bluuebunny/crossref_metadata_2025_split huggingface dataset:
Circulating Tumor Cells in Patients with Castration-Resistant Prostate Cancer Baseline Values and Correlation with Prognostic Factors
Authors: Goodman Oscar B. , Fink Louis M. , Symanowski James T. , Wong Bryan , Grobaski Beth , Pomerantz David , Ma Yupo , Ward David C. , Vogelzang Nicholas J. 
Published: June 2009

Abstract
Purpose: Circulating tumor cells (CTC) have been recently accepted by the Food and Drug Administration of the United States as a prognostic tool in advanced prostate cancer. However, a number of questions remain about the use of the test. The optimal clinical cut-off has never been determined. Also, the predictive value of CTCs in the setting of low-burden advanced prostate cancer has not been evaluated. Herein we describe our experience with the CellSearch method of CTC enumeration.
Experimental Design: CTCs enumerated from 100 patients with castration-resistant prostate cancer were correlated with clinicopathologic characteristics and conventional biomarkers, such as prostate-specific antigen and lactate dehydrogenase. Patients received ongoing medical oncologic follow-up for up to 26 months, and overall survival status was documented.
Results: Forty-nine of the patients (49%) were alive at the end of the study. CTC counts correlate well with overall survival (P &lt; 0.001) but are also tightly interrelated to other biomarkers. Threshold analysis identified 4 CTC/7.5 cc (compared with the approved value of 5) as an optimal cut-off value with respect to correlation with survival outcomes as well as predictive of metastatic disease. Univariate analysis confirmed a tight interrelationship between cut-off CTC values and biomarkers. Multivariate analysis with bootstrap sampling validation identified lactate dehydrogenase (P = 0.002) and CTCs (P = 0.001) as independently prognostically significant.
Conclusions: Baseline CTC values provide important prognostic information and specific prediction of metastatic disease. Their presence correlates with classic biomarkers. (Cancer Epidemiol Biomarkers Prev 2009;18(6):1904–13)
Factors Associated with Awareness of Infection Status among Chronic Hepatitis B and C Carriers in Korea
Authors: Shin Aesun , Cho Eo Rin , Kim Jeongseon , Sung Joohon , Park Kyung Woo , Lim Min-Kyung , Shin Hai-Rim 
Published: June 2009

Abstract
Hepatitis B (HBV) and hepatitis C (HCV) viral infections are the most important risk factors for hepatocellular carcinoma (HCC), which is responsible for 17.5% of cancer deaths in Korea. The objectives of this study were to identify demographic characteristics that may affect hepatitis carriers' awareness of their infection status, and to assess whether health-related behaviors differed by awareness of the infection. Among 18,636 persons who were recruited from a cancer screenee cohort, 904 were HBV carriers and 146 were HCV carriers. Among the HBV carriers, 74.2% were aware of their infection status. Higher education (odds ratio, 1.8; college versus middle school or less), family history of liver cancer or disease, and marriage were associated with awareness of HBV infection status. Participants who were aware of their HBV carrier status were more likely to be former smokers or drinkers than those who were not aware of their status. Only 34.9% of HCV carriers were aware of their HCV infection status. No demographic characteristics were related to awareness of HCV infection status among HCV carriers. However, HCV carriers who were aware of their infection status were more likely to be former drinkers (odds ratio, 9.2; 95% confidence interval, 1.8-47.2). In conclusion, two thirds of HCV carriers and one fourth of HBV carriers in this study population were not aware of their infection status, and awareness of hepatitis infection status was significantly associated with other risk behaviors, such as alcohol consumption and cigarette smoking. (Cancer Epidemiol Biomarkers Prev 2009;18(6):1894–8)
Apoptosis in the Colonic Crypt, Colorectal Adenomata, and Manipulation by Chemoprevention
Authors: West Nicholas J. , Courtney Edward D.J. , Poullis Andrew P. , Leicester Roger J. 
Published: June 2009

AbstractThis review discusses the biology and the methods of assessment of apoptosis, of which, the monoclonal antibody M30 would seem to be the most useful; the role of apoptosis in the etiology of colorectal cancer; and its use as a marker to monitor the beneficial effects of chemopreventative interventions to reduce the development of colorectal cancer within the context of clinical trials. (Cancer Epidemiol Biomarkers Prev 2009;18(6):1680–7)
Bias Associated With Self-Report of Prior Screening Mammography
Authors: Cronin Kathleen A. , Miglioretti Diana L. , Krapcho Martin , Yu Binbing , Geller Berta M. , Carney Patricia A. , Onega Tracy , Feuer Eric J. , Breen Nancy , Ballard-Barbash Rachel 
Published: June 2009

Abstract
Background: Self-reported screening behaviors from national surveys often overestimate screening use, and the amount of overestimation may vary by demographic characteristics. We examine self-report bias in mammography screening rates overall, by age, and by race/ethnicity.
Methods: We use mammography registry data (1999-2000) from the Breast Cancer Surveillance Consortium to estimate the validity of self-reported mammography screening collected by two national surveys. First, we compare mammography use from 1999 to 2000 for a geographically defined population (Vermont) with self-reported rates in the prior two years from the 2000 Vermont Behavioral Risk Factor Surveillance System. We then use a screening dissemination simulation model to assess estimates of mammography screening from the 2000 National Health Interview Survey.
Results: Self-report estimates of mammography use in the prior 2 years from the Vermont Behavioral Risk Factor Surveillance System are 15 to 25 percentage points higher than actual screening rates across age groups. The differences in National Health Interview Survey screening estimates from models are similar for women 40 to 49 and 50 to 59 years and greater than for those 60 to 69, or 70 to 79 (27 and 26 percentage points versus 14, and 14, respectively). Overreporting is highest among African American women (24.4 percentage points) and lowest among Hispanic women (17.9) with non-Hispanic White women in between (19.3). Values of sensitivity and specificity consistent with our results are similar to previous validation studies of mammography.
Conclusion: Overestimation of self-reported mammography usage from national surveys varies by age and race/ethnicity. A more nuanced approach that accounts for demographic differences is needed when adjusting for overestimation or assessing disparities between populations. (Cancer Epidemiol Biomarkers Prev 2009;18(6):1699–705)
Cancer Incidence in the U.S. Military Population: Comparison with Rates from the SEER Program
Authors: Zhu Kangmin , Devesa Susan S. , Wu Hongyu , Zahm Shelia Hoar , Jatoi Ismail , Anderson William F. , Peoples George E. , Maxwell Larry G. , Granger Elder , Potter John F. , McGlynn Katherine A. 
Published: June 2009

Abstract
The U.S. active-duty military population may differ from the U.S. general population in its exposure to cancer risk factors and access to medical care. Yet, it is not known if cancer incidence rates differ between these two populations. We therefore compared the incidence of four cancers common in U.S. adults (lung, colorectal, prostate, and breast cancers) and two cancers more common in U.S. young adults (testicular and cervical cancers) in the military and general populations. Data from the Automated Central Tumor Registry (ACTUR) of the Department of Defense and the nine cancer registries of the Surveillance, Epidemiology and End Results (SEER) of the National Cancer Institute for the years 1990 to 2004 for persons with ages 20 to 59 years were analyzed. Incidence rates were significantly lower in the military population for colorectal cancer in White men, lung cancer in White and Black men and White women, and cervical cancer in Black women. In contrast, incidence rates of breast and prostate cancers were significantly higher in the military among Whites and Blacks. Incidence rates of testicular cancer did not differ between ACTUR and SEER. Although the numbers of diagnoses among military personnel were relatively small for temporal trend analysis, we found a more prominent increase in prostate cancer in ACTUR than in SEER. Overall, these results suggest that cancer patterns may differ between military and nonmilitary populations. Further studies are needed to confirm these findings and explore contributing factors. (Cancer Epidemiol Biomarkers Prev 2009;18(6):1740–5)
Sam-Pointed Domain Containing Ets Transcription Factor in Luminal Breast Cancer Pathogenesis
Authors: Sood Ashwani K. , Wang Jianmin , Mhawech-Fauceglia Paulette , Jana Bagirathan , Liang Ping , Geradts Joseph 
Published: June 2009

Abstract
We previously described frequent overexpression of Sam-pointed domain containing Ets transcription factor (SPDEF), also known as PDEF, in human breast cancer, and suggested a role for this transcription factor in breast tumor progression. To seek evidence in support of this hypothesis, the MCF-12A breast epithelial cell line was transfected with an SPDEF expression plasmid or with control vector plasmid and the transfected cells tested for their tumorigenic growth in vivo. The data showed that SPDEF expression in MCF-12A cells induced accelerated tumor growth in severe combined immune deficient mice compared with vector-transfected MCF-12A cells. Furthermore, Gene Expression Omnibus and Oncomine databases were mined to determine any correlation between SPDEF expression levels and clinical outcome. High SPDEF expression correlated with poor overall survival of patients with estrogen receptor+ breast cancer, in three independent data sets. In contrast, little correlation was observed between SPDEF expression and cancer relapse or remote metastases. SPDEF expression was further found to be restricted to tumors arising in the luminal epithelial lineage including estrogen receptor+ luminal subtype breast tumors, Her2/neu-positive tumors, and apocrine carcinomas. In contrast, little SPDEF expression was found in the basal subtype of breast tumors. Based on these results, we hypothesize that SPDEF has a function in the specification of the progenitor cells of the luminal epithelial lineage that become targets of oncogenesis in luminal breast cancer. (Cancer Epidemiol Biomarkers Prev 2009;18(6):1899–903)
Single and Multigenic Analysis of the Association between Variants in 12 Steroid Hormone Metabolism Genes and Risk of Prostate Cancer
Authors: Beuten Joke , Gelfond Jonathan A.L. , Franke Jennifer L. , Weldon Korri S. , Crandall AnaLisa C. , Johnson-Pais Teresa L. , Thompson Ian M. , Leach Robin J. 
Published: June 2009

AbstractTo estimate the prostate cancer risk conferred by individual single nucleotide polymorphisms (SNPs), SNP-SNP interactions, and/or cumulative SNP effects, we evaluated the association between prostate cancer risk and the genetic variants of 12 key genes within the steroid hormone pathway (CYP17, HSD17B3, ESR1, SRD5A2, HSD3B1, HSD3B2, CYP19, CYP1A1, CYP1B1, CYP3A4, CYP27B1, and CYP24A1). A total of 116 tagged SNPs covering the group of genes were analyzed in 2,452 samples (886 cases and 1,566 controls) in three ethnic/racial groups. Several SNPs within CYP19 were significantly associated with prostate cancer in all three ethnicities (P = 0.001-0.009). Genetic variants within HSD3B2 and CYP24A1 conferred increased risk of prostate cancer in non-Hispanic or Hispanic Caucasians. A significant gene-dosage effect for increasing numbers of potential high-risk genotypes was found in non-Hispanic and Hispanic Caucasians. Higher-order interactions showed a seven-SNP interaction involving HSD17B3, CYP19, and CYP24A1 in Hispanic Caucasians (P = 0.001). In African Americans, a 10-locus model, with SNPs located within SRD5A2, HSD17B3, CYP17, CYP27B1, CYP19, and CYP24A1, showed a significant interaction (P = 0.014). In non-Hispanic Caucasians, an interaction of four SNPs in HSD3B2, HSD17B3, and CYP19 was found (P &lt; 0.001). These data are consistent with a polygenic model of prostate cancer, indicating that multiple interacting genes of the steroid hormone pathway confer increased risk of prostate cancer. (Cancer Epidemiol Biomarkers Prev 2009;18(6):1869–80)
Molecular Subtypes of Breast Cancer Emerging in Young Women in Taiwan: Evidence for More Than Just Westernization as a Reason for the Disease in Asia
Authors: Lin Ching-Hung , Liau Jau-Yu , Lu Yen-Shen , Huang Chiun-Sheng , Lee Wei-Chung , Kuo Kuan-Ting , Shen Ying-Chun , Kuo Sung-Hsin , Lan Chieh , Liu Jacqueline Ming , Kuo Wun-Hon , Chang King-Jen , Cheng Ann-Lii 
Published: June 2009

Abstract
Background: In the past two decades, the incidence of breast cancer in young Taiwanese females has been rapidly increasing, approaching the risk level of western countries. As a first step to investigate the possible etiology, we examined the molecular subtypes of female breast cancer in Taiwan.
Methods: This study included 1,028 consecutive patients with breast cancer diagnosed in National Taiwan University Hospital between 2004 and 2006. Estrogen receptor (ER), progesterone receptor (PR), human epidermal growth factor receptor-2, cytokeratin 5/6, and epidermal growth factor receptor expression and/or gene amplification were analyzed.
Results: Younger (≤50 years) breast cancer patients had a higher prevalence of luminal A (67% versus 57%; P &lt; 0.001) and a lower prevalence of basal-like subtype (9% versus 17%; P &lt; 0.001) compared with older (&gt;50 years) patients. The higher prevalence of luminal A subtype was mainly attributed to a higher ER (75% versus 63%; P &lt; 0.001) and PR (47% versus 33%; P &lt; 0.001) expression rate in younger patients than older patients. Tumors with histologic grade 3 were less prevalent in younger patients than in older patients (23% versus 30%; P = 0.01). For very young (&lt;35 years) patients, the molecular subtype distribution, ER and/or PR expression rate, and histologic grade were not significantly different from those of less young (35-50 years) patients.
Conclusions: Young breast cancer patients in Taiwan are characterized by a high prevalence of luminal A subtype and low prevalence of histologic grade 3 tumor and/or basal-like subtype. These features are distinct from young breast cancer patients in western countries. (Cancer Epidemiol Biomarkers Prev 2009;18(6):1807–14)
Detection of Urothelial Bladder Cancer Cells in Voided Urine Can Be Improved by a Combination of Cytology and Standardized Microsatellite Analysis
Authors: Wild Peter J. , Fuchs Thomas , Stoehr Robert , Zimmermann Dieter , Frigerio Simona , Padberg Barbara , Steiner Inbal , Zwarthoff Ellen C. , Burger Maximilian , Denzinger Stefan , Hofstaedter Ferdinand , Kristiansen Glen , Hermanns Thomas , Seifert Hans-Helge , Provenzano Maurizio , Sulser Tullio , Roth Volker , Buhmann Joachim M. , Moch Holger , Hartmann Arndt 
Published: June 2009

Abstract
Purpose: To evaluate molecular and immunohistochemical markers to develop a molecular grading of urothelial bladder cancer and to test these markers in voided urine samples.
Experimental Design: 255 consecutive biopsies from primary bladder cancer patients were evaluated on a tissue microarray. The clinical parameters gender, age, adjacent carcinoma in situ, and multifocality were collected. UroVysion fluorescence in situ hybridization (FISH) was done. Expression of cytokeratin 20, MIB1, and TP53 was analyzed by immunohistochemistry. Fibroblast growth factor receptor 3 (FGFR3) status was studied by SNaPshot mutation detection. Results were correlated with clinical outcome by Cox regression analysis. To assess the predictive power of different predictor subsets to detect high grade and tumor invasion, logistic regression models were learned. Additionally, voided urine samples of 119 patients were investigated. After cytologic examination, urine samples were matched with their biopsies and analyzed for loss of heterozygosity (LOH), FGFR3 mutation, polysomy, and p16 deletion using UroVysion FISH. Receiver operator characteristic curves for various predictor subsets were plotted.
Results: In biopsies, high grade and solid growth pattern were independent prognostic factors for overall survival. A model consisting of UroVysion FISH and FGFR3 status (FISH + FGFR3) predicted high grade significantly better compared with a recently proposed molecular grade (MIB1 + FGFR3). In voided urine, the combination of cytology with LOH analysis (CYTO + LOH) reached the highest diagnostic accuracy for the detection of bladder cancer cells and performed better than cytology alone (sensitivity of 88.2% and specificity of 97.1%).
Conclusions: The combination of cytology with LOH analysis could reduce unpleasant cystoscopies for bladder cancer patients. (Cancer Epidemiol Biomarkers Prev 2009;18(6):1798–806)
Effects of Nickel on Cyclin Expression, Cell Cycle Progression and Cell Proliferation in Human Pulmonary Cells
Authors: Ding Jin , He Guoping , Gong Wenfeng , Wen Wen , Sun Wen , Ning Beifang , Huang Shanna , Wu Kun , Huang Chuanshu , Wu Mengchao , Xie Weifen , Wang Hongyang 
Published: June 2009

Abstract
Frequent exposure to nickel compounds has been considered as one of the potential causes of human lung cancer. However, the molecular mechanism of nickel-induced lung carcinogenesis remains obscure. In the current study, slight S-phase increase, significant G2/M cell cycle arrest, and proliferation blockage were observed in human bronchial epithelial cells (Beas-2B) upon nickel exposure. Moreover, the induction of cyclin D1 and cyclin E by nickel was shown for the first time in human pulmonary cells, which may be involved in nickel-triggered G1/S transition and cell transformation. In addition, we verified that hypoxia-inducible factor-1α, an important transcription factor of nickel response, was not required for the cyclin D1 or cyclin E induction. The role of p53 in nickel-induced G2/M arrest was excluded, respecting that its protein level, ser15 phosphorylation, and transcriptional activity were not changed in nickel response. Further study revealed that cyclin A was not activated in nickel response, and cyclin B1, which not only promotes G2/M transition but also prevents M-phase exit of cells if not degraded in time, was up-regulated by nickel through a manner independent of hypoxia-inducible factor. More importantly, our results verified that overexpressed cyclin B1, veiling the effect of cyclin D1 or cyclin E, mediated nickel-caused M-phase blockage and cell growth inhibition, which may render pulmonary cells more sensitive to DNA damage and facilitates cancer initiation. These results will not only deepen our understanding of the molecular mechanism involved in nickel carcinogenecity, but also lead to the further study on chemoprevention of nickel-associated human cancer. (Cancer Epidemiol Biomarkers Prev 2009;18(6):1720–9)
Matrix Metalloproteinase-2Polymorphisms and Breast Cancer Susceptibility
Authors: Beeghly-Fadiel Alicia , Lu Wei , Long Ji-Rong , Shu Xiao-ou , Zheng Ying , Cai Qiuyin , Gao Yu-Tang , Zheng Wei 
Published: June 2009

AbstractMatrix metalloproteinase-2 (MMP-2) is a well-known mediator of cancer metastasis but is also thought to be involved in several aspects of cancer development, including cell growth and inflammation. We comprehensively characterized genetic variation across the MMP-2 gene and evaluated associations with breast cancer risk using a two-phase (phase 1 and phase 2) study design. A total of 39 polymorphisms were genotyped among 6,066 Chinese women participating in the Shanghai Breast Cancer Study, a population-based case-control study. Two MMP-2 promoter polymorphisms were found to have consistent results between phase 1 and phase 2 participants, and to be significantly associated with breast cancer risk among all genotyped participants. Minor allele homozygotes for rs11644561 (G/A) were found to have a decreased risk of breast cancer [odds ratio (OR), 0.6; 95% confidence interval (CI), 0.3-1.0] compared with major allele homozygotes, as were minor allele homozygotes for rs11643630 (T/G) compared with major allele homozygotes (OR, 0.8; 95% CI, 0.7-1.0). When analyzed together, a rare haplotype (4.4%) with both rs11644561 A and rs11643630 G was found to have a significantly reduced risk of breast cancer (OR, 0.6; 95% CI, 0.4-0.8). In addition, rare allele homozygotes for rs243865 (−1306 C/T) tended to have an increased risk of breast cancer (OR, 1.4; 95% CI, 0.9-2.4). Together, these findings support a role for MMP-2 genetic variation in breast cancer susceptibility. (Cancer Epidemiol Biomarkers Prev 2009;18(6):1770–6)
Increase in Incidence of Colorectal Cancer Among Young Men and Women in the United States
Authors: Siegel Rebecca L. , Jemal Ahmedin , Ward Elizabeth M. 
Published: June 2009

AbstractThe recent, accelerated decline in colorectal cancer incidence rates has largely been attributed to an increase in screening rates among adults 50 years and older. We used data from 13 Surveillance, Epidemiology, and End Results cancer registries to report on colorectal cancer incidence trends from 1992 through 2005 among adults under age 50 years, for whom screening is not recommended for persons at average risk, by sex, race/ethnicity, age, stage at diagnosis, and anatomic subsite. Overall, incidence rates of colorectal cancer per 100,000 young individuals (ages 20-49 years) increased 1.5% per year in men and 1.6% per year in women from 1992 to 2005. Among non-Hispanic Whites, rates increased for both men and women in each 10-year age grouping (20-29, 30-39, and 40-49 years) and for every stage of diagnosis. The increase in incidence among non-Hispanic Whites was predominantly driven by rectal cancer, for which there was an average increase of 3.5% per year in men and 2.9% per year in women over the 13-year study interval. In contrast to the overall decreasing trend in colorectal cancer incidence in the United States, rates are increasing among men and women under age 50 years. Further studies are necessary to elucidate causes for this trend and identify potential prevention and early detection strategies. (Cancer Epidemiol Biomarkers Prev 2009;18(6):1695–8)