bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract A89: Examination of ancestral informative markers and self-reported race with tumor characteristics of breast cancer among black and white women
Authors: Reding Kerryn W. , Carlson Christopher S. , Malone Kathleen E. , Chen Christina T. , Doody David R. , Ornelas India , Chen Chu , Lowe Kimberly , Weiss Linda , Simon Michael , Strom Brian 
Published: June 2012

Abstract
African American (AA) women have higher mortality from breast cancer (BC) compared to European American (EA) women. This may be due to the higher proportion of AA women with tumors that are diagnosed at advanced stage and are estrogen receptor negative (ER-) /progesterone receptor negative (PR-). Our study sought to determine whether self-reported race and percent African ancestry were associated with BC tumor characteristics. In a multi-center, population-based case-control study of BC, we determined percent African ancestry using ancestry informative markers (AIM) among women self-reporting as Black. While self-reported race was associated with several BC tumor characteristics, AIMs markers among AA women were not. Specifically, women self-reporting as Black were at a 30% reduction in ER+/PR+ tumors (95% CI: 0.6–0.9), a non-significant risk of ER-/PR-tumors (OR = 1.3 [95% CI: 0.9–1.7]), a 1.4-fold increased risk of regional/distant stage (95% CI: 1.1–1.7) and a 1.5-fold increased risk of high grade tumors (95% CI: 1.2–1.9) compared to EA women. Percent African ancestry was not associated with any BC tumor characteristics (OR=1.0 for ER+/PR+ [95% CI: 0.6–1.8], OR = 0.9 for ER-/PR-[95% CI: 0.5–1.6], OR = 1.3 for regional/distant stage [95% CI: 0.8–2.1], and OR=0.9 for high-grade tumors [95% CI: 0.6–1.4] comparing those with ≥95% African ancestry to those with &lt;80% African ancestry). This analysis suggests that factors unrelated to AA women's genetic ancestry contribute to racial differences in BC tumor characteristics.
Citation Information: Cancer Epidemiol Biomarkers Prev 2011;20(10 Suppl):A89.
Abstract B31: Molecular signature discriminating triple-negative breast tumors between African American and Caucasian women
Authors: Ellsworth Rachel , Field Lori , Shriver Craig 
Published: June 2012

Abstract
Background: Triple negative (TN) tumors are characterized by aggressive behavior and, the negative hormone receptor and HER2 status precludes the use of personalized therapies such as tamoxifen and trastuzumab. African American women have higher rates of both breast cancer mortality as well as TN breast tumors. What remains unknown is how much of these disparities can be attributed to molecular differences between populations.
Methods: The Clinical Breast Care Project database was queried to identify African American women with triple negative, high-grade tumors. Caucasian women with highgrade TN tumors were then matched by age at diagnosis, tumor stage, size and lymph node status. RNA was isolated after laser microdissection of the tumor and hybridized to HG U133A 2.0 microarrays. Data was analyzed using Partek Genomics Suite.
Results: Principal Component Analysis accurately clustered the triple negative specimens by ethnicity. Using a false-discovery rate (FDR) p-value &lt;0.05 with a minimum 2.0-fold change of expression, 132 probes from 117 genes were differentially expressed. Hierarchical clustering using a subset of these probes (P&lt;0.00001) representing 23 known genes reliably partitioned all samples as African American or Caucasian. Genes differentially expressed include lower expression of AQP5, VEGF and RAD51C and higher expression of hemoglobin B, and complement factors CFD and C4A in tumors from African Americans.
Discussion: Despite matching of tumors by clinicopathological characteristics, molecular profiles of triple negative breast tumors differed between AAW and CW. These differences may serve as molecular targets for the development of novel prevention strategies and therapeutics to reduce the risk of developing and improve treatment of African American women with triple negative breast cancer.
Citation Information: Cancer Epidemiol Biomarkers Prev 2011;20(10 Suppl):B31.
Abstract B64: Low estrogen receptor expression level and early age of breast cancer onset are the common breast cancer features in Arab population
Authors: Dhaheri Mariam Al 
Published: June 2012

Abstract
Breast cancer is the common malignant related disease of Women worldwide. In clinic, molecular classification of the disease is a key to setup therapeutic strategy for patients. To date, few reports describe the molecular basis of the disease, survival rate and therapeutic strategies that applied to encounter breast cancer in the Arab population. Nevertheless, advancement of medical research varied among Arab nations. This study reviews published data of breast cancer in the Arab World and integrate the available data to propose a model that describes the common molecular features of breast cancer in the Arab population. In conclusion, almost all of Arab nations share an early onset of breast cancer. Grade I cases accounted for ≤10% of the total cases, while grade III cases accounted for ≥40% of the total diagnosed cases. In general, breast tumor poor differentiation is associated with decrease in estrogen receptor (ER) and B-cell lymphoma 2 (Bcl2) expression and an increase of protein 53 (p53) protein expression. Human epidermal growth factor receptor 2 (HER2/neu) expression is varied, yet it is associated with poor differentiation. Most importantly ER expression level is relatively lower compared to the reported ER expression level in breast cancer cases detected in Western countries. This could be due to the fact that the majority of breast cancer cases detected in Arab population were grade II or III of cancer progression. The dominance of advanced form of the disease with early age of onset urge to screen samples to identify biomarkers associated with breast cancer onset in Arab population. In deed; identifying new biomarkers responsible of early onset of the disease might advance our understanding of disease progression and/ or discover new molecular therapeutic targets.
Citation Information: Cancer Epidemiol Biomarkers Prev 2011;20(10 Suppl):B64.
Abstract B75: Association of insurance status and age with stage at diagnosis among cervical cancer patients, National Cancer Database 2000–2007
Authors: Fedewa Stacey A. , Virgo Katherine S. , Bandi Priti , Saslow Debbie , Ward Elizabeth M. , Cokkinides Vilma 
Published: June 2012

Abstract
Introduction: Late stage cervical cancer at diagnosis is associated with greater morbidity and mortality and higher treatment costs. Few studies have examined the association between insurance status and cervical cancer stage at diagnosis. Existing studies have been either state-specific or limited to elderly Medicare recipients. This study aims to examine the relationship between patient characteristics, with a particular focus on age at diagnosis and insurance status, and stage in a large number of cervical cancer patients aged 21–85 in the National Cancer Database (NCDB).
Methods: Women diagnosed with their first primary invasive cervical cancer between 2000 and 2007 were selected from the NCDB. We evaluated the association between late stage (stage III/IV) and insurance and age while adjusting for race/ethnicity and other socio-demographic and clinical factors. Multivariate log binomial models were used to estimate risk ratios (RR) and 95% confidence intervals (CIs), respectively.
Results: Among the 69,739 evaluable patients, the rate of late stage disease increased from 16.53% in 21–34 year olds to 42.44% in women ≥70. The adjusted risk of advanced stage of disease among women 50 years and older was 2.2 to 2.5 times that of patients aged 21–34. Uninsured (RR=1.44, 95% CI 1.40–1.49), Medicaid (RR=1.37, 95% CI 1.34–1.41), Younger Medicare (RR=1.12, 95% CI 1.06–1.19), and Older Medicare (RR=1.20, 95% CI 1.15–1.26) patients had a higher risk of late stage disease compared to privately insured patients. African Americans (RR=1.05, 95%CI 1.02–1.08) had slightly higher risks of advanced stage disease while Hispanics (RR=0.86, 95%CI 0.83–0.89) and other race/ethnicities (RR=0.88, 95%CI 0.84–0.92) had a lower risks compared to whites.
Conclusion: In a large national sample of women diagnosed with cervical cancer, the strongest predictor of late stage at diagnosis was age. Patients without private insurance were also more likely to be diagnosed at later stages, particularly uninsured and Medicaid insured patients. Screening should be encouraged for those women for whom it is recommended, especially those at higher risk of advanced stage disease. Consideration of these findings in developing future guidelines for cervical cancer screening among older women is recommended.
Citation Information: Cancer Epidemiol Biomarkers Prev 2011;20(10 Suppl):B75.
Abstract B83: Factors influencing adherence to mammography screening guidelines in Appalachian women participating in a mobile mammography program
Authors: Vyas Ami , Madhavan S. Suresh , Lemasters Traci , Atkins Elvonna , Kennedy Stephenie , Kelly Kimberly , Vona-Davis Linda , Halverson Joel , Remick Scot 
Published: June 2012

Abstract
Objectives: The objectives of this study were to evaluate the characteristics (demographic, access to care, health-related behavioral, self and family medical history, psychosocial) of women age 40 years and above who participated in a mobile mammography screening program conducted throughout West Virginia to determine the factors influencing their self-reported adherence to mammography screening guidelines.
Methods: The data were collected from 738 women who participated in the Bonnie Wells Wilson Mobile Mammography Program and completed a six-page Preventive Care Survey. Data were analyzed using the Andersen Behavioral Model of Healthcare Utilization framework to determine the factors associated with adherence to mammography screening guidelines in these women.
Results: Of the 686 women included in the analysis, 46.2% reported having had a mammogram in the past two years as per current mammography screening guidelines. The unadjusted model showed predisposing factors such as older age and unemployed status, visit to a gynecologist in the past year (an enabling factor) and need-related factors such as having a family history of breast cancer (BC), having had breast problems in the past, having had breast biopsy in the past, having had a Pap test in past two years, and having had all the screenings for cholesterol, blood glucose, bone mineral density and high blood pressure in past two years to be significant predictors of self-reported adherence to mammography guidelines. In the adjusted model, being of age 65 and above (OR=3.787), having a family history of BC (OR=1.909), having had breast problems in the past (OR=1.992) and having had a Pap test (OR=6.035) were significant predictors of self-reported mammography screening adherence.
Conclusions: Forty-six percent of the sample reported having had a mammogram in the past two years as per current mammography screening guidelines which is lower than the 70% goal of Healthy People 2010. Breast cancer related events seem to be associated with mammography screening adherence in this rural Appalachian population. Increasing adherence to mammography screening may require targeted, community-based educational interventions that precede and complement visits by the mobile mammography unit.
Citation Information: Cancer Epidemiol Biomarkers Prev 2011;20(10 Suppl):B83.
Abstract ED03-01: Validation and quantitation of DNA methylation changes
Authors: Kwabi-Addo Bernard 
Published: June 2012

Abstract
Advances in the molecular mechanisms underlying prostate cancer demonstrates that prostate cancer cells carry a myriad of genomic defects including both genetic and epigenetic alterations such as DNA methylation. Underlying this aberrant DNA methylation is the accumulating body of data hinting that normal prostate cells may be subjected to a relentless barrage of genome-damaging stresses due to both exogenous and endogenous carcinogens, with damage accumulating over time and age. There are increasing numbers of genes that show aberrant DNA methylation changes in human prostate cancer. In addition, recent reports indicate widespread methylation changes that correlate with a broad range of clinical behavior in prostate cancer patients. Thus aberrant DNA methylation changes may represent the integration of environmental or lifestyle exposures and genetic predisposition to prostate cancer. Such events may differ between individuals belonging the same ethnic group or individuals belonging to different ethnic groups. We hypothesize that differential methylation patterns maybe associated with ethnicity and could potentially contribute to the incidence and mortality of prostate cancer. Our research studies validate and quantify selected regions of genes from a genome-wide methylation analysis in a large sample number from African American and Caucasian male patients with prostate cancer. Our preferred method for studying DNA methylation is pyrosequencing over other methods of methylation analysis in that it is processive and quantitative. The principle of pyrosequencing is the real-time detection of pyro-phosphate (PPi), released after each incorporation of a specific nucleotide, initiated by simple primer extension on a PCR product template. Pyrosequencing has both qualitative and quantitative applications, and is optimal for allele quantification, DNA methylation estimation, and for regions that contain multiple polymorphisms (SNPs, IN/DELs) adjacent or in close proximity. Using this approach, we have observed significant differences in the methylation pattern for several genes in prostate tissue samples from African American and Caucasian men. Such alterations can contribute to the biological differences underlying prostate cancer disparity.
Citation Information: Cancer Epidemiol Biomarkers Prev 2011;20(10 Suppl):ED03-01.
Abstract PL04-02: Efficacy of PSA screening for prostate cancer: A case-control study of Caucasian and African American Medicare beneficiaries
Authors: Godley Paul A. , Carpenter William R. , Edwards Lloyd J. , Talcott James A. , Zullig Leah L. , Peacock Sharon , Schenck Anna P. 
Published: June 2012

Abstract
Background: PSA screening has become standard practice in the US although mortality data from controlled trials is lacking to assess the efficacy of screening of African American men. We investigated whether PSA screening efficacy is similar among elderly Caucasian and African American men.
Methods: This case-control study compared PSA exposure history of Surveillance, Epidemiology, and End Results (SEER) dataset-derived cases deceased from prostate cancer to that of control subjects from a linked Medicare dataset. The prostate cancer cases include males diagnosed with prostate cancer between 1992 and 2005 that subsequently died from the disease (matched with 3:1 on race, age, and SEER region).
Results: We identified 8,846 cases deceased from prostate cancer, and 23,538 age-, race-, and SEER site-matched controls. African Americans comprised about 10% of both the cases (779) and controls (2,337). Conditional logistic regression analyses were used to calculate prostate cancer-specific mortality among African American (1.09 [95% CI 0.917–1.303]) and Caucasian subjects (1.14 [95% CI 1.076–1.201]) who were asymptomatic at the time of their PSA screening test.
Conclusions: The results of this large, claims-based, case-control study suggest that the efficacy of PSA screening among elderly African American men is not dissimilar to that of elderly Caucasian men, and that neither group benefitted from reduced mortality attributable to screening.
Citation Information: Cancer Epidemiol Biomarkers Prev 2011;20(10 Suppl):PL04-02.
Predictive Value of XRCC1 Gene Polymorphisms on Platinum-Based Chemotherapy in Advanced Non–Small Cell Lung Cancer Patients: A Systematic Review and Meta-analysis
Authors: Wu Junjie , Liu Jie , Zhou Yuhao , Ying Jun , Zou Houdong , Guo Shicheng , Wang Lei , Zhao Naiqing , Hu Jianjun , Lu Daru , Jin Li , Li Qiang , Wang Jiu-Cun 
Published: June 2012

Abstract
Purpose: Published data have shown conflicting results about the relationship between X-ray repair cross-complementing group 1 (XRCC1) gene polymorphisms (Arg399Gln and Arg194Trp) and clinical outcome of platinum-based chemotherapy in patients with advanced non–small cell lung cancer (NSCLC). A meta-analysis is needed to provide a systematic review of the published findings.
Experimental Design: We conducted a systematic review and meta-analysis to evaluate the predictive value of XRCC1 gene polymorphisms on clinical outcome up to October 1, 2010. The quality of each study was scored on the basis of predefined criteria.
Results: A total of 13 eligible follow-up studies met all the inclusion criteria. The XRCC1194Trp allele was found to be significantly associated with a favorable response rate relative to 194Arg [Trp vs. Arg: OR, 1.88; 95% confidence interval (CI), 1.48–2.38]. XRCC1399Gln was less favorably associated with both response rate (Gln vs. Arg: OR, 0.67; 95% CI, 0.52–0.87) and overall survival (Gln vs. Arg: HR, 1.30; 95% CI, 1.04–1.63) than 399Arg in analyses using all available studies; but these associations became insignificant when only high-quality studies were used.
Conclusion: These findings suggest a predictive role for XRCC1 gene polymorphisms in clinical outcome. However, the role of 399Gln could be considered controversial because its impact on clinical outcome was insignificant in high-quality studies. These findings show the importance of establishing suitable criteria, including genetic epidemiologic, phenotypic, and clinical criteria, to improve quality control of study design and methods in pharmacogenomic studies related to XRCC1 gene polymorphism. Clin Cancer Res; 18(14); 3972–81. ©2012 AACR.
Abstract A105: Phase 2 trials of linifanib (ABT-869) in advanced hepatocellular, renal cell and non-small cell lung cancer: Associations of response by CT or DCE-MRI with patient outcome
Authors: Toh Han Chong , Yong Wei Peng , Wong Yu-Ning , tan Eng-Huat , Kollmannsberger Christian K. , Devanarayan Viswanath , Zhang Ke , Luo Yanping , Chen Daniel , Ashton Edward , Ricker Justin L. , Carlson Dawn , Chen Pei-Jer 
Published: June 2012

Abstract
Background: Linifanib is a novel orally active and selective inhibitor of VEGF and PDGF families of receptor tyrosine kinases. Linifanib has demonstrated antitumor activity in a variety of advanced solid tumors in phase 1 and 2 trials. The objective of this analysis was to assess associations between pt outcome (PFS or OS) and response by CT (per RECIST or tumor volume change), or DCE-MRI (per Ktrans), in patients (pts) enrolled in ongoing phase 2 linifanib monotherapy trials.
Methods: Three open-label, phase 2 monotherapy studies were conducted internationally in advanced/metastatic solid tumor pts with hepatocellular carcinoma (HCC), non-small cell lung cancer (NSCLC) and renal cell carcinoma (RCC). Interim efficacy and safety results have been previously reported. A retrospective exploratory analysis of associations between pt outcome and CT or DCE-MRI response was conducted. An independent centralized review of tumor response assessment by CT (baseline, and Q8 wks) and DCE-MRI (baseline, and 2 wks) was performed using a uniform charter. CT assessed tumor volume and best percent change from baseline and pts were classified as PR, SD, or PD by RECIST. Baseline Ktrans and percent change in Ktrans were derived from DCE-MRI. Statistical analysis was performed using the Cox proportional hazard model and logrank test, and significance considered at the level of P≥0.05. Threshold estimates were determined by the Bootstrapping & Aggregating Thresholds from Trees (BATTing).
Results: Across the 3 phase 2 trials, 236 pts were enrolled from 08/07 to 10/08 at 34 centers: 44 pts with HCC, 53 pts with RCC, and 139 pts with NSCLC. Based on the BATTing methodology, 79/191 evaluable pts had a maximum CT tumor volume decrease of &gt;32%. This was associated with improved OS (log-rank p&lt;0.001) and PFS (log-rank p&lt;0.001). Pts with confirmed or unconfirmed PR (n=27) per RECIST had better OS (p=0.021) and PFS (p=0.017) than those who did not achieve a PR (n=181). Among the 236 pts, 117 had DCE-MRI scans at baseline and Day 15. Of these, 68/117 pts (58%) had baseline Ktrans above the BATTing cutoff of 0.055 and this was associated with improved OS (log-rank, p=0.011), but not PFS (log-rank, p=0.835). DCE-MRI response (Ktrans decrease) at 2 wks was not associated with significant improvement in PFS or OS.
Conclusions: CT tumor volume reduction and CT response were associated with improved OS and PFS. Greater baseline Ktrans was associated with improved OS but not PFS. Ktrans changes at 2 wks were not associated with improvement in pt outcome.
Citation Information: Mol Cancer Ther 2009;8(12 Suppl):A105.
Abstract A155: Activation of PI3K/Akt signaling pathway mediates acquired resistance to sorafenib in hepatocellular carcinoma cells
Authors: Chen Kuen-Feng , Feng Wen-Chi , Hsu Chih-Hung , Chen Pei-Jer , Cheng Ann-Lii 
Published: June 2012

Abstract
Background: Hepatocellular carcinoma (HCC) is one of the most common and lethal human malignancies. Sorafenib, a tyrosine kinase inhibitor, was recently approved by FDA for HCC.
Material and Methods: We established two sorafenib-resistant HCC cell lines (Huh7-R1 and Huh7-R2) from Huh7, a human HCC cell line, by chronic exposure of cells to sorafenib. The mechanisms of resistance were investigated.
Results: Sorafenib induced significant apoptosis in Huh7 cells. However, Huh7-R1 and Huh7-R2 showed significant resistance to sorafenib-induced apoptosis at the clinical relevant concentrations (up to 10 M). Thorough comparisons of the molecular changes between Huh7 and resistant cells, we found PI3K/Akt signaling pathways played a significant role in mediating acquired resistance to sorafenib in Huh7-R1 and Huh7-R2 cells. Our data showed that phospho-Akt and p85 (a regulatory subunit of PI3K) were up-regulated, while PTEN was down-regulated in these resistant cells. In addition, ectopic expression of constitutive Akt in Huh7 demonstrated similar resistance to sorafenib. Knocking down Akt by RNA-interference reversed the resistance to sorafenib in Huh7-R1, indicating the importance of Akt in drug sensitivity. Furthermore, the combination of MK-2206, a novel allosteric Akt inhibitor, and sorafenib restored the sensitivity of resistant cells to sorafenib-induced apoptosis.
Conclusions: Activation of PI3K/Akt signaling pathway medicates acquired resistance to sorafenib in HCC cells. The combination of sorafenib with MK-2206, an Akt inhibitor, overcomes the resistance at clinical achievable concentrations. This study is supported by NTUH 98P03, NSC 98-3112-B-002-037, DOH (94–98)-TD-B-111-001 and MK-2206 was kindly provided by Merck & Co., Inc. (Whitehouse Station, NJ, USA).
Citation Information: Mol Cancer Ther 2009;8(12 Suppl):A155.