current study was conducted to examine the effect of ethnicity as a host-related factor for survival of gastric cancer patients in British Columbia, Canada.
Methods: Data were obtained from the population-based BC Cancer Registry for patients diagnosed with invasive gastric cancer between 1984 and 2006. The ethnicity of patients was estimated according to their names and categorized as Chinese, South Asian, Iranian or Other (more than 80% of “Other” are British and Western Europeans). Cox proportional hazards regression analysis was used to estimate the effect of ethnicity adjusted for patient sex and age, disease histology, tumor location, disease stage and treatment.
Results: Results from this study indicate significantly different survival of gastric cancer patients depending on their ethnic group (p&lt;0.01). When considered separately according to the presence or absence of metastatic disease, significant differences were only found for non-metastatic disease (p&lt;0.01). Furthermore, the association between survival and ethnicity was only significant for patients with non-metastatic disease who received therapeutic surgery (p&lt;0.01). In multivariate analyses adjusting for patient factors, disease factors and treatment, there was a significant difference among ethnic groups. Only Chinese had significantly longer survival compared to the Other ethnicities, but this survival advantage was only seen for non-metastatic disease (HR=0.78, 95% CI=0.64-0.95).
Conclusion: The difference observed in patient survival is not likely to be due to healthcare disparities among minority groups, as all BC residents are covered for healthcare through the BC Medical Services Plan (MSP). Ethnicity may represent underlying genetic factors. Such factors could influence host-tumor interactions by altering the tumor's etiology and therefore its chance of spreading. Alternatively, genetic factors may determine response to treatments. Finally, ethnicity may represent non-genetic factors that affect survival. Differences in survival support the importance of ethnicity as a prognostic factor, and may provide clues for the future identification of genetic or lifestyle factors that underlie these observations.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 4676. doi:10.1158/1538-7445.AM2011-4676
Abstract 4678: Post-diagnosis use of lipophilic statins and breast cancer recurrence: A Danish nationwide cohort study
Authors: Ahern Thomas P. , Pedersen Lars , Cronin-Fenton Deirdre P. , Tarp Maja , Silliman Rebecca A. , Sørensen Henrik Toft , Lash Timothy L. 
Published: June 2012

Abstract
Statins may affect non-cardiovascular endpoints, including cancer incidence and survival. These effects may depend on the solubility of the specific medicine. Our objective was to measure the association between post-diagnosis lipophilic and hydrophilic statin use and recurrence among non-metastatic breast cancer patients.
We ascertained incident cases of stage I-III invasive breast cancer diagnosed in Denmark between 1996 and 2006 from the Danish Breast Cancer Cooperative Group registry, and linked these records to the Register of Medicinal Products (RMP), which automatically logs pharmacy transactions in Denmark. We determined statin prescriptions filled by cohort members by searching the RMP for appropriate ATC codes. Statins were classified by solubility (Table 1) and exposure status was updated yearly. Follow-up began upon completion of primary therapy and continued until the first of breast cancer recurrence, death from any cause, emigration from Denmark, or the end of 2006. Associations were estimated with time-dependent crude and multivariate Cox regression models.
We enrolled 18,769 breast cancer patients, with a median follow-up of 6.2 years. Of the 3,282 women ever prescribed a statin after diagnosis, 2,518 were exclusively prescribed lipophilic statins and 210 were exclusively prescribed hydrophilic statins.
Crude and multivariate models yielded similar estimates. Lipophilic (but not hydrophilic) statin use was associated with a reduced rate of breast cancer recurrence (compared with no statin use: multivariate HR for lipophilic statin use = 0.65, 95% CI: 0.55, 0.76; multivariate HR for hydrophilic statin use = 0.89, 95% CI: 0.61, 1.3). Associations were similar when estimated in the subset of women with no pre-diagnosis statin exposure.
In this population-based prospective cohort study with complete information on prognostic and treatment variables, breast cancer patients who took lipophilic statins had a reduced rate of breast cancer recurrence.

(a) Hazard ratios adjusted for age, menopausal status, tumor stage, ER status, adjuvant hormonal therapy, type of surgery, comorbidity, and co-prescription of aspirin. Estimates were similar in models further adjusted for chemotherapy, type of surgery, receipt of radiotherapy, and co-prescription of hormone replacement therapy, NSAIDs, anticoagulants and ACE inhibitors.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 4678. doi:10.1158/1538-7445.AM2011-4678
Abstract 4679: A multi-stage genome-wide association study on response to chemotherapy in ovarian cancer
Authors: MacGregor Stuart , Lu Yi , Johnatty Sharon , Beesley Jonathan , Chen Xiao Qing , Fridley Brooke , Webb Penny , Gurney Howard , Harnett Paul , Haber Michelle , Goode Ellen , De Fazio Anna , Chenevix-Trench Georgia 
Published: June 2012

Abstract
We performed a multi-stage genome-wide association study (GWAS) for drug response in ovarian cancer. We selected 313 chemotherapy treated patients from the Australian Ovarian Cancer Study (AOCS). Patients were treated with paclitaxel/carboplatin and the trait of interest was Progression Free Survival (PFS). We maximized power for a fixed genotyping budget by genotyping individuals from the tails of the distribution: 94 with good survival and 94 with poor survival, taking into account extent of residual disease following surgery. Patients were genotyped on Illumina HumanOmni1-Quad arrays (1140419 loci).Two further cohorts with measures of PFS and whole genome data available; 134 ovarian patients from the Mayo clinic (genotyped on Illumina HumanHap 610 arrays, 620901 loci) and 68 patients from The Cancer Genome Atlas ovarian cancer set (genotyped on Illumina Human1M arrays, 1199187 loci) were meta-analyzed with the AOCS set (stage 1).
We have imputed all the stage 1 samples with reference of the 1000 Genome data to allow more direct comparison of SNPs not common to all of the arrays used (up to 6 million SNPs with good imputation quality).
Based on the chemotherapy treatment received by each patient, we assigned the patients into primary and secondary analysis, with primary analysis using a more strictly defined treatment subgroup.
We followed up the stage 1 findings by genotyping 26 SNPs in more than 3,000 samples collected from 8 study sites of Ovarian Cancer Association Consortium (OCAC). These 26 SNPs were mainly genotyped SNPs, chosen from 23 distinct regions showing the strongest association with chemotherapy response from either primary or secondary analysis. 2 SNPs showed nominal significance in the replication sample (chr 12: rs1861932, chr 22: rs708444). We are currently genotyping more regions to seek replication of the initial findings.
In summary, we sought to identify genes that underlie individual differences in chemoresistance. In the future, typing variations in these genes will be important for personalizing drug regimes for patients.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 4679. doi:10.1158/1538-7445.AM2011-4679
Abstract 4684: Vitamin D may impair glucocorticoid cytotoxicity in acute lymphoblastic leukemia cells
Authors: Antony Reuben , Sheng Xia , Pramanik Rocky , Ehsanipour Ehsan A. , Klemm Lars , Ichihara Brian , Ng Pik Lam , Mittelman Steven D. 
Published: June 2012

Abstract
Vitamin D deficiency has been associated with increased incidence and mortality in several types of cancer. Vitamin D has been shown to be cytotoxic to cancer cells in vitro, and may act synergistically with chemotherapy to kill cancer cells. Although vitamin D deficiency is common in children with cancer, the clinical implications of this remain unclear. Since acute lymphoblastic leukemia (ALL) is the most common type of cancer in children and relapsed leukemia remains a major problem, the present study was designed to test our hypothesis that active Vitamin D (Calcitriol) would induce apoptosis in ALL cells and potentiate the effect of chemotherapy on ALL cells.
We cultured several human ALL cell lines and primary human ALL cells with and without Calcitriol, and quantified survival using trypan blue exclusion. Contrary to our hypothesis, Calcitriol did not negatively affect the viability or impair proliferation in the human ALL cell lines RS4; 11, SD1, BV173, or RCH-ACV, or in primary human ALL cells US7 or TXL 2. We then tested whether Calcitriol would synergize with dexamethasone, a glucocorticoid used almost universally in the treatment of childhood ALL. Again, contrary to our hypothesis, we found that rather than augment dexamethasone-induced cytotoxicity, supraphysiological doses of Calcitriol protected RS4;11 cells from the cytotoxic effect of 72 hour exposure to 100 nM dexamethasone (dexamethasone alone: 10±5% of initially plated cells viable; dexamethasone plus 300 nM Calcitriol: 27±14% of initially plated cells viable, n=4, p=0.04). More physiological doses of Calcitriol (10nM) showed similar protection (12.5±5% vs 31.5±19% of initially plated cells were viable at 72 hrs, n=4, p=0.05). Preliminary flow cytometry using Annexin/7AAD suggests that Calcitriol decreases dexamethasone-induced apoptosis in RS4;11 cells (dexamethasone alone: 94% of cells in apoptosis; dexamethasone plus 100 nM Calcitriol: 75% of cells in apoptosis, n=1)
In summary, the active form of vitamin D appears to protect ALL cells from dexamethasone. This finding could be important, since glucocorticoid sensitivity of ALL cells is highly predictive of outcome and likelihood of relapse. Our findings could have major health implications given the high prevalence of Vitamin D deficiency in children and adolescents worldwide.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 4684. doi:10.1158/1538-7445.AM2011-4684
Abstract 4687: Novel functions of the AMPK pathway to maintain spindle orientation during mitosis
Authors: Thaiparambil Jose T. , Marcus Adam I. 
Published: June 2012

Abstract
AMP activated protein kinase (AMPK) functions as an energy sensor that regulates cell signaling. It is phosphorylated by the tumor suppressor, LKB1 at times of energy stress in both the cell polarity and motility pathways. Here we show that phosphorylated AMPKα (Thr-172) localizes to the spindle poles at gamma tubulin sites during mitosis in an LKB1-independent manner and serves as an essential regulator of mitotic spindle orientation. Phosphorylated AMPK levels peak during mitosis and siRNA-based disruption AMPK-α1& α2 function, results in spindles that are mis-oriented relative to the normal spindle axis. This phenotype is accompanied by an aberrant, double-ring actin cage that encompasses the microtubule spindle, as well as reduced astral microtubules. Similar results were obtained by live cell imaging using compound C (AMPK pharmacological inhibitor) treated cells. Molecular studies show that AMPK regulates spindle orientation through a PI3k-AKT pathway at the spindle poles that signals to myosin regulatory light chain (MRLC). We postulate that AMPK is regulating astral microtubule docking onto actin through this pathway and when compromised spindles become misaligned. Taken together, this study reveals a novel PI3K-AKT-p-AMPK-MRLC mitotic signaling axis that regulates spindle orientation during mitosis.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 4687. doi:10.1158/1538-7445.AM2011-4687
Abstract 4688: Met receptor tyrosine kinase cross-talk in tumorigenesis
Authors: Lai Andrea , Park Morag 
Published: June 2012

Abstract
The Met receptor tyrosine kinase (RTK) is a cell surface, transmembrane protein that is activated in response to the growth factor Hepatocyte Growth Factor (HGF) and initiates multiple downstream signaling pathways that predominantly promote cell migration and invasive cell growth. These processes are essential for Met-dependent signals during development. Dysregulated signaling of Met has been characterized in cancers, and include mechanisms such as point mutations, gene amplification, overexpression, and loss of negative regulation and more recently evidence of Met cross talk with other RTKs has been established. However, the role of Met cross-talk with other cell surface receptors in tumorigenesis, is still poorly understood.
Recent studies in non-small cell lung cancer cell lines have established that amplification of MET contributes to acquired resistance to the EGFR inhibitor gefitinib through phosphorylation of HER3, a member of the EGF receptor family of RTKs. As HER3 phosphorylation was demonstrated to occur under conditions of MET amplification, we have investigated whether HER3 phosphorylation and signaling is a common event in other cell lines where MET is amplified. In gastric cancer cell lines with MET amplification where Met is overexpressed and constitutively active, HER3 is phosphorylated. Met and HER3 are also found in a complex, as established through co-immunoprecipitation. Interestingly, upon treatment with a small molecule kinase inhibitor targeting Met, HER3 phosphorylation and association between the two receptors decreases. Thus, in cells that express high levels of constitutively active Met, cross-talk with other receptors, such as HER3, may be another mechanism through which Met promotes tumorigenesis. The interaction of Met with HER3 will be addressed at the mechanistic level and these data will be presented.
Kinase inhibitors that target single RTKs have proven susceptible to resistance. Inhibition of one RTK often results in upregulation of signaling through another receptor, and in this way, re-establish pathways essential for tumorigenesis. Determining how and under what conditions RTKs cross-talk with one another may allow identification of potential resistance mechanisms, as well as other targets for multi-targeted therapies.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 4688. doi:10.1158/1538-7445.AM2011-4688