bluuebunny/crossref_metadata_2025_split huggingface dataset:
The utility of magnetic resonance imaging and spectroscopy for predicting insignificant prostate cancer: an initial analysis
Authors: Shukla‐Dave Amita , Hricak Hedvig , Kattan Michael W. , Pucar Darko , Kuroiwa Kentaro , Chen Hui‐Ni , Spector Jessica , Koutcher Jason A. , Zakian Kristen L. , Scardino Peter T. 
Published: January 2007

OBJECTIVETo design new models that combine clinical variables and biopsy data with magnetic resonance imaging (MRI) and MR spectroscopic imaging (MRSI) data, and assess their value in predicting the probability of insignificant prostate cancer.PATIENTS AND METHODSIn all, 220 patients (cT stage T1c or T2a, prostate‐specific antigen level <20 ng/mL, biopsy Gleason score 6) had MRI/MRSI before surgery and met the inclusion criteria for the study. The probability of insignificant cancer was recorded retrospectively and separately for MRI and combined MRI/MRSI on a 0–3 scale (0, definitely insignificant; − 3, definitely significant). Insignificant cancer was defined from surgical pathology as organ‐confined cancer of ≤ 0.5 cm3 with no poorly differentiated elements. The accuracy of predicting insignificant prostate cancer was assessed using areas under receiver operating characteristic curves (AUCs), for previously reported clinical models and for newly generated MR models combining clinical variables, and biopsy data with MRI data (MRI model) and MRI/MRSI data (MRI/MRSI model).RESULTSAt pathology, 41% of patients had insignificant cancer; both MRI (AUC 0.803) and MRI/MRSI (AUC 0.854) models incorporating clinical, biopsy and MR data performed significantly better than the basic (AUC 0.574) and more comprehensive medium (AUC 0.726) clinical models. The P values for the differences between the models were: base vs medium model, <0.001; base vs MRI model, <0.001; base vs MRI/MRSI model, <0.001; medium vs MRI model, <0.018; medium vs MRI/MRSI model, <0.001.CONCLUSIONSThe new MRI and MRI/MRSI models performed better than the clinical models for predicting the probability of insignificant prostate cancer. After appropriate validation, the new MRI and MRI/MRSI models might help in counselling patients who are considering choosing deferred therapy.
Kgtests: a simple Excel Macro program to detect signatures of population expansion using microsatellites
Authors: BİLGİN RAİT 
Published: January 2007

AbstractA simple Microsoft Excel Macro application (kgtests) that performs the k and g tests for detecting population expansion is described. The application, being an Excel Macro, facilitates the ease of preparation of the input file and makes it possible to use the application in any machine that can run Excel.
Microsatellite loci for the progenetic trematode, Coitocaecum parvum (Opecoelidae)
Authors: LAGRUE CLÉMENT , WATERS JONATHAN M. , POULIN ROBERT , KEENEY DEVON B. 
Published: January 2007

AbstractNine polymorphic microsatellite loci were characterized from the freshwater trematode Coitocaecum parvum. This parasite can either reproduce sexually in the definitive host or produce eggs by selfing inside its second intermediate host. Two to 11 alleles per locus were detected in 24 trematode sporocysts and observed heterozygosities ranged from 0.04 to 0.96. These loci will be useful for identifying parasite genetic clones within hosts and testing for effects of relatedness on parasite life history strategy.
Comparison of a SYBR Green I-Based Assay with a Histidine-Rich Protein II Enzyme-Linked Immunosorbent Assay for In Vitro Antimalarial Drug Efficacy Testing and Application to Clinical Isolates
Authors: Bacon David J. , Latour Christine , Lucas Carmen , Colina Olga , Ringwald Pascal , Picot Stéphane 
Published: January 2007

ABSTRACT

In vitro drug susceptibility testing with the malaria parasite has been used to assess the antimalarial activities of new compounds and to monitor drug resistance in field isolates. We investigated the validity of a SYBR green I fluorescent-based assay under various culture conditions and compared the assay results to those of previously published histidine-rich protein II (HRPII) enzyme-linked immunosorbent assay (ELISA) methods. Reference strains of
Plasmodium falciparum
were cultured in vitro by using standard conditions in complete medium with and without phenol red before they were dispensed into 96-well plates predosed with chloroquine, mefloquine, or quinine. Following incubation, the culture supernatants were divided and the 50% inhibitory concentrations (IC
50
s) were determined by using a SYBR green I-based method and the HRPII capture ELISA method. There were no significant differences in IC
50
values when phenol red was included in the medium. The IC
50
s and the IC
90
s of the antimalarials tested by both methods were similar or identical for each of the reference strains. Fresh clinical isolates of
P. falciparum
collected from imported cases of malaria in Lyon, France, were tested for in vitro resistance to chloroquine and mefloquine by using the validated SYBR green I and HRPII ELISA methods. The SYBR green I-based method was able to calculate IC
50
and IC
90
values similar or identical to those calculated by the HRPII assay with fresh clinical samples without removal of white blood cells. The SYBR green I-based method for determination of drug sensitivity levels produced results comparable to those produced by other methods, showing that this method can be used routinely to conduct surveillance for drug resistance in
P. falciparum
with fresh or cultured parasites.
Mutagenesis and Repair in
Bacillus anthracis
: the Effect of Mutators
Authors: Zeibell Krystle , Aguila Sharon , Yan Shi Vivian , Chan Andrea , Yang Hanjing , Miller Jeffrey H. 
Published: January 2007

ABSTRACT

We have generated mutator strains of
Bacillus anthracis
Sterne by using directed gene knockouts to investigate the effect of deleting genes involved in mismatch repair, oxidative repair, and maintaining triphosphate pools. The single-knockout strains are deleted for
mutS
,
mutY
,
mutM
, or
ndk
. We also made double-knockout strains that are
mutS ndk
or
mutY mutM
. We have measured the levels of mutations in the
rpoB
gene that lead to the Rif
r
phenotype and have examined the mutational specificity. In addition, we examined the mutational specificity of two mutagens, 5-azacytidine and
N
-methyl-
N
′-nitro-
N
-nitroso-guanidine. The
mutY
and
mutM
single knockouts are weak mutators by themselves, but the combination of
mutY mutM
results in very high mutation rates, all due to G:C → T:A transversions. The situation parallels that seen in
Escherichia coli
. Also,
mutS
knockouts are strong mutators and even stronger in the presence of a deletion of
ndk
. The number of sites in
rpoB
that can result in the Rif
r
phenotype by single-base substitution is more limited than in certain other bacteria, such as
E. coli
and
Deinococcus radiodurans
, although the average mutation rate per mutational site is roughly comparable. Hotspots at sites with virtually identical surrounding sequences are organism specific.
Familial Effects of BRCA1 Genetic Mutation Testing: Changes in Perceived Family Functioning
Authors: Stroup Antoinette M. , Smith Ken R. 
Published: January 2007

Abstract
This study expands recent research that examines how the receipt of BRCA1 genetic test results affects family adaptability and cohesion 1 year after genetic risk notification. Study participants were members of a large Utah-based kindred with an identified mutation at the BRCA1 locus. The final sample, 90 men and 132 women, contributed information before genetic testing (baseline) and 4 months and/or 1 year after receipt of genetic test results. After controlling for other factors such as family coping resources (Family Crises–Oriented Personal Evaluation Scale) and strains (Family Strains Index) and the tested individual's anxiety levels before genetic testing (state anxiety subscale), men and women reported significant declines in family cohesion 1 year after genetic risk notification (P &lt; 0.01). There is suggestive evidence that carrier men reported increasing adaptability 1 year after risk notification (+0.21 points per month; P &lt; 0.10). Having a carrier sister had a positive influence on women's perceived family cohesion and adaptability levels, whereas a personal history of cancer, having a great deal of caregiving involvement for a female relative with cancer, anxiety, and some types of coping resources had a negative effect on men's perceived family cohesion and adaptability levels. Although results showed that tested parents are perceiving a decline in family functioning after genetic risk notification, there is no evidence to suggest that the decline is due to carrier status. In fact, it is other life circumstances that exist at the time of the genetic testing process that seem to influence the degree to which families adjust to the experience and test results. (Cancer Epidemiol Biomarkers Prev 2007;16(1):135–41)
Haplotype-Based Analysis of Common Variation in the Growth Hormone Receptor Gene and Prostate Cancer Risk
Authors: McKay James D. , Kaaks Rudolf , Johansson Mattias , Biessy Carine , Wiklund Fredik , Bälter Katarina , Adami Hans-Olov , Boillot Catherine , Gioia-Patricola Lydie , Canzian Federico , Stattin Pär , Grönberg Henrik 
Published: January 2007

Abstract
The growth hormone receptor (GHR) is potentially involved in prostate cancer through its role in stimulating insulin-like growth factor I production and its cellular effects on prostate epithelium. We have used a haplotype-based tagging approach within CAncer Prostate Sweden, a large retrospective case-control study of 2,863 cases and 1,737 controls to investigate if genetic variation in the GHR gene influences prostate cancer risk. One haplotype in the 3′ region of the GHR gene was found associated with prostate cancer risk in elderly men (&gt;65 years old at the time of diagnosis), with heterozygote haplotype carriers having an odds ratio of 1.65 (95% confidence interval, 1.21-2.16; P = 0.0009, Pcorrected = 0.03). GHR function has been implicated in the determination of body mass index. Interestingly, the same haplotype associated with risk in the 3′ end of the GHR gene was also associated with a decrease in body mass index in controls (P = 0.003, Pcorrected = 0.05), possibly indicating some functionality with this haplotype. These results suggest that whereas genetic variation in the GHR gene does not seem to play a major role in prostate cancer etiology, one haplotype in the 3′ region may be potentially relevant to cases with later onset of prostate cancer. (Cancer Epidemiol Biomarkers Prev 2007;16(1):169–73)
A Case-Control Investigation of Immune Function Gene Polymorphisms and Risk of Testicular Germ Cell Tumors
Authors: Purdue Mark P. , Sakoda Lori C. , Graubard Barry I. , Welch Robert , Chanock Stephen J. , Sesterhenn Isabel A. , Rubertone Mark V. , Erickson R. Loren , McGlynn Katherine A. 
Published: January 2007

Abstract
There is reason to suspect that testicular germ cell tumor (TGCT) development may be influenced by cytokines, secreted proteins that modulate tumor immune surveillance activity as well as a variety of processes in the testis. To address this hypothesis, we conducted a case-control analysis (508 cases, 608 controls) of 32 putatively functional single-nucleotide polymorphisms (SNP) in 16 immune function genes among non-Hispanic Caucasian participants in the U.S. Servicemen's Testicular Tumor Environmental and Endocrine Determinants Study. The TGFB1 Ex5−73C&gt;T variant was positively associated with TGCT (CT/TT versus CC: odds ratio, 1.73; 95% confidence interval, 1.01-2.95; Ptrend = 0.05); additionally, haplotypes of the assessed TGFB1 SNPs (−509C&gt;T, 327C&gt;T, Ex1−282C&gt;G, and Ex5−73C&gt;T) differed in frequency between cases and controls (all TGCT, P 0.07; seminoma, P 0.04; nonseminoma, P 0.11). We also observed excess frequencies among TGCT cases versus controls of LTA 252G (Ptrend = 0.08) and of the TNF variants −1042C (Ptrend = 0.06), −1036T (Ptrend = 0.07), and −238G (Ptrend = 0.09). Analyses of haplotypes for LTA-TNF SNPs (LTA −91C&gt;A, LTA 252A&gt;G, TNF −863C&gt;A, TNF −857C&gt;T, TNF −308G&gt;A, and −238G&gt;A) were similarly suggestive of an association with TGCT (P = 0.06) and nonseminoma (P = 0.04), but not seminoma (P = 0.21). Polymorphisms in other genes were found to be associated only with seminoma (IL2) or nonseminoma (IFNGR2 and IL10). However, none of the associations remained noteworthy after applying the false discovery rate method to control for multiple testing. In conclusion, our findings suggest that polymorphisms in TGFB1 and LTA/TNF, and possibly other immune function genes, may influence susceptibility to TGCT. (Cancer Epidemiol Biomarkers Prev 2007;16(1):77–83)
Global DNA Methylation Level in Whole Blood as a Biomarker in Head and Neck Squamous Cell Carcinoma
Authors: Ting Hsiung Debra , Marsit Carmen J. , Houseman E. Andres , Eddy Karen , Furniss C. Sloane , McClean Michael D. , Kelsey Karl T. 
Published: January 2007

Abstract
Background: Head and neck squamous cell carcinoma (HNSCC) is commonly associated with tobacco and alcohol exposures, although dietary factors, particularly folate, and human papillomavirus, are also risk factors. Epigenetic alterations are increasingly implicated in the initiation and progression of cancer. Genome-wide (global) hypomethylation seems to occur in early neoplasia and is a feature of genomic DNA derived from solid tumor tissues, including HNSCC. This study aimed to determine whether global methylation in DNA derived from whole blood, a proxy tissue, is associated with HNSCC and to assess potential modification of this property by environmental or behavioral risk factors.
Methods: Global DNA methylation levels were assessed using a modified version of the combined bisulfite restriction analysis of the LRE1 sequence in a population-based case-control study of HNSCC from the Boston area.
Results: Hypomethylation lead to a significant 1.6-fold increased risk for disease (95% confidence interval, 1.1-2.4), in models controlled for other HNSCC risk factors. Smoking showed a significant differential effect (P &lt; 0.03) on blood relative methylation between cases and controls. Furthermore, in cases, variant genotype in the MTHFR gene and low folate intake showed relationships with decreased global methylation, whereas in controls, antibody response to human papillomavirus 16 was associated with an increased global methylation level.
Discussion: DNA hypomethylation in nontarget tissue was independently associated with HNSCC and had a complex relationship with the known risk factors associated with the genesis of HNSCC. (Cancer Epidemiol Biomarkers Prev 2007;16(1):108–14)
Type-Specific Persistence of High-Risk Human Papillomavirus Infections in the New Independent States of the former Soviet Union Cohort Study
Authors: Kulmala Satu-Maria A. , Shabalova Irena P. , Petrovitchev Nikolay , Syrjänen Kari J. , Gyllensten Ulf B. , Johansson Bo C. , Syrjänen Stina M. ,   and the New Independent States of the former Soviet Union Cohort Study Group
Published: January 2007

Abstract
Background: Prospective follow-up studies have recently suggested that persistent high-risk human papillomavirus (HPV) infections play a key role in the progression of CIN lesions and in the development of cervical cancer. However, data on type-specific persistence, viral integration, and the role of multiple infections are scanty.
Materials and Methods: A cross-sectional/cohort study was conducted between 1998 and 2002 in three New Independent States of the former Soviet Union comprising a cohort of 3,187 women, of whom 854 women were followed up for a mean of 17 months (SD, 11.6). HPV genotyping was done with real-time PCR, detecting HPV types 16, 18/45, 31, 33/52/58, 35, and 39. The integration status of HPV16 was examined by using a novel Taqman-based PCR method.
Results: The mean clearance time for the individual high– risk–type infection was 16.5 months (range = 0.9-34.9 months). HPV16 and HPV31 were the most persistent infections (clearance times = 18.1 and 16.2 months, respectively), whereas HPV39 infections cleared most rapidly. The mean copies per cell in HPV18/45, HPV31, HPV33/52/58, and HPV39 infections were higher in persisting HPV infections than in HPV infections that cleared, but the difference was not significant. Integration of HPV16 was not found to correlate with HPV persistence.
Conclusions: A large proportion of women remained high-risk HPV positive after 18 months. Coinfection with multiple HPV types, viral load, or integration status did not correlate with persistence of high-risk HPV infections. (Cancer Epidemiol Biomarkers Prev 2007;16(1):17–22)
Risk for High-Grade Cervical Intraepithelial Neoplasia Associated with Variants of Human Papillomavirus Types 16 and 18
Authors: Xi Long Fu , Koutsky Laura A. , Hildesheim Allan , Galloway Denise A. , Wheeler Cosette M. , Winer Rachel L. , Ho Jesse , Kiviat Nancy B. 
Published: January 2007

Abstract
Background: Although the variant lineages of human papillomavirus (HPV) types 16 and 18 are well established, their individual associations with high-grade cervical intraepithelial neoplasia (CIN) have not been extensively evaluated.
Methods: Study subjects were women participating in the Atypical Squamous Cells of Undetermined Significance/Low-Grade Squamous Intraepithelial Lesion Triage Study who were positive for HPV16 or HPV18 at enrollment. These women were followed every 6 months for 2 years. Viral isolates from enrollment samples were characterized by DNA sequencing and classified as variant lineages.
Results: Over a 2-year study period, CIN3 was histologically diagnosed in 291 of the 779 HPV16-positive women and 47 of the 275 HPV18-positive women. Among women without CIN2-3 at enrollment, the risk of subsequent CIN3 was 2.7-fold greater for those with HPV16 African-2 [95% confidence interval (95% CI), 1.0-7.0] and 3.1-fold greater for those with HPV16 Asian American (95% CI, 1.6-6.0), compared with European variants. Relative to infection with HPV18 African variants, the risk associating subsequent CIN3 was 3.8 (95% CI, 0.9-17.2) for infection with HPV18 European variants and 4.8 (95% CI, 1.0-23.6) for infection with HPV18 Asian American variants. Similar associations were observed when the 2-year prevalence of CIN3 was used as the end point. Further, for those with HPV16 European variants, the 2-year prevalence of CIN3 was higher in White women than in African American women (P = 0.01); this trend was reversed for those with HPV16 African-1 variants (P = 0.22). A similar pattern was present for infections with HPV18 European versus African variants.
Conclusions: The lineages of HPV16 and HPV18 variants are associated with differing risks for high-grade CIN. (Cancer Epidemiol Biomarkers Prev 2007;16(1):4–10)
Variant in Sex Hormone-Binding Globulin Gene and the Risk of Prostate Cancer
Authors: Berndt Sonja I. , Chatterjee Nilanjan , Huang Wen-Yi , Chanock Stephen J. , Welch Robert , Crawford E. David , Hayes Richard B. 
Published: January 2007

Abstract
Sex hormones have been implicated in prostate carcinogenesis and are thought to modulate cell proliferation and growth. To investigate the association between polymorphisms in hormone-related genes and prostate cancer risk, we conducted a two-stage, case-control study within the screening arm of the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. Using DNA extracted from blood specimens, we initially genotyped 14 single nucleotide polymorphisms in genes involved in hormone regulation or metabolism (AKR1C3, CYP1A1, CYP1B1, CYP3A4, ESR1, GNRH1, HSD173B, HSD3B2, SHBG, and SRD5A2) in 488 prostate cancer cases and 617 matched controls. Heterozygotes at SHBG D356N were found to be associated with an increased risk of prostate cancer compared with the homozygous wild type, particularly among non-Hispanic whites (odds ratio, 1.54; 95% confidence interval, 1.13-2.09; P = 0.006). No significant associations were observed with the other polymorphisms. The SHBG D356N polymorphism, which has potential functional significance, was subsequently genotyped in additional 769 cases and 1,168 controls. Overall, SHBG D356N heterozygotes were found to have an increased risk of prostate cancer among whites (odds ratio, 1.34; 95% confidence interval, 1.10-1.63; P = 0.0007). This study suggests that genetic variation in SHBG may influence prostate cancer susceptibility. (Cancer Epidemiol Biomarkers Prev 2007;16(1):165–8)
Body Mass Index, Weight Change, and Risk of Prostate Cancer in the Cancer Prevention Study II Nutrition Cohort
Authors: Rodriguez Carmen , Freedland Stephen J. , Deka Anusila , Jacobs Eric J. , McCullough Marjorie L. , Patel Alpa V. , Thun Michael J. , Calle Eugenia E. 
Published: January 2007

AbstractBackground: Obesity has been associated with aggressive prostate cancer. The extent of this association, which varies by stage and grade, remains unclear. The role of recent weight change had not been previously examined.Methods: We examined body mass index (BMI) and weight change in relation to incident prostate cancer by disease stage and grade at diagnosis among 69,991 men in the Cancer Prevention Study II Nutrition Cohort. Participants provided information on height and weight in 1982, and again at enrollment in 1992. During follow-up through June 30, 2003 (excluding the first 2 years of follow-up), we documented 5,252 incident prostate cancers. Cox proportional hazards models were used to estimate rate ratios (RR) and 95% confidence intervals (95% CI).Results: The association between BMI in 1992 and risk of prostate cancer differed by stage and grade at diagnosis. BMI was inversely associated with risk of nonmetastatic low-grade prostate cancer (RR, 0.84; 95% CI, 0.66-1.06), but BMI was positively associated with risk of nonmetastatic high-grade prostate cancer (RR, 1.22; 95% CI, 0.96-1.55) and risk of metastatic or fatal prostate cancer (RR, 1.54; 95% CI, 1.06-2.23). Compared with weight maintenance, men who lost &gt;11 pounds between 1982 and 1992 were at a decreased risk of nonmetastatic high-grade prostate cancer (RR, 0.58; 95% CI, 0.42-0.79).Conclusion: Obesity increases the risk of more aggressive prostate cancer and may decrease either the occurrence or the likelihood of diagnosis of less-aggressive tumors. Men who lose weight may reduce their risk of prostate cancer. (Cancer Epidemiol Biomarkers Prev 2007;16(1):63–9)