bluuebunny/crossref_metadata_2025_split huggingface dataset:
PREDICTION OF NONLINEAR SYSTEM IN OPTICS USING GENETIC PROGRAMMING
Authors: RADI AMR 
Published: June 2007

It is difficult to predict the dynamics of systems which are nonlinear and whose characteristic is unknown. In order to build a model of the system from input and output data without any knowledge about the system, we try automatically to build prediction model by Genetic Programming (GP). GP has been used to discover the function that describes nonlinear system to study the effect of wavelength and temperature on the refractive index of the fiber core. The predicted distribution from the GP based model is compared with the experimental data. The discovered function of the GP model has proved to be an excellent match to the experimental data.
Promoter Hypermethylation of Tumor Suppressor Genes in Urine from Patients with Cervical Neoplasia
Authors: Feng Qinghua , Hawes Stephen E. , Stern Joshua E. , Dem Amadou , Sow Papa Salif , Dembele Birama , Toure Papa , Sova Pavel , Laird Peter W. , Kiviat Nancy B. 
Published: June 2007

Abstract
We examined the feasibility of using detection of high-risk human papillomavirus (HPV) DNA in combination with the presence of aberrantly methylated genes (DAPK1, RARB, TWIST1, and CDH13) for urine-based cervical cancer screening. Urine samples from 129 Senegalese women, aged 35 years or older, 110 with (same day) biopsy-proven cervical neoplasia [cervical intraepithelial neoplasia grade 1 (CIN-1): n = 9; CIN-2–3/carcinoma in situ (CIS): n = 29; invasive cervical cancer (ICC): n = 72], and 19 without cervical neoplasia on biopsy were examined. Hypermethylation of at least one of the four genes identified 62% of ICC and 28% of CIN-2–3/CIS and was present in only 4% of CIN-1 or normal urines. High-risk HPV DNA was detected in urine in 70% of those with biopsy-proven ICC, 59% of those with CIN-2–3/CIS on biopsy, 44% of those with CIN-1 on biopsy, and only 11% of women negative for cervical neoplasia on biopsy. Urine-based detection of either high-risk HPV or hypermethylation of any of the four genes identified 84% of ICC, 64% of CIN-2–3/CIS, 44% of CIN-1, but only 19% of women negative for cervical neoplasia. The sensitivity for detection of CIN-2–3/CIS/ICC by high-risk HPV DNA or aberrant DNA methylation of four genes seems to be comparable to that of an exfoliated cervical cytology. This study shows the potential feasibility of using molecular markers detected in urine for cervical cancer screening. (Cancer Epidemiol Biomarkers Prev 2007;16(6):1178–84)
Exposure to Magnetic Fields and Survival after Diagnosis of Childhood Leukemia: A German Cohort Study
Authors: Svendsen Anne Louise , Weihkopf Thomas , Kaatsch Peter , Schüz Joachim 
Published: June 2007

Abstract
Inspired by a recent U.S. study showing poorer survival among children with acute lymphoblastic leukemia (ALL) exposed to magnetic fields above 0.3 μT, we examine this relationship in a German cohort of childhood leukemia cases derived from previous population-based case-control studies conducted between 1992 and 2001. A total of 595 ALL cases with 24-h magnetic field measurements are included in the analysis with a median follow-up of 9.5 years. We calculate the hazard ratios (HR) using the Cox proportional hazards model for overall survival, adjusted for age at diagnosis, calendar year of diagnosis, and gender. Elevated hazards are found for exposures between 0.1 and 0.2 μT [HR, 2.6; 95% confidence interval (95% CI), 1.3-5.2], based on 34 cases with 9 deaths as well as for exposures above 0.2 μT (HR, 1.6; 95% CI, 0.6-4.4), based on 18 cases with 4 deaths. After adjustment for prognostic risk group, the hazard for exposures above 0.2 μT increases to HR, 3.0 (95% CI, 0.9-9.8). In conclusion, this study is generally consistent with the previous finding; however, we report the excess risk at field levels lower than those in the U.S. study. In all, the evidence is still based on small numbers, and a biological mechanism to explain the findings is not known. (Cancer Epidemiol Biomarkers Prev 2007;16(6):1167–71)
Acceleration to Death from Liver Cancer in People with Hepatitis B Viral Mutations Detected in Plasma by Mass Spectrometry
Authors: Chen Jian Guo , Kuang Shuang Yuan , Egner Patricia A. , Lu Jian Hua , Zhu Yuan Rong , Wang Jin Bing , Zhang Bao Chu , Chen Tao Yang , Muñoz Alvaro , Kensler Thomas W. , Groopman John D. 
Published: June 2007

Abstract
Liver cancer is the leading cause of cancer death in many regions of the world. With the goal to discover biomarkers that reflect subsets of high-risk individuals and their prognosis, we nested our study in a male cohort of 5,581 hepatitis B surface antigen carriers in Qidong, People's Republic of China, who were recruited starting in 1989. By December 2003, 667 liver cancer cases were diagnosed in this group and plasma samples collected at the initial screening at enrollment were available in 515 cases who had succumbed to liver cancer. Hepatitis B virus (HBV) DNA could be isolated in 355 (69%) of these samples. In 14%, 15%, 19%, 31%, and 22%, screening took place at ≤1.5, 1.51 to 3, 3.01 to 5, 5.01 to 9, and &gt;9 years before death, respectively; and 39% died at age below 45 years. The relation between mutations in HBV and time to death were determined by logistic regression for the odds of mutation and by survival analyses methods with age as the time scale. In 279 (79%) of these individuals, the samples contained a two-nucleotide 1762T/1764A HBV mutation. Sixteen samples lacking the 1762T/1764A mutation had novel mutations elsewhere in the 1761 to 1767 region of the HBV genome. There was a statistically significant difference (P = 0.012) for the high prevalence of the HBV mutations in the men who died from hepatocellular carcinoma under the age of 45 years relative to those who died after 55 years of age and HBV mutations accelerated death (relative hazard, 1.40; 95% confidence interval, 1.06-1.85) and that the effect was attenuated by age from 2.04 for age 35 years to 1.0 for age 65 years with the 90% confidence band being above 1 for ages &lt;50 years. These findings provide a conceptual framework to explain the acceleration of mortality in individuals infected with HBV. (Cancer Epidemiol Biomarkers Prev 2007;16(6):1213–8)
The Future of Tobacco-Control Research
Authors: Morgan Glen D. , Backinger Cathy L. , Leischow Scott J. 
Published: June 2007

Abstract
Recent epidemiologic data on the stabilization of adult and youth smoking rates underscore the need for vigorous research across the cancer control spectrum on tobacco use interventions. The steady decline in adult rates of smoking has stalled for the first time in 8 years, and certain race, ethnic, and population groups are disproportionately at risk to tobacco-related cancers because of disparities in tobacco use or access to effective interventions. Although substantial progress has been made across levels of basic through applied research, tobacco-control research across the discovery and delivery continuum must be accelerated to further reduce the cancer burden. Following a brief review of the prevalence and trends affecting tobacco use initiation and cessation, we identify and describe four domains of extraordinary research opportunities: genetics and gene-environment interactions, bioinformatics and health informatics, disparities and disproportionate risk, and prevention and treatment. Evolutionary scientific changes, like rapidly advancing technology and emphasis on the paradigm of team science research approaches, provide both a challenge as well as unparalleled opportunities for scientific advancement and public health progress. (Cancer Epidemiol Biomarkers Prev 2007;16(6):1077–80)
Family History and the Risk of Kidney Cancer: a Multicenter Case-control Study in Central Europe
Authors: Hung Rayjean J. , Moore Lee , Boffetta Paolo , Feng Bing-Jian , Toro Jorge R. , Rothman Nathanial , Zaridze David , Navratilova Marie , Bencko Vladimir , Janout Vladimir , Kollarova Helena , Szeszenia-Dabrowska Neonila , Mates Dana , Chow Wong-Ho , Brennan Paul 
Published: June 2007

Abstract
An elevated familial relative risk may indicate either an important genetic component in etiology or shared environmental exposures within the family. Incidence rates of kidney cancer are particularly high in Central Europe, although no data were available on the familial aggregation or genetic background of kidney cancer in this region. We have, therefore, investigated the role of family history in first-degree relatives in a large multicenter case-control study in Central Europe. A total number of 1,097 cases of kidney cancer and 1,555 controls were recruited from 2000 to 2003 from seven centers in Czech Republic, Poland, Romania, and Russia. The risk of kidney cancer increased with the increasing number of relatives with history of any cancer [odds ratio (OR), 1.15; 95% confidence interval (95% CI), 1.00-1.31 per affected relative], and this association seemed to be more prominent among subjects with young onset (OR, 1.55; 95% CI, 1.09-2.20 per affected relative). Overall, the OR was 1.40 (95% CI, 0.71- 2.76) for the subjects who had at least one first-degree relative with kidney cancer after adjusting for tobacco smoking, body mass index, and medical history of hypertension, and this association was most apparent among subjects with affected siblings (OR, 4.09; 95% CI, 1.09-15.4). Based on the relative risk to siblings in our study population, we estimated that 80% of the kidney cancer cases are likely to occur in 20% of the population with the highest genetic risk, which indicate the importance of further investigation of genetic factors in cancer prevention for kidney cancer. (Cancer Epidemiol Biomarkers Prev 2007;16(6):1287–90)
Human Papillomavirus Prevalence and Type Distribution in Male Anogenital Sites and Semen
Authors: Nielson Carrie M. , Flores Roberto , Harris Robin B. , Abrahamsen Martha , Papenfuss Mary R. , Dunne Eileen F. , Markowitz Lauri E. , Giuliano Anna R. 
Published: June 2007

Abstract
Background: Human papillomavirus (HPV) is sexually transmitted and causes cervical cancer. Although HPV can infect men and women, little is known about infection in men. Specifically, the prevalence of type-specific HPV infection and the distribution of infections by anogenital anatomic site in men are incompletely characterized.
Methods: We tested 463 men ages 18 to 40 years for HPV at the glans/corona, penile shaft, scrotum, urethra, perianal area, anal canal, and in a semen sample. Eligible men acknowledged no history of genital warts and had sexual intercourse with a woman within the past year. HPV testing by PCR and reverse line blot genotyping for 37 types was conducted on each of the specimens from the seven sampling sites.
Results: When HPV results from any sampling site were considered, 237 (51.2%) men were positive for at least one oncogenic or nononcogenic HPV type, and another 66 (14.3%) men were positive for an unclassified HPV type. The types with the highest prevalence were HPV-16 (11.4%) and 84 (10.6%). External genital samples (glans/corona, shaft, and scrotum) were more likely than anal samples to contain oncogenic HPV (25.1% versus 5.0%). HPV-positive penile shaft and glans/corona samples were also more likely to be infected with multiple HPV types than other sites.
Conclusions: More complete anogenital sampling and sensitive detection for 37 HPV types resulted in a higher HPV prevalence in primarily asymptomatic men than reported previously. The penile shaft was the site most likely to be HPV positive and harbored the greatest proportion of multiple type and oncogenic infections. These results have implications for research of HPV among men and transmission between partners. (Cancer Epidemiol Biomarkers Prev 2007;16(6):1107–14)
The Role of Osteopontin in Tumor Progression and Metastasis in Breast Cancer
Authors: Rodrigues Lígia R. , Teixeira José A. , Schmitt Fernando L. , Paulsson Marie , Lindmark-Mänsson Helena 
Published: June 2007

Abstract
The use of cancer biomarkers to anticipate the outlines of disease has been an emerging issue, especially as cancer treatment has made such positive steps in the last few years. Progress in the development of consistent malignancy markers is imminent because advances in genomics and bioinformatics have allowed the examination of immense amounts of data. Osteopontin is a phosphorylated glycoprotein secreted by activated macrophages, leukocytes, and activated T lymphocytes, and is present in extracellular fluids, at sites of inflammation, and in the extracellular matrix of mineralized tissues. Several physiologic roles have been attributed to osteopontin, i.e., in inflammation and immune function, in mineralized tissues, in vascular tissue, and in kidney. Osteopontin interacts with a variety of cell surface receptors, including several integrins and CD44. Binding of osteopontin to these cell surface receptors stimulates cell adhesion, migration, and specific signaling functions. Overexpression of osteopontin has been found in a variety of cancers, including breast cancer, lung cancer, colorectal cancer, stomach cancer, ovarian cancer, and melanoma. Moreover, osteopontin is present in elevated levels in the blood and plasma of some patients with metastatic cancers. Therefore, suppression of the action of osteopontin may confer significant therapeutic activity, and several strategies for bringing about this suppression have been identified. This review looks at the recent advances in understanding the possible mechanisms by which osteopontin may contribute functionally to malignancy, particularly in breast cancer. Furthermore, the measurement of osteopontin in the blood or tumors of patients with cancer, as a way of providing valuable prognostic information, will be discussed based on emerging clinical data. (Cancer Epidemiol Biomarkers Prev 2007;16(6):1087–97)
Association of Polymorphisms in One-Carbon Metabolism Genes and Postmenopausal Breast Cancer Incidence
Authors: Stevens Victoria L. , McCullough Marjorie L. , Pavluck Alexandre L. , Talbot Jeffrey T. , Feigelson Heather S. , Thun Michael J. , Calle Eugenia E. 
Published: June 2007

Abstract
The interconversion of folates by the one-carbon metabolism pathway is essential for the synthesis of precursors used in DNA synthesis, repair, and methylation. Perturbations in this pathway can disrupt these processes and are hypothesized to facilitate carcinogenesis. We investigated associations of 25 candidate polymorphisms in nine one-carbon metabolism genes with risk of postmenopausal breast cancer using 502 cases and 505 controls from the Cancer Prevention II Nutrition Cohort. Four single nucleotide polymorphisms (SNP) in three different genes were significantly associated with breast cancer. The nonsynonymous R134K SNP in methylenetetrahydrofolate dehydrogenase/methenyltetrahydrofolate cyclohydrolase/formyltetrahydrofolate synthase [MTHFD1; odds ratio (OR), 1.40; 95% confidence interval (95% CI), 1.06-1.85 for CT + TT] and an intronic SNP in formyltetrahydrofolate dehydrogenase (FTHFD; OR, 2.23; 95% CI, 1.09-4.54 for CC) were associated with a significant increase in risk. Significantly decreased risk was associated with an intronic SNP in FTHFD (OR, 0.75; 95% CI, 0.58-0.98 for CT + CC) and the A360A SNP in cystathionine β-synthase (CBS; OR, 0.63; 95% CI, 0.41-0.96 for TT). The presence of at least one variant from both the methylenetetrahydrofolate reductase (MTHFR) C677T and A1298C SNPs was also associated with increased risk (OR, 2.16; 95% CI, 1.34-3.48 for 677 CT + TT/1,298 AC + CC). Investigations into interactions of the associated SNPs with each other and with dietary factors yielded inconclusive results. Our findings indicate that genetic variation in multiple one-carbon metabolism genes may influence risk of postmenopausal breast cancer and may involve changes in methyl donor synthesis. However, larger studies are needed to further examine gene/gene and gene/diet interactions in this pathway. (Cancer Epidemiol Biomarkers Prev 2007;16(6):1–8)
Sun Exposure and Prostate Cancer Risk: Evidence for a Protective Effect of Early-Life Exposure
Authors: John Esther M. , Koo Jocelyn , Schwartz Gary G. 
Published: June 2007

Abstract
Mounting experimental and epidemiologic evidence supports the hypothesis that vitamin D reduces the risk of prostate cancer. Some evidence suggests that prostate cancer risk may be influenced by sun exposure early in life. We analyzed data from the National Health and Nutrition Examination Survey I Epidemiologic Follow-up Study to examine associations of prostate cancer risk with early-life and adult residential sun exposure and adult sun exposures that were assessed through self-report, physician report, and dermatologic examination. We used solar radiation in the state of birth as a measure of sun exposure in early life. Follow-up from 1971 to 1975 (baseline) to 1992 identified 161 prostate cancer cases (102 nonfatal and 59 fatal) among non-Hispanic white men for whom sun exposure data were available. Significant inverse associations were found for men born in a region of high solar radiation (relative risk, 0.49, 95% confidence interval, 0.27-0.90 for high versus low solar radiation), with a slightly greater reduction for fatal than for nonfatal prostate cancer. Frequent recreational sun exposure in adulthood was associated with a significantly reduced risk of fatal prostate cancer only (relative risk, 0.47; 95% confidence interval, 0.23-0.99). These findings suggest that, in addition to sun exposure in adulthood, sun exposure in early life protects against prostate cancer. (Cancer Epidemiol Biomarkers Prev 2007;16(6):1283–6)
Association between Germline Variation in theFHITGene and Prostate Cancer in Caucasians and African Americans
Authors: Levin Albert M. , Ray Anna M. , Zuhlke Kimberly A. , Douglas Julie A. , Cooney Kathleen A. 
Published: June 2007

AbstractMany studies have established that loss of heterozygosity and/or altered expression of the fragile histidine triad (FHIT) gene is a common event in a number of tumor types including prostate carcinoma. Encompassing the most active fragile site in the human genome, FRA3B, FHIT has become the model fragile site–associated tumor suppressor gene. In a recent study, linkage and association between germline genetic variation in FHIT (specifically single nucleotide polymorphism rs760317) and prostate cancer were reported. We sought to confirm this finding in two independent samples: (a) a family-based sample of 817 men with (n = 434) and without (n = 383) prostate cancer from 323 Caucasian families, and (b) a community-based case-control sample of African American men with (n = 133) and without (n = 342) prostate cancer. Using a family-based association test, rs760317 was associated with prostate cancer in Caucasians (P = 0.031), with a reduction in the risk of prostate cancer among carriers of the minor allele (odds ratio, 0.66; 95% confidence interval, 0.42-1.04; P = 0.074). African American carriers experienced a similar risk reduction (odds ratio, 0.63; 95% confidence interval, 0.42-0.96; P = 0.032). These results are remarkably consistent across ethnic samples but are in opposition to results from the original study, which showed an association between the minor allele of rs760317 and an increased risk of prostate cancer. Taken together, the consistently significant but flipped association between single nucleotide polymorphism rs760317 and prostate cancer in three independent samples suggests that rs760317 may be in linkage disequilibrium with one or more prostate cancer susceptibility variants in or near FHIT. (Cancer Epidemiol Biomarkers Prev 2007;16(6):1294–7)
Serum Insulin-like Growth Factor (IGF)-I and IGF-Binding Protein-3 Concentrations and Prostate Cancer Risk: Results from the European Prospective Investigation into Cancer and Nutrition
Authors: Allen Naomi E. , Key Timothy J. , Appleby Paul N. , Travis Ruth C. , Roddam Andrew W. , Rinaldi Sabina , Egevad Lars , Rohrmann Sabine , Linseisen Jakob , Pischon Tobias , Boeing Heiner , Johnsen Nina Føns , Tjønneland Anne , Grønbæk Henning , Overvad Kim , Kiemeney Lambartus , Bueno-de-Mesquita H. Bas , Bingham Sheila , Khaw Kay Tee , Tumino Rosario , Berrino Franco , Mattiello Amalia , Sacerdote Carlotta , Palli Domenico , Quirós José Ramón , Ardanaz Eva , Navarro Carmen , Larrañaga Nerea , Gonzalez Carlos , Sanchez Maria-José , Trichopoulou Antonia , Travezea Cryssoula , Trichopoulos Dimitrios , Jenab Mazda , Ferrari Pietro , Riboli Elio , Kaaks Rudolf 
Published: June 2007

Abstract
Background: Some studies suggest that elevated serum insulin-like growth factor (IGF)-I concentrations are associated with an increased risk of prostate cancer and, in particular, with an increased risk of advanced-stage prostate cancer.
Methods: We analyzed the association between prediagnostic serum concentrations of IGF-I and IGF-binding protein-3 (IGFBP-3) and prostate cancer risk in a case-control study nested in the European Prospective Investigation into Cancer and Nutrition. This study includes 630 incident prostate cancer cases and 630 matched control subjects. Odds ratios and their 95% confidence intervals (95% CI) were calculated for prostate cancer risk associated with increasing IGF-I and IGFBP-3 concentrations using conditional logistic regression.
Results: The risk of total prostate cancer in the highest versus the lowest third of serum peptide concentration was 1.35 (95% CI, 0.99-1.82; Ptrend = 0.08) for IGF-I, 1.39 (95% CI, 1.02-1.89; Ptrend = 0.12) for the IGF-I residuals after adjusting for IGFBP-3, 1.22 (95% CI, 0.92-1.64; Ptrend = 0.38) for IGFBP-3, and 1.01 (95% CI, 0.74-1.37; Ptrend = 0.75) for the IGFBP-3 residuals after adjusting for IGF-I. There was no significant difference in the association of peptide hormones and prostate cancer by stage of disease, although the association of serum IGF-I concentration with risk was slightly stronger for advanced-stage disease; the odds ratio for the highest versus the lowest third was 1.65 (95% CI, 0.88-3.08; Ptrend = 0.21) for IGF-I and 1.76 (95% CI, 0.92-3.40; Ptrend = 0.11) for IGF-I adjusted for IGFBP-3.
Conclusions: In this large nested case-control study, serum IGF-I concentration is not strongly associated with prostate cancer risk, although the results are compatible with a small increase in risk, particularly for advanced-stage disease; no association for IGFBP-3 was observed. (Cancer Epidemiol Biomarkers Prev 2007;16(6):1121–7)