bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract LB-276: Effect of lay health worker intervention on complinace of hepatitis B vaccinations in Asian Americans: Randomizd control trial
Authors: Juon Hee-Soon , Kim Frederic , Strong Carol , Park Eunmi 
Published: August 2015

Abstract
Background/Context: Asian Americans are at high risk with contracting the Hepatitis B virus (HBV). There are preventive measures with vaccinations that could be administered. However, there are several barriers that preclude Asian Americans from receiving the proper care.
Purpose: To implement lay health worker (LHW) telephone intervention using randomized control trial.
Setting: Asian American community-based organizations in the Baltimore-Washington Metropolitan area from April 2013 to March 2014.
Participants: 232 Asian American adults who were unprotected and 18 years of age or older.
Intervention: Calling those in the intervention group to remind to receive a 3-shot series for HBV vaccinations at month 1, 2, and 5.
Data collection/analysis: In a parent study, 600 Asian Americans participated in study by completing pretest, reading photo novel, and doing free Hepatitis B screening. A week later, participants received the results (i.e., protected, unprotected, and infected). In this study, those unprotected was assigned to either intervention or control group. The intervention group received the LHW intervention. Seven months after the pretest, those unprotected (n = 187) were followed by phone. The outcome measure was whether they had received a series of vaccines over 6 months with 3 groups (none, 1 or 2 vaccines, and completed). Multinomial logistic regressions were used.
Results: We found that those in the intervention group were more likely to have 1 or more vaccines than the control group, compared to no vaccination group (OR = 3.04, 95% CI, 1.16, 8.00). Also, those in the intervention group were more likely to complete a series of vaccinations than the control group, compared to no vaccination group (OR = 7.29, 95% CI 3.39, 5.67). We also found that time is the most important barriers preventing them from seeking hepatitis B vaccinations.
Conclusion: The LHW intervention was successful in increasing the chances to protect them from HBV infection in high risk group of Asian Americans. This study suggests that it is very critical to implement this culturally integrated LHW intervention program to reduce liver cancer health disparities among Asian Americans.
Mulitivariate mulitinomial logistic regression model for having hepatitis B vaccinations (n = 187)None vs. 1or 2 vaccinesNone vs completedOR (95% CI)OR (95% CI)Control1.001.00Intervention3.04 (1.16, 8.00)7.29 (3.39, 5.67)
Citation Format: Hee-Soon Juon, Frederic Kim, Carol Strong, Eunmi Park. Effect of lay health worker intervention on complinace of hepatitis B vaccinations in Asian Americans: Randomizd control trial. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr LB-276. doi:10.1158/1538-7445.AM2015-LB-276
Abstract LB-279: Quantitative flux measurements of serum protein catabolism in PDAC and other KRAS-mutant cancers
Authors: Nofal Michel , Zhang Kevin , Rabinowitz Josh 
Published: August 2015

Abstract
Activating KRAS mutations are prevalent in human cancer and are associated with poor prognosis. Among these malignancies is pancreatic ductal adenocarcinoma (PDAC), which is universally KRAS-driven and almost universally lethal. PDAC tumors are extremely fibrotic and hypovascularized, limiting perfusion of nutrients into the tumor, and tumor cells exhibit an altered metabolic program to support survival and proliferation in this environment. One metabolic activity upregulated in these tumor cells is the uptake and catabolism of serum protein. This process yields a substantial alternative source of amino acids and can support the proliferation of cultured cells lacking free essential amino acids. However, existing methods for assaying the uptake and degradation of intact protein provide qualitative outputs, and as such, do not yield accurate estimates of flux from serum protein to amino acid monomers. Here, we present a method for quantitative measurement of the catabolic production of amino acids from serum protein in cultured cells. By culturing cells in medium containing fully 13C-labeled glucose and amino acids supplemented with unlabeled albumin, we distinguish amino acids taken up as monomers from the medium from serum protein-derived amino acids. Using a variant of classical metabolic flux analysis, we derive flux estimates for serum protein catabolism from measurements of amino acid abundance and isotopic labeling over time. Our method is highly sensitive (i.e. can estimate “baseline” serum protein catabolism in KRAS wild-type cell lines) and yields precise estimates of amino acid influx from serum protein for all proteinogenic amino acids. We have measured serum protein catabolism in a variety of cultured cell lines and find that protein catabolism yields amino acids in comparable amounts to conventional uptake in various pancreatic and non-pancreatic lines. This approach enables estimation of protein catabolic flux in any cell line and can be used to assay the effects of various genetic and pharmacological perturbations on serum protein catabolism with high sensitivity and while accounting for growth rate differences.
Citation Format: Michel Nofal, Kevin Zhang, Josh Rabinowitz. Quantitative flux measurements of serum protein catabolism in PDAC and other KRAS-mutant cancers. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr LB-279. doi:10.1158/1538-7445.AM2015-LB-279
Abstract LB-287: iKnife in neurosurgery: intraoperative real-time, in vivo biochemical characterization of brain tumors with high spatial resolution
Authors: Vaqas Babar , Balog Julia , Roncaroli Federico , Takats Zoltan , O'Neill Kevin 
Published: August 2015

Abstract
The purpose of this study was to prove that rapid intraoperative tissue identification of brain tumours using Rapid Evaporative Ionization Mass Spectrometry (REIMS, used surgically as the iKnife) with high spatial resolution is possible in order to help establish a tissue diagnosis and to maximise the extent of tumour resection.
A single centre prospective observational study was designed involving a consecutive series of patients undergoing craniotomy and resection of WHO grade II, III and IV tumours. A neuronavigation system was used to register iKnife readings for the first time during surgery for brain tumour resection. Precise intraoperative readings from different tumour zones were taken and compared to matched core biopsy samples verified by routine histopathology.
This protocol worked well, allowing in-vivo mass spectrometry readings to be taken with accurate histology. Analysis of data from the first 6 cases shows distinct phospholipid spectral patterns for Grade II and IV tumours. An increased intensity of sulfatides were observed in the white matter of the grade II tumours.
Our neuronavigational platform for the iKnife has revealed unique in-vivo spectra for different intrinsic brain tumours. As more cases are added to our spectral database we hope to describe in-vivo intra-tumoural variations which may shed important light into intrinsic brain tumour biology.
Citation Format: Babar Vaqas, Julia Balog, Federico Roncaroli, Zoltan Takats, Kevin O'Neill. iKnife in neurosurgery: intraoperative real-time, in vivo biochemical characterization of brain tumors with high spatial resolution. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr LB-287. doi:10.1158/1538-7445.AM2015-LB-287
Abstract LB-296: Small RNA profiling of human testicular germ cell tumor tissue samples shows abundant tRNA fragments and global loss of piRNA
Authors: Rounge Trine B. , Furu Kari , Skotheim Rolf , Haugen Trine B. , Enerly Espen , Grotmol Tom 
Published: August 2015

Abstract
Small non-coding RNAs play essential roles in tumorigenesis. However, their role in testicular germ cell tumor (TGCT), the most common malignancy in young males in most western countries, is largely unknown. In particular, a comprehensive analysis of the small RNA composition, including microRNAs (miRNAs), PIWI-interacting RNAs (piRNAs), and tRNA-derived small RNAs and their interactions, are lacking. tRNA-derived small RNAs have been shown to bind to the piRNA-associated protein HIWI2, indicating crosstalk between small RNA pathways.
We have employed small RNA sequencing on 22 human TGCT samples from 5 histological subtypes, 3 carcinoma in situ, and 12 normal testis samples. The sequences from each sample group were analyzed according to sequence length, base composition, and their association with repeats, exons, tRNAs, piRNAs, and miRNAs. Most sequences 24-32 nucleotides in length, displayed piRNA characteristics. Expression analyses of the small RNA contigs demonstrated global loss of small RNAs in TGCT compared to normal testis.
A large proportion of the 33-36 nt RNA sequences derives from mature tRNAs, predominantly from the 5′ end. We did not identify differences in the expression of 5′ tRNA halves between normal and cancer tissue samples; however, 3 shorter 5′ tRNA fragments showed differential expression. Although components of the same pathways might be involved in piRNA and tRNA-derived small RNAs biogenesis, expression differences in TGCT samples suggest independent regulation of key components in response to the carcinogenic process.
Our results show subtype-specific microRNA expression, as well as a global loss of piRNAs in all TGCT histological subtypes when compared to normal testicular tissue. In addition, we document the presence of large amounts of tRNA-derived sequences in both TGCT and normal samples, which may provide new insight into the association between the tRNA fragments and piRNA biogenesis. These results may be valuable in the identification of new biomarkers for TGCT.
Citation Format: Trine B. Rounge, Kari Furu, Rolf Skotheim, Trine B. Haugen, Espen Enerly, Tom Grotmol. Small RNA profiling of human testicular germ cell tumor tissue samples shows abundant tRNA fragments and global loss of piRNA. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr LB-296. doi:10.1158/1538-7445.AM2015-LB-296
Abstract SY02-02: Shared risk factors for diabetes, cardiovascular disease, and cancer in a low-income population
Authors: Blot William J. , Hargreaves Margaret , Zheng Wei 
Published: August 2015

Abstract
Diabetes, cardiovascular disease (CVD) and cancer are the three most common chronic disease afflicting Americans today, but few investigations have compared and contrasted disease-specific risk factors, especially among low-income populations where incidence of the conditions is elevated. Herein we examine major lifestyle and social determinants of the illnesses, including cigarette smoking, obesity, physical activity, and socioeconomic status, and how they predict subsequent disease-specific mortality within the Southern Community Cohort Study (SCCS). The SCCS is tracking a population of approximately 85,000 adults age 40-79, two-thirds African American, recruited during 2002-2009 predominantly from community health centers (CHCs) across 12 southeastern states. Since CHCs provide basic health care and preventative services in underserved areas, the cohort comprises many individuals, both black and white, with low income and educational levels. Participants enrolling at CHCs were interviewed using a structured comprehensive questionnaire and then followed for mortality via linkage with the National Death Index. CVD and cancer were the leading causes among the nearly 7,500 deaths observed, and diabetes was reported by nearly 20% of participants at cohort entry. In Cox modeling, mortality hazard ratios (HRs) rose markedly and steadily with increasing cigarette smoking amounts for both CVD and cancer, but more so for cancer. HRs were elevated among the obese, but only mildly and only for CVD and not cancer. Diabetes prevalence, however, was very strongly and linearly related to body mass index (BMI), with 6- and 12-fold higher odds of diabetes among blacks and whites, respectively, with BMI ≥ 40 vs &lt;25 kg/m2. HRs were modestly elevated among the most sedentary (and modestly decreased among the most physically active), more so for CVD than cancer. Low socioeconomic status, especially low income, was a strong (for CVD), modest (for diabetes) and weak (for cancer) risk factor. The findings indicate that these common diseases tend to share many of the same determinants, raising the possibility that mechanisms by which these exposures affect cardiovascular disease and diabetes may also relate to cancer risk and that public health measures aimed at other chronic diseases may have benefits for cancer prevention.
Citation Format: William J. Blot, Margaret Hargreaves, Wei Zheng. Shared risk factors for diabetes, cardiovascular disease, and cancer in a low-income population. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr SY02-02. doi:10.1158/1538-7445.AM2015-SY02-02
Abstract SY30-04: Can protein discovery with complete molecular specificity increase return on investment for cancer biomarkers
Authors: Kelleher Neil 
Published: August 2015

Abstract
Bottom-up proteomics relies on the use of proteases and is the method of choice for identifying thousands of protein groups in complex samples. Top-down proteomics has been shown to be robust for direct analysis of small proteins and offers a solution to the “peptide-to-protein” inference problem inherent with bottom-up. This talk will focus on the results in our recently accepted manuscript which describes the first large-scale integration of genomic, bottom-up and top-down proteomic data for comparative analysis of patient-derived mouse xenograft models of basal and luminal B human breast cancer, WHIM2 and WHIM16, respectively. Using these well-characterized xenograft models established by the National Cancer Institute Clinical Proteomic Tumor Analysis Consortium, we compared and contrasted the performance of bottom-up and top-down proteomics to detect cancer-specific aberrations at the peptide and proteoform levels, and to measure differential expression of proteins and proteoforms. For proteins in the range of 0-30 kDa, bottom-up proteomics quantified 3,519 protein groups from 49,185 peptides, while top-down proteomics quantified 982 proteoforms mapping to 358 proteins. Examples of both concordant and discordant quantitation were found in an approximately 60:40 ratio, providing a unique opportunity for top-down to fill in missing information. The two techniques showed complementary performance, with bottom-up yielding 8 times more identifications of 0-30 kDa proteins in xenograft proteomes, but failing to detect differences in post-translational modifications, such as phosphorylation pattern changes of alpha-endosulfine. This initial study illustrates the potency of a combined bottom-up and top-down proteomics approach to deepen our knowledge of cancer biology, especially when genomic data are available.
Citation Format: Neil Kelleher. Can protein discovery with complete molecular specificity increase return on investment for cancer biomarkers. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr SY30-04. doi:10.1158/1538-7445.AM2015-SY30-04
Abstract SY45-01: Defining the origin of tumor heterogeneity in epithelial cancers
Authors: Blanpain Cedric 
Published: August 2015

Abstract
Different theories have been proposed to explain tumor heterogeneity including the cancer cell of origin. Here, we developed genetically engineered mouse models allowing lineage tracing together with oncogenic activation in different cell lineages, and assessed whether the cancer cell of origin controls tumor heterogeneity. Mouse skin squamous cell carcinoma (SCC) arising from the interfollicular epidermis (IFE) are all well-differentiated SCCs. In contrast, tumors that arise from the same oncogenic hits in the hair follicle (HF) lineages displayed considerable heterogeneity ranging from well-differentiated SCCs to fibroblastic-like cancers exhibiting epithelial to mesenchymal transition (EMT) features. I will discuss further evidence that the cancer cell of origin controls EMT-related tumor heterogeneity and the underlying molecular mechanisms that promote multilineage differentiation, tumor propagation, EMT and metastasis in primary skin SCCs. Breast cancer is the most frequent cancer in women and consists of heterogeneous types of tumors that are classified into different histological and molecular subtypes. PIK3CA and p53 are the two most frequently mutated genes and are associated with different types of human breast cancers. I will present new results uncovering the cellular origin of mammary tumors. These results have important implications for our understanding of the mechanisms controlling tumor heterogeneity and the development of new strategies to block tumor initiation.
This work is supported by the WELBIO, the FNRS, the Fondation Bettencourt-Schuler and the Fondation Baillet-Latour.
Citation Format: Cedric Blanpain. Defining the origin of tumor heterogeneity in epithelial cancers. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr SY45-01. doi:10.1158/1538-7445.AM2015-SY45-01
Genetic Architecture of Lacunar Stroke
Authors: Traylor Matthew , Bevan Steve , Baron Jean-Claude , Hassan Ahamad , Lewis Cathryn M. , Markus Hugh S. 
Published: August 2015

Background and Purpose—
Lacunar strokes comprise ≈20% of all strokes. Despite this frequency, their pathogenesis is poorly understood. Previous genome-wide association studies in lacunar stroke have been disappointing, which may be because of phenotypic heterogeneity. Pathological and radiological studies suggest that there may be different pathologies underlying lacunar strokes. This has led to the suggestion of 2 subtypes: isolated lacunar infarcts and multiple lacunar infarcts and leukoaraiosis.

Methods—
We performed genome-wide analyses in a magnetic resonance imaging–verified cohort of 1012 younger onset lacunar stroke cases and 964 controls. Using these data, we first estimated the heritability of lacunar stroke and its 2 hypothesized subtypes, and secondly, we determined whether this is enriched for regulatory regions in the genome, as defined by data from Encyclopedia of DNA Elements (ENCODE) and other sources. Finally, we determine the evidence for a polygenic contribution from rare variation to lacunar stroke and its subtypes.

Results—
Our results indicate a substantial heritable component to magnetic resonance imaging–verified lacunar stroke (20%–25%) and its 2 subtypes (isolated lacunar infarct, 15%–18%; multiple lacunar infarcts/leukoaraiosis, 23%–28%). This heritable component is significantly enriched for sites affecting expression of genes. In addition, we show that the risk of the 2 subtypes of lacunar stroke in isolation, but not in combination, is associated with rare variation in the genome.

Conclusions—
Lacunar stroke, when defined on magnetic resonance imaging, is a highly heritable complex disease. Much of this heritability arises from regions of the genome affecting gene regulation. Rare variation affects 2 subtypes of lacunar in isolation, suggesting that they may have distinct genetic susceptibility factors.
The Truth Before and After: Brain Potentials Reveal Automatic Activation of Event Knowledge during Sentence Comprehension
Authors: Nieuwland Mante S. 
Published: August 2015

AbstractHow does knowledge of real-world events shape our understanding of incoming language? Do temporal terms like “before” and “after” impact the online recruitment of real-world event knowledge? These questions were addressed in two ERP experiments, wherein participants read sentences that started with “before” or “after” and contained a critical word that rendered each sentence true or false (e.g., “Before/After the global economic crisis, securing a mortgage was easy/harder”). The critical words were matched on predictability, rated truth value, and semantic relatedness to the words in the sentence. Regardless of whether participants explicitly verified the sentences or not, false-after-sentences elicited larger N400s than true-after-sentences, consistent with the well-established finding that semantic retrieval of concepts is facilitated when they are consistent with real-world knowledge. However, although the truth judgments did not differ between before- and after-sentences, no such sentence N400 truth value effect occurred in before-sentences, whereas false-before-sentences elicited an enhanced subsequent positive ERPs. The temporal term “before” itself elicited more negative ERPs at central electrode channels than “after.” These patterns of results show that, irrespective of ultimate sentence truth value judgments, semantic retrieval of concepts is momentarily facilitated when they are consistent with the known event outcome compared to when they are not. However, this inappropriate facilitation incurs later processing costs as reflected in the subsequent positive ERP deflections. The results suggest that automatic activation of event knowledge can impede the incremental semantic processes required to establish sentence truth value.
Task-positive Functional Connectivity of the Default Mode Network Transcends Task Domain
Authors: Elton Amanda , Gao Wei 
Published: August 2015

Abstract
The default mode network (DMN) was first recognized as a set of brain regions demonstrating consistently greater activity during rest than during a multitude of tasks. Originally, this network was believed to interfere with goal-directed behavior based on its decreased activity during many such tasks. More recently, however, the role of the DMN during goal-directed behavior was established for internally oriented tasks, in which the DMN demonstrated increased activity. However, the well-documented hub position and information-bridging potential of midline DMN regions indicate that there is more to uncover regarding its functional contributions to goal-directed tasks, which may be based on its functional interactions rather than its level of activation. An investigation of task-related changes in DMN functional connectivity during a series of both internal and external tasks would provide the requisite investigation for examining the role of the DMN during goal-directed task performance. In this study, 20 participants underwent fMRI while performing six tasks spanning diverse internal and external domains in addition to a resting-state scan. We hypothesized that the DMN would demonstrate “task-positive” (i.e., positively contributing to task performance) changes in functional connectivity relative to rest regardless of the direction of task-related changes in activity. Indeed, our results demonstrate significant increases in DMN connectivity with task-promoting regions (e.g., anterior insula, inferior frontal gyrus, middle frontal gyrus) across all six tasks. Furthermore, canonical correlation analyses indicated that the observed task-related connectivity changes were significantly associated with individual differences in task performance. Our results indicate that the DMN may not only support a “default” mode but may play a greater role in both internal and external tasks through flexible coupling with task-relevant brain regions.