bluuebunny/crossref_metadata_2025_split huggingface dataset:
A Novel Nonobese Diabetic/Severe Combined Immunodeficient Xenograft Model for Chronic Lymphocytic Leukemia Reflects Important Clinical Characteristics of the Disease
Authors: Dürig Jan , Ebeling Peter , Grabellus Florian , Sorg Ursula R. , Möllmann Michael , Schütt Philipp , Göthert Joachim , Sellmann Ludger , Seeber Siegfried , Flasshove Michael , Dührsen Ulrich , Moritz Thomas 
Published: September 2007

Abstract
We here describe a novel xenograft model of chronic lymphocytic leukemia (CLL) generated by infusion of human primary CLL cells into immunodeficient nonobese/severe combined immunodeficient (NOD/SCID) mice. Combined i.v. and i.p. injection of peripheral blood mononuclear cells (PBMC) from 39 patients with CLL resulted in highly reproducible splenic (37 of 39) and peritoneal (35 of 39) engraftment, which remained stable over a time span of 4 to 8 weeks. By comparison, recovery of leukemic cells from bone marrow (21 of 39) or peripheral blood (8 of 22) was substantially lower. The engraftment pattern of CLL PBMC 4 weeks posttransplant was correlated with clinical disease activity: infusion of PBMC from donors with Binet stage A, lymphocyte doubling time of &gt;12 months, and normal lactate dehydrogenase (LDH) serum levels led to marked engraftment of T cells whereas comparably few tumor cells could be detected. In contrast, NOD/SCID mice receiving PBMC from donors with advanced stage Binet C, lymphocyte doubling time of &lt;12 months, and elevated LDH serum levels exhibited predominant engraftment of tumor cells and comparably low numbers of T cells. These results suggest that this model reflects the heterogeneity and important clinical characteristics of the disease, and thus may serve as a tool for preclinical drug testing and investigation of the pathophysiology of CLL. [Cancer Res 2007;67(18):8653–61]
Mastermind-like 1 Is a Specific Coactivator of β-Catenin Transcription Activation and Is Essential for Colon Carcinoma Cell Survival
Authors: Alves-Guerra Marie-Clotilde , Ronchini Chiara , Capobianco Anthony J. 
Published: September 2007

Abstract
Misregulation of the Wnt signaling pathway has been linked to many human cancers including colon carcinoma and melanoma. The primary mediator of the oncogenic effects of the Wnt signaling pathway is β-catenin. Accumulation of nuclear β-catenin and transcription activation of lymphoid enhancer factor 1 (LEF1)/T-cell factor (TCF) target genes underlie the oncogenic activity. However, the mechanism of β-catenin–mediated transcriptional activation remains poorly understood. In this study, we identified Mastermind-like 1 (Maml1), which is thought to be a specific coactivator for the Notch pathway, as a coactivator for β-catenin. We found that Maml1 participates in the Wnt signaling by modulating the β-catenin/TCF activity. We show in vivo that Maml1 is recruited by β-catenin on the cyclin D1 and c-Myc promoters. Importantly, we show that Maml1 functions in the Wnt/β-catenin pathway independently of Notch signaling. Finally, we show that the knockdown of Mastermind-like family proteins in colonic carcinoma cells results in cell death by affecting β-catenin–induced expression of cyclin D1 and c-Myc. This is the first demonstration of a role for the Mastermind-like family in another signaling pathway and that the knockdown of Mastermind-like family function leads to tumor cell death. [Cancer Res 2007;67(18):8690–8]
Gestational Age and Fetal Growth in Relation to Maternal Ovarian Cancer Risk in a Swedish Cohort
Authors: Mucci Lorelei A. , Dickman Paul W. , Lambe Mats , Adami Hans-Olov , Trichopoulos Dimitrios , Riman Tomas , Hsieh Chung-cheng , Cnattingius Sven 
Published: September 2007

Abstract
Background: Pregnancy influences subsequent maternal ovarian cancer risk. To date, there is limited evidence whether two characteristics of pregnancy, gestational age and birth weight, could modify risk.
Materials and Methods: We studied 1.1 million Swedish women who delivered singleton births between 1973 and 2001. Information on infant gestational age and birth weight was abstracted from the nationwide Swedish Birth Register. Women were followed prospectively through linkage with other population-based registers for occurrence of ovarian cancer, death, or emigration through 2001. Hazard ratios [relative risk (RR), 95% confidence interval (95% CI)] from Cox models were used to estimate associations between gestational age, birth weight, and epithelial ovarian cancer risk.
Results: During 12.6 million person-years, 1,017 epithelial ovarian cancers occurred. Mean age at diagnosis was 43 years. Compared with women with term deliveries (≥40 weeks), women with moderately (35-36 weeks) or very (&lt;35 weeks) preterm deliveries had increased risks of epithelial ovarian cancer (RR 1.4, 95% CI 1.0-2.0 and RR 2.3, 95% CI 1.3-3.8, respectively). In contrast, women giving birth to small-for-gestational-age babies had a reduced risk (RR 0.7, 95% CI 0.4-1.0). Stratifying on birth weight and gestational age, there was a strong protective effect of low birth weight on maternal risk of epithelial ovarian cancer among term deliveries, whereas birth weight seemed to have little effect among preterm births (Pinteraction = 0.022).
Conclusions: Our results lend further support that the hormonal milieu of a pregnancy may modify long-term risk of developing ovarian cancer. (Cancer Epidemiol Biomarkers Prev 2007;16(9):1828–32)
Atypia and DNA Methylation in Nipple Duct Lavage in Relation to Predicted Breast Cancer Risk
Authors: Euhus David M. , Bu Dawei , Ashfaq Raheela , Xie Xian-Jin , Bian Aihua , Leitch A. Marilyn , Lewis Cheryl M. 
Published: September 2007

AbstractBackground: Tumor suppressor gene (TSG) methylation is identified more frequently in random periareolar fine needle aspiration samples from women at high risk for breast cancer than women at lower risk. It is not known whether TSG methylation or atypia in nipple duct lavage (NDL) samples is related to predicted breast cancer risk.Methods: 514 NDL samples obtained from 150 women selected to represent a wide range of breast cancer risk were evaluated cytologically and by quantitative multiplex methylation-specific PCR for methylation of cyclin D2, APC, HIN1, RASSF1A, and RAR-β2.Results: Based on methylation patterns and cytology, NDL retrieved cancer cells from only 9% of breasts ipsilateral to a breast cancer. Methylation of ≥2 genes correlated with marked atypia by univariate analysis, but not multivariate analysis, that adjusted for sample cellularity and risk group classification. Both marked atypia and TSG methylation independently predicted abundant cellularity in multivariate analyses. Discrimination between Gail lower-risk ducts and Gail high-risk ducts was similar for marked atypia [odds ratio (OR), 3.48; P = 0.06] and measures of TSG methylation (OR, 3.51; P = 0.03). However, marked atypia provided better discrimination between Gail lower-risk ducts and ducts contralateral to a breast cancer (OR, 6.91; P = 0.003, compared with methylation OR, 4.21; P = 0.02).Conclusions: TSG methylation in NDL samples does not predict marked atypia after correcting for sample cellularity and risk group classification. Rather, both methylation and marked atypia are independently associated with highly cellular samples, Gail model risk classifications, and a personal history of breast cancer. This suggests the existence of related, but independent, pathogenic pathways in breast epithelium. (Cancer Epidemiol Biomarkers Prev 2007;16(9):1812–21)
The Association of a Tobacco-Specific Biomarker and Cigarette Consumption and Its Dependence on Host Characteristics
Authors: Lubin Jay H. , Caporaso Neil , Hatsukami Dorothy K. , Joseph Anne M. , Hecht Stephen S. 
Published: September 2007

AbstractThe tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is a potent carcinogen, which can be characterized by urinary concentrations of the metabolite 4-(methylnitrosamino)-1-(3-pyridyl)-butanol (NNAL) and its glucuronide. Using baseline data in current smokers from four clinical trials, we examine the associations of urinary cotinine with CPD and of total NNAL with cotinine and the modification of these associations by several host factors. There was a linear relationship between ln(cotinine) and ln(CPD) within categories of the Fagerstrom Test of Nicotine Dependence and of age. The increasing trend was significantly smaller for subjects with high and very high nicotine addiction and for older subjects and larger in females than males. The regression of ln(total NNAL/cotinine) on ln(cotinine) declined linearly, suggesting reduced NNK uptake per unit cotinine with increasing cotinine. The decline in trend was greater in subjects with increased CPD, with greater nicotine addiction, and at older ages and was smaller in females, although gender differences were small. Variations in the ratio with host characteristics were generally similar to a recent epidemiologic analysis of effect modification of the association between lung cancer and cigarette smoking. (Cancer Epidemiol Biomarkers Prev 2007;16(9):1852–7)
Noninvasive Prediction of Prostatic DNA Damage by Oxidative Stress Challenge of Peripheral Blood Lymphocytes
Authors: Waters David J. , Shen Shuren , Xu Huiping , Kengeri Seema S. , Cooley Dawn M. , Chiang Emily C. , Chen Yu , Schlittler Deborah , Oteham Carol , Combs Gerald F. , Glickman Lawrence T. , Morris J. Steven , Bostwick David G. 
Published: September 2007

Abstract
To move closer to the goal of individualized risk prediction for prostate cancer, we used an in vivo canine model to evaluate whether the susceptibility of peripheral blood lymphocytes (PBLs) to oxidative stress-induced DNA damage could identify those individuals with the highest prostatic DNA damage. This hypothesis was tested in a population of 69 elderly male beagle dogs after they had completed a 7-month randomized feeding trial to achieve the broad range of dietary selenium status observed in U.S. men. The alkaline Comet assay was used to directly compare the extent of DNA damage in PBLs with prostatic DNA damage in each dog. Using stepwise logistic regression, the sensitivity of PBLs to oxidative stress challenge with hydrogen peroxide (H2O2) predicted dogs in the highest tertile of prostatic DNA damage. Dogs with PBLs highly sensitive to H2O2 were 7.6 times [95% confidence interval (95% CI), 1.5-38.3] more likely to have high prostatic DNA damage than those in the H2O2-resistant group. This risk stratification was observed in multivariate analysis that considered other factors that might influence DNA damage, such as age, toenail selenium concentration, and serum testosterone concentration. Our data show that the sensitivity of PBLs to oxidative stress challenge, but not endogenous DNA damage in PBLs, provides a noninvasive surrogate marker for prostatic DNA damage. These findings lend support to the concept that oxidative stress contributes to genotoxic damage, and that oxidative stress challenge may stratify men for prostate cancer risk. (Cancer Epidemiol Biomarkers Prev 2007;16(9):1906–10)
Oral Contraceptives and Survival in Breast Cancer Patients Aged 20 to 54 Years
Authors: Trivers Katrina F. , Gammon Marilie D. , Abrahamson Page E. , Lund Mary Jo , Flagg Elaine W. , Moorman Patricia G. , Kaufman Jay S. , Cai Jianwen , Porter Peggy L. , Brinton Louise A. , Eley J. William , Coates Ralph J. 
Published: September 2007

Abstract
Recent oral contraceptive (OC) use is associated with modestly higher breast cancer incidence among younger women, but its impact on survival is unclear. This study examined the relationship between OC use before breast cancer diagnosis and survival. A population-based sample of 1,264 women aged 20 to 54 years with a first primary invasive breast cancer during 1990 to 1992 were followed up for 8 to 10 years. OC and covariate data were obtained by interviews conducted shortly after diagnosis and from medial records. All-cause mortality was ascertained through the National Death Index (n = 292 deaths). Age- and income-adjusted hazard ratios (HR) and 95% confidence intervals (95% CI) were estimated by Cox regression methods. All-cause mortality was not associated with ever use of OCs or duration of use. Compared with nonusers, mortality estimates were elevated among women who were using OCs at diagnosis or stopped use in the previous year (HR, 1.57; 95% CI, 0.95-2.61). The HR for use of high-dose estrogen pills within 5 years before diagnosis was double that of nonusers (HR, 2.39; 95% CI, 1.29-4.41) or, if the most recent pill included the progestin levonorgestrel, compared with nonusers (HR, 2.01; 95% CI, 1.03-3.91). Because subgroup estimates were based on small numbers of OC users, these results should be cautiously interpreted. Overall, most aspects of OC use did not seem to influence survival, although there is limited evidence that OC use just before diagnosis, particularly use of some pill types, may negatively impact survival in breast cancer patients aged 20 to 54 years. (Cancer Epidemiol Biomarkers Prev 2007;16(9):1822–7)
Carbonic Anhydrase IX Is Highly Expressed in Hereditary Nonpolyposis Colorectal Cancer
Authors: Niemelä Anssi M. , Hynninen Piritta , Mecklin Jukka-Pekka , Kuopio Teijo , Kokko Antti , Aaltonen Lauri , Parkkila Anna-Kaisa , Pastorekova Silvia , Pastorek Jaromir , Waheed Abdul , Sly William S. , Ørntoft Torben F. , Kruhøffer Mogens , Haapasalo Hannu , Parkkila Seppo , Kivelä Antti J. 
Published: September 2007

Abstract
Carbonic anhydrase (CA) II, CA IX, and CA XII are expressed in various neoplasias and have been linked to tumorigenesis. We examined their expression in three different groups of colorectal cancer [i.e., microsatellite stable (MSS), microsatellite instable (MSI), and hereditary nonpolyposis colorectal cancer (HNPCC)]. First, we analyzed gene expression profiles of 113 specimens by a microarray method to study the expression of various CA isozymes in the subgroups of colorectal cancer. The results indicated that mRNAs for CA II and CA XII are down-regulated and CA IX mRNA is up-regulated in all three tumor categories when compared with the normal tissue. The up-regulation of CA IX was greatest in the HNPCC group. For more information, 77 specimens were immunohistochemically stained to study the levels of CA II, CA IX, and CA XII. Immunohistochemical analyses further confirmed that the subgroups express CA II, CA IX, and CA XII differentially, and the HNPCC tumors express high levels of CA IX. Expression of these CAs did not correlate to Dukes stage or grade of differentiation. Our results show that CAs are differentially expressed in the subgroups of colorectal cancer, and CA IX expression seems to be very high in most cases of HNPCC. CA IX could be a potential diagnostic and therapeutic target in HNPCC. (Cancer Epidemiol Biomarkers Prev 2007;16(9):1760–6)
Cytoplasmic Clusterin Expression Is Associated with Longer Survival in Patients with Resected Non–Small Cell Lung Cancer
Authors: Albert Jeffrey M. , Gonzalez Adriana , Massion Pierre P. , Chen Heidi , Olson Sandra J. , Shyr Yu , Diaz Roberto , Lambright Eric S. , Sandler Alan , Carbone David P. , Putnam Joe B. , Johnson David H. , Lu Bo 
Published: September 2007

Abstract
Background: Clusterin is a glycoprotein that has been implicated in many processes, including apoptosis, cell cycle regulation, and DNA repair. Previous studies have examined the prognostic value of clusterin expression in various malignancies. In the present study, we examined clusterin staining in tumors resected from patients with non–small cell lung cancer (NSCLC).
Materials and Methods: Tumor specimens were obtained for 113 patients with completely resected NSCLC from paraffin-embedded tissue microarrays and stained with an antibody specific for clusterin. Staining patterns were observed and graded based on intensity and then correlated with clinical data.
Results: Positive cytoplasmic clusterin staining was observed in 44 patients, and weak/negative staining was observed in 62 patients. Patients who had tumors that stained positive for cytoplasmic clusterin had significantly longer survival in multivariate analysis (hazard ratio 0.487, 95% confidence interval 0.27-0.89). A correlation was also observed for recurrence-free survival, which approached statistical significance (hazard ratio 0.345, 95% confidence interval 0.12-1.02). In univariate analysis, patients with clusterin-positive tumors had a 63% 3-year survival, whereas patients with clusterin-negative tumors had a 42% 3-year survival (P = 0.0108); clusterin-positive tumors also had significantly less recurrence (P = 0.0231).
Conclusions: Cytoplasmic clusterin staining is present in a substantial number of NSCLC tumors and may be a biomarker for longer survival in patients with surgically resected NSCLC. (Cancer Epidemiol Biomarkers Prev 2007;16(9):1845–51)
Accuracy of Colorectal Polyp Self-Reports: Findings from the Colon Cancer Family Registry
Authors: Madlensky Lisa , Daftary Darshana , Burnett Terrilea , Harmon Patricia , Jenkins Mark , Maskiell Judi , Nigon Sandra , Phillips Kerry , Templeton Allyson , Limburg Paul J. , Haile Robert W. , Potter John D. , Gallinger Steven , Baron John A. 
Published: September 2007

Abstract
Introduction: Colorectal adenomas and other types of polyps are commonly used as end points or risk factors in epidemiologic studies. However, it is not known how accurately patients are able to self-report the presence or absence of adenomas following colonoscopy.
Methods: Participants in the Colon Cancer Family Registry provided self-reports of recent colorectal cancer (CRC) screening activity, and whether or not they had ever been told they had a polyp. Positive and negative predictive values for polyp self-report were calculated by comparing medical records with self-reports from 488 participants.
Results: The positive predictive value for self-reported polyp was 80.9%, and the negative predictive value was 85.8%. The predictive values did not differ by age group or sex, but participants with a previous diagnosis of CRC had a lower negative predictive value (76.2%) than participants with no personal history of CRC (89.0%; P = 0.04).
Conclusions: Predictive values for self-reports of polyps are fairly high, but researchers needing accurate polyp data should obtain medical record confirmation. Pursuing medical records on only those participants self-reporting a polyp could result in an underestimation of the polyp prevalence in a study population. (Cancer Epidemiol Biomarkers Prev 2007;16(9):1898–901)
Demographic and Pathologic Differences in the Incidence of Invasive Penile Cancer in the United States, 1995-2003
Authors: Goodman Marc T. , Hernandez Brenda Y. , Shvetsov Yurii B. 
Published: September 2007

Abstract
Objective: Penile cancer is an uncommon malignancy, so few descriptive or analytic studies have been reported in the literature. The objective of this analysis was to describe the distribution of penile cancer in the United States by demographic, pathologic, and clinical features.
Methods: Penile cancer among 6,539 men was identified through 29 population-based registries in the United States during the period 1995-2003. These registries were estimated to represent 68% of the U.S. population. Age-adjusted incidence rates were calculated per million population using counts derived from the 2000 U.S. census. A subset of nine registries was used to examine time trends in penile cancer between 1973 and 2003.
Results: Squamous cell carcinomas were the most common histologic type of penile cancer, representing 93% of all malignancies. Hispanic men had the highest age-adjusted incidence rates per million for penile cancer (6.58 per million), followed by Blacks (4.02 per million), Whites (3.90 per million), American Indians (2.81 per million), and Asian-Pacific Islanders (2.40 per million). The highest rates of penile cancer were found among Hispanic men (46.9 per million) and Black men (36.2 per million) of ages ≥85 years. Penile malignancy was rare among males under age 20 years. Time trend analysis supported a significant decrease in the incidence of penile cancer for Blacks (annual percent change, −1.9%) and Whites (annual percent change, −1.2%). The majority (61%) of penile cancers were diagnosed at a localized stage among all racial and ethnic groups, although Hispanic and Black men tended to be diagnosed at more advanced stages than Whites. No racial or ethnic differences in tumor grade were identified. The incidence of penile cancer was highest in the South (4.42 per million) and lowest in the West (3.28 per million) of the United States. The highest age-adjusted incidence rate was found among Black men in the South (4.77 per million) and the lowest rate among Asian-Pacific Islanders in the West (1.84 per million).
Conclusions: This analysis showed significant racial/ethnic and regional variation in the incidence of penile cancer. The high rate of penile cancer among Hispanic and Southern Black men suggests differences in risk factors for this malignancy, such as circumcision, hygiene, or human papillomavirus exposure. (Cancer Epidemiol Biomarkers Prev 2007;16(9):1833–9)
Genetic Variability in Iron-Related Oxidative Stress Pathways (Nrf2, NQ01, NOS3, andHO-1), Iron Intake, and Risk of Postmenopausal Breast Cancer
Authors: Hong Chi-Chen , Ambrosone Christine B. , Ahn Jiyoung , Choi Ji-Yeob , McCullough Marjorie L. , Stevens Victoria L. , Rodriguez Carmen , Thun Michael J. , Calle Eugenia E. 
Published: September 2007

AbstractOxidative stress resulting from excess reactive oxygen species and/or deficiencies in antioxidant capabilities may play a role in breast cancer etiology. In a nested case-control study of postmenopausal women (505 cases and 502 controls) from the American Cancer Society Prevention II Nutrition Cohort, we examined relationships between breast cancer risk and genetic polymorphisms of enzymes involved in the generation and removal of iron-mediated reactive oxygen species. Using unconditional logistic regression, genetic variations in Nrf2 (11108C&gt;T), NQO1 (609C&gt;T), NOS3 (894G&gt;T), and HO-1 [(GT)n dinucleotide length polymorphism] were not associated with breast cancer risk in a multivariate model. A significant dose trend (P trend = 0.04), however, was observed for total number of putative “at-risk” alleles (Nrf T, NQO1 T, NOS T, and HO-1 LL and LM genotypes), with those carrying three or more at-risk alleles having an odds ratio (OR) of 1.56 [95% confidence interval (95% CI), 0.97-2.51] compared with those having none. When examined in relation to iron, carriage of three or more high-risk alleles in the highest tertile of iron intake (OR, 2.27; 95% CI, 0.97-5.29; P trend = 0.02; P interaction = 0.30) or among users of supplemental iron (OR, 2.39; 95% CI, 1.09-5.26; P trend = 0.02; P interaction = 0.11) resulted in a greater than 2-fold increased risk compared with women with no high-risk alleles. Increased risk was also observed among supplement users with the HO-1 LL or LM genotypes (OR, 1.56; 95% CI, 1.01-2.41; P interaction = 0.32) compared with S allele carriers and MM genotypes combined. These results indicate that women with genotypes resulting in potentially higher levels of iron-generated oxidative stress may be at increased risk of breast cancer and that this association may be most relevant among women with high iron intake. (Cancer Epidemiol Biomarkers Prev 2007;16(9):1784–94)