bluuebunny/crossref_metadata_2025_split huggingface dataset:
Serum Levels of Hepatocyte Growth Factor in Patients with Breast Cancer
Authors: Sheen-Chen Shyr-Ming , Liu Yueh-Wei , Eng Hock-Liew , Chou Fong-Fu 
Published: September 2005

Abstract
Objective: Hepatocyte growth factor (HGF) has been reported the cause of many biological events, including cell proliferation, movement, invasiveness, morphogenesis, and angiogenesis. Elevated hepatocyte growth factor content in tumor tissue was reported to predict a more aggressive biology in non–small cell lung cancer patients. However, there is still limited knowledge about the role of HGF in breast cancer. This study was designed with the aim to elucidate the possible relationship between the preoperative circulating soluble HGF and breast cancer.
Materials and Methods: One hundred twenty-four consecutive patients with invasive breast cancer undergoing surgery were prospectively included and evaluated. Venous blood samples were collected before the surgery. Sera were obtained by centrifugation and stored at −70°C until assayed. The control group consisted of 35 patients with benign breast tumor (20 with fibrocystic disease and 15 with fibroadenoma). Serum concentrations of soluble HGF were measured by the quantitative sandwich enzyme immunoassay technique. The data on primary tumor staging, age, estrogen receptor status, lymph node status, distant metastases status, histologic grading, and tumor-node-metastasis (TNM) staging were reviewed and recorded.
Results: The mean value of serum soluble HGF in patients with invasive breast cancer was 529.05 ± 123.33 pg/mL and that of control group was 343.00± 31.03 pg/mL and the difference was significant (P &lt; 0.001). Furthermore, there were significantly higher serum levels of soluble HGF in patients with negative estrogen receptor (P = 0.035), in patients with poorer differentiated tumor (P &lt; 0.001), in patients with more advanced primary tumor staging (P &lt; 0.001), in patients with more advanced lymph node status (P &lt; 0.001), in patients with distant metastases (P &lt; 0.001), and in patients with more advanced TNM staging (P &lt; 0.001). In multivariate analysis by the multiple linear regression method, TNM staging (P &lt; 0.001) seemed an independent factor regarding the significant higher serum levels of soluble HGF.
Conclusion: Patients with more advanced TNM staging were shown to have higher serum soluble HGF. Thus, preoperative serum soluble HGF levels might reflect the severity of invasive breast cancer and deserve further evaluation.
Surveillance Patterns and Polyp Recurrence following Diagnosis and Excision of Colorectal Polyps in a Medicare Population
Authors: Amonkar Mayur M. , Hunt Timothy L. , Zhou Zhiyuan , Jin Xiaodong 
Published: September 2005

Abstract
Objective: Study objectives were to determine surveillance and polyp recurrence rates among older, increased-risk patients who have been diagnosed and excised of colorectal polyps. The high incidence of colorectal cancers in the Medicare-eligible population, the strong evidence linking reductions in mortality from colorectal cancer by removal of colorectal polyps, and the paucity of postpolypectomy surveillance data in this population all supported the need for this study.
Methods: This retrospective study used Medicare claims data to identify a cohort of 19,895 beneficiaries ages ≥65 years diagnosed and excised of colorectal polyps in 1994. Survival analysis was used to compute surveillance and polyp recurrence rates over 5 years. Log-rank test was used for all statistical comparisons.
Results: Median time to first surveillance was 2.6 years. Surveillance rates for 1, 3, and 5 years were 17.6%, 55.8%, and 74.5%, respectively. Twenty-six percent had no surveillance event. Polyp recurrence rates for 1, 3, and 5 years were 10.9%, 38.2%, and 52.6%, respectively. Males and younger patients were more likely to undergo surveillance and showed higher polyp recurrence rates.
Conclusions: The high likelihood of polyp recurrence underscores the need for continued efforts to promote awareness of and compliance with postpolypectomy surveillance. Efforts to increase surveillance rates among individuals diagnosed with colorectal polyps and making available additional treatment options that may prevent the recurrence of polyps and/or their possible progression to colorectal cancer should help make significant progress in reaching the Healthy People 2010 goal of reducing colorectal cancer deaths by 34% by the year 2010.
Alcohol Dehydrogenase 3 and Risk of Squamous Cell Carcinomas of the Head and Neck
Authors: Wang Donghong , Ritchie Justine M. , Smith Elaine M. , Zhang Zugui , Turek Lubomir P. , Haugen Thomas H. 
Published: September 2005

Abstract
In order to examine the association between alcohol dehydrogenase 3 (ADH3) genotypes and risk of head and neck squamous cell carcinomas (HNSCC), we conducted a hospital based case-control study including 348 cases and 330 controls. DNA isolated from exfoliated cells from the oral cavity were genotyped for ADH3 polymorphisms using PCR followed by SspI digestion. Odds ratios (OR) and hazards ratios (HR) were done by unconditional logistic regression and Cox regression. Relative to ADH32-2 carriers, ADH31-1 [OR, 0.7; 95% confidence interval (CI), 0.4-1.1] and ADH31-2 (OR, 0.8; 95% CI, 0.5-1.2) had a nonsignificant reduced risk of HNSCC. ADH1-2 smokers of &gt;30 pack-years were at decreased risk of oral cavity squamous cell carcinomas compared with ADH32-2 (OR, 0.3, 0.1-0.9), whereas ADH31-1 smokers were not. After adjustment, those with ADH31-2 had significantly worse overall survival compared with ADH31-1 (HR, 0.3, 0.2-0.6) or ADH32-2 (HR, 0.4, 0.2-0.9) and increased recurrence (ADH31-1, 0.2, 0.1-0.6; ADH32-2, 0.6, 0.2-1.3). Our data did not show that ADH3 genotypes had a significantly independent effect on the risk of HNSCC, nor did they modify the risks increased by alcohol or tobacco consumption and high-risk human papillomavirus infection. However, participants with ADH31-2 genotype were associated with poorer survival compared with those who had the other two ADH3 genotypes and a higher rate of recurrence than participants with ADH31-1 genotype.
Dietary Patterns Associated with Male Lung Cancer Risk in the Netherlands Cohort Study
Authors: Balder Helena F. , Goldbohm R. Alexandra , van den Brandt Piet A. 
Published: September 2005

Abstract
The objective of this article was to study the association between dietary patterns and lung cancer incidence in the Netherlands Cohort Study on Diet and Cancer. The baseline measurement of this prospective case cohort study that was completed by 58,279 men in 1986 included a self-administered questionnaire on dietary intake, smoking habits, and other covariates. Follow-up was established by computerized record linkage to cancer registries and a pathology register. After 9.3 years of follow-up, 1,426 confirmed cases of incident male lung cancer were detected. Five dietary patterns were identified by exploratory factor analysis in a randomly sampled subcohort (n = 2,190). The dietary pattern labeled “salad vegetables” was associated with decreased risk of lung cancer [rate ratios (RR)Q5, 0.75; 95% confidence interval (CI), 0.55-1.01], after multivariate adjustment. This inverse association was most evident among current and former smokers. A dietary pattern labeled “sweet foods” was also inversely associated with lung cancer risk (RRQ5, 0.62; 95% CI, 0.43-0.89). However, the higher intake of monosaccharides and disaccharides, fruits, and lower consumption of alcohol associated with this pattern could not account for its full protective effect. The “pork, processed meat, and potatoes” pattern was nonsignificantly associated with increased risk (RRQ5, 1.44; 95% CI, 0.99-2.09), and this positive association was most evident among current smokers. The other dietary patterns characterized by brown/white bread substitution and by consumption of cooked vegetables were not associated with lung cancer risk. These results show how studying both single factors and dietary patterns gives more insight into the complex, and often seemingly inconsistent, associations between diet and cancer.
Sex Steroid Hormones and the Androgen Receptor Gene CAG Repeat and Subsequent Risk of Prostate Cancer in the Prostate-Specific Antigen Era
Authors: Platz Elizabeth A. , Leitzmann Michael F. , Rifai Nader , Kantoff Philip W. , Chen Yen-Ching , Stampfer Meir J. , Willett Walter C. , Giovannucci Edward 
Published: September 2005

Abstract
Objective: Sex steroid hormones are thought to contribute to the growth, differentiation, and progression of prostate cancer. We investigated plasma levels of sex steroid hormones and length of the androgen receptor gene CAG repeat in relation to incident prostate cancer diagnosed in the prostate-specific antigen (PSA) era.
Methods: Using a nested case-control design, we included 460 prostate cancer cases diagnosed after providing a blood specimen in 1993 but before February 1998 among men in the Health Professionals Follow-up Study. Controls were 460 age-matched men without prostate cancer who had a screening PSA test after the date of providing a blood specimen. We measured plasma concentrations of total testosterone, free testosterone, dihydrotestosterone, androstanediol glucuronide, estradiol, and sex hormone binding globulin (SHBG) and determined the length of the androgen receptor gene CAG repeat. Conditional logistic regression was used to estimate odds ratios (OR) and 95% confidence intervals (CI) of prostate cancer.
Results: Mean concentrations of the sex steroids adjusted for SHBG, and mean CAG repeat length did not differ significantly between the prostate cancer cases and controls. No significant associations with total prostate cancer were detected for plasma total testosterone concentration (comparing highest versus lowest quartiles: OR, 0.78; 95% CI, 0.48-1.28; Ptrend = 0.73) or the other sex hormones after adjusting for SHBG. However, plasma total testosterone concentration was positively associated with low-grade disease (Gleason sum &lt; 7: OR, 1.91; 95% CI, 0.89-4.07; Ptrend = 0.02) and inversely associated with high-grade disease (Gleason sum ≥ 7: OR, 0.26; 95% CI, 0.10-0.66; Ptrend = 0.01). Similar patterns for grade were observed for free testosterone. Short CAG repeat length was not associated with total prostate cancer (≤ 19 versus ≥ 24: OR, 0.84; 95% CI, 0.57-1.23; Ptrend = 0.22) or grade of disease. No clear associations with regionally invasive or metastatic (≥ T3b, N1, or M1) were found for any of the hormones or the CAG repeat, although the number of these cases was small.
Conclusions: The overall lack of association of prostate cancer diagnosed in the PSA era with sex steroid hormones and the androgen receptor gene CAG repeat length is consistent with the hypothesis that these factors do not substantially contribute to the development of early prostate cancer in the PSA era. The influence of plasma total and free testosterone concentrations on prostate cancer grade merits further evaluation.
Clinicopathologic Correlation of Up-regulated Genes Identified Using cDNA Microarray and Real-time Reverse Transcription-PCR in Human Colorectal Cancer
Authors: Chiu Sou-Tyau , Hsieh Fon-Jou , Chen Shi-Wen , Chen Chun-Lieh , Shu Hwei-Fan , Li Hung 
Published: September 2005

Abstract
Purpose: We hypothesize that changes in the transcription of up-regulated genes are biologically meaningful and may be linked to variations in tumor behavior and clinical features. This study aimed to find individual up-regulated genes responsible for clinicopathologic variations in human colorectal cancer.
Experimental Design: Genes up-regulated concurrently in four microarray experiments were taken as candidate genes; 20 candidate genes were verified using real-time reverse transcription-PCR in these four experiments, along with 27 new samples. The presence or absence of up-regulation of these genes was correlated with 10 clinicopathologic variables from 31 patients. The mRNA transcript levels of these 20 candidate genes in the 31 paired samples were also correlated with each other to disclose any expression relationship.
Results: Forty percent (8/20) of the candidate genes were verified by real-time reverse transcription-PCR to have a tumor/normal expression ratio &gt; 2. Up-regulation of THY1 and PHLAD1 was associated with the presence of anemia in colon cancer patients (P = 0.036 and 0.009, respectively). Up-regulation of HNRPA1 was more significant in cancer growing in the right-sided colon than the left side (P = 0.027). Up-regulated GPX2 was related to a higher degree of tumor differentiation (P = 0.019). c-MYC was significantly over-expressed in specimens from male compared with female colon cancer patients (P = 0.012). GRO1 was significantly up-regulated in patients younger than 65 years old (P = 0.010) and was found to be frequently over-expressed when cancers were less invasive. In addition, we found that normalized transcript levels of HNRPA1 were tightly associated with that of c-MYC (r = 0.948).
Conclusions: Validation of microarray data using another independent laboratory approach is mandatory and statistical correlation between gene expression status and the patient's clinical features may reveal individual genes relevant to tumor behavior and clinicopathologic variations in human colorectal cancer.
Multiplexed Immunobead-Based Cytokine Profiling for Early Detection of Ovarian Cancer
Authors: Gorelik Elieser , Landsittel Douglas P. , Marrangoni Adele M. , Modugno Francesmary , Velikokhatnaya Lyudmila , Winans Matthew T. , Bigbee William L. , Herberman Ronald B. , Lokshin Anna E. 
Published: September 2005

Abstract
Early detection of ovarian cancer might improve clinical outcome. Some studies have shown the role of cytokines as a new group of tumor markers for ovarian cancer. We hypothesized that a panel comprised of multiple cytokines, which individually may not show strong correlation with the disease, might provide higher diagnostic power. To evaluate the diagnostic utility of cytokine panel, we used a novel multianalyte LabMAP profiling technology that allows simultaneous measurement of multiple markers. Concentrations of 24 cytokines (cytokines/chemokines, growth, and angiogenic factors) in combination with cancer antigen-125 (CA-125), were measured in sera of 44 patients with early-stage ovarian cancer, 45 healthy women, and 37 patients with benign pelvic tumors. Six markers, i.e., interleukin (IL)-6, IL-8, epidermal growth factor (EGF), vascular endothelial growth factor (VEGF), monocyte chemoattractant protein-1 (MCP-1), and CA-125, showed significant differences in serum concentrations between ovarian cancer and control groups. Out of this group, IL-6, IL-8, VEGF, EGF, and CA-125, were used in a classification tree analysis that resulted in 84% sensitivity at 95% specificity. The receiver operator characteristic curve created using the combination of markers produced sensitivities between 90% and 100% in the area of 80% to 90% specificity, whereas the receiver operator characteristic curve for CA-125 alone resulted in sensitivities of 70% to 80%. The classification tree analysis for discrimination of benign condition from ovarian cancer used CA-125, granulocyte colony-stimulating factor (G-CSF), IL-6, EGF, and VEGF resulting in 86.5% sensitivity and 93.0% specificity. The presented data show that simultaneous testing of a panel of serum cytokines and CA-125 using LabMAP technology may present a promising approach for ovarian cancer detection.
Comparison of Human Papillomavirus Messenger RNA and DNA Detection: A Cross-sectional Study of 4,136 Women &gt;30 Years of Age with a 2-Year Follow-up of High-Grade Squamous Intraepithelial Lesion
Authors: Molden Tor , Kraus Irene , Karlsen Frank , Skomedal Hanne , Nygård Jan F. , Hagmar Bjørn 
Published: September 2005

Abstract
The purpose of this study was to compare the detection of human papillomavirus (HPV) DNA with detection of mRNA. The study included 4,136 women &gt;30 years of age. E6/E7 mRNA expression from the carcinogenic HPV types 16, 18, 31, 33, and 45 was detected by the PreTect HPV-Proofer assay, whereas the presence of HPV DNA was detected by Gp5+/6+ consensus PCR followed by type-specific PCR. A total of 4.0% had an abnormal cytologic diagnosis, 3.0% were positive by PreTect HPV-Proofer, 4.4% by type-specific PCR, and 10.4% by consensus PCR. For detection of HPV in high-grade squamous intraepithelial lesion (HSIL), no significant difference was observed between PreTect HPV-Proofer and consensus PCR. For women with a cytologic normal, atypical squamous cell of uncertain significance, and low-grade SIL diagnosis, the detection rate of HPV was significantly higher by Gp5+/6+ consensus PCR (P &lt; 0.005) than by PreTect HPV-Proofer. Histology confirmed 14 of 23 cytologic HSIL as cervical intraepithelial neoplasia grade &gt;2. Of these women, PreTect HPV-Proofer and type-specific PCR detected 12, whereas consensus PCR detected 13. In conclusion, for HSIL, detection of E6/E7 transcripts from HPV types 16, 18, 31, 33, and 45 are present to the same degree as DNA detected by consensus PCR. Equally important, only a small proportion of the HPV DNA–positive women with a normal, atypical squamous cell of uncertain significance or low-grade SIL diagnosis had a detectable mRNA expression. HPV E6/E7 mRNA detection by PreTect HPV-Proofer represents a new promising test as an adjunct to cytology.
Polymorphisms in XRCC1 Modify the Association between Polycyclic Aromatic Hydrocarbon-DNA Adducts, Cigarette Smoking, Dietary Antioxidants, and Breast Cancer Risk
Authors: Shen Jing , Gammon Marilie D. , Terry Mary Beth , Wang Lianwen , Wang Qiao , Zhang Fangfang , Teitelbaum Susan L. , Eng Sybil M. , Sagiv Sharon K. , Gaudet Mia M. , Neugut Alfred I. , Santella Regina M. 
Published: September 2005

Abstract
The variability in DNA repair capacity of the general population may depend in part upon common variants in DNA repair genes. X-ray repair cross complementing group 1 (XRCC1) is an important DNA base excision repair gene and exhibits polymorphic variation. Using the Long Island Breast Cancer Study Project, a population-based case-control study, we evaluated the hypothesis that two common single nucleotide polymorphisms of XRCC1 (codon 194 Arg→Trp and 399 Arg→Gln) influence breast cancer susceptibility and interact with polycyclic aromatic hydrocarbon (PAH)-DNA adducts, cigarette smoking, and intake of fruits and vegetables and antioxidants. The available sample for genotyping included 1,067 cases and 1,110 controls. Genotyping was done by a high-throughput single-nucleotide extension assay with fluorescence polarization detection of the incorporated nucleotide. We observed no significant increases in risk among all subjects who were carriers of XRCC1 194Trp or 399Gln alleles. Among never smokers, we observed an increased risk of breast cancer in 399Gln carriers [odds ratio (OR), 1.3; 95% confidence interval (CI), 1.0-1.7). Further analysis indicated a suggestive weak additive interaction between the 399Gln allele and detectable PAH-DNA adducts (OR for exposure with mutant genotype, 1.9; 95% CI, 1.2-3.1). The estimated age-adjusted interaction contrast ratio (ICR) and 95% CI (ICR, 0.38; 95% CI, −0.32 to 1.10) indicated that the departure from additivity was not statistically significant, but that there was some suggestion of a relative excess risk due to the interaction. In subjects with at least one copy of XRCC1 194Trp allele, there was a moderate interaction with high intake of fruits and vegetables (≥35 half-cup servings per week of any fruits, fruit juices, and vegetables, OR, 0.58; 95% CI, 0.38-0.89; ICR, −0.49; 95% CI, −0.03 to −0.95), and dietary plus supplement antioxidant intake with 33% to 42% decreases in breast cancer risk compared with those with the Arg194Arg genotype and low-intake individuals. These results do not show that the two genetic polymorphisms of XRCC1 independently influence breast cancer risk. However, there is evidence for interactions between the two XRCC1 single nucleotide polymorphisms and PAH-DNA adducts or fruit and vegetable and antioxidant intake on breast cancer risk. Further understanding of the biological function of XRCC1 variants and their interactions with PAH-DNA adducts, antioxidants, and other genes in the pathway are needed.
Serum Insulin-Like Growth Factor-I Levels and Prostatic Intraepithelial Neoplasia: A Clue to the Relationship Between IGF-I Physiology and Prostate Cancer Risk
Authors: Nam Robert K. , Trachtenberg John , Jewett Michael A.S. , Toi Ants , Evans Andrew , Emami Marjan , Narod Steven A. , Pollak Michael 
Published: September 2005

Abstract
Serum insulin-like growth factor-I (IGF-I) levels at the higher end of the reference range have been associated with increased risk for the future development of prostate cancer. We determined whether high serum IGF-I levels are associated with precancerous lesions of the prostate. We conducted a case-control study to determine whether high serum IGF-I levels were associated with the presence of high-grade prostatic intraepithelial neoplasia (HGPIN) among patients who presented for prostate biopsy because of an abnormal serum prostate-specific antigen level or digital rectal exam. We measured serum IGF-I and insulin-like growth factor binding protein-3 (IGFBP-3) prior to prostate biopsy and compared them between 103 men with HGPIN (cases) and 205 men with normal prostate histology (controls). The mean IGF-I level in patients with HGPIN (130.2 ng/mL) was significantly higher compared with controls (118.8 ng/mL, P = 0.01). The mean IGFBP-3 level in patients with HGPIN (2,393.9 ng/mL) was also higher compared with controls (2,276.0 ng/mL, P = 0.06). After adjusting for age, prostate-specific antigen, digital rectal examination, and ethnic background, the odds ratio for a HGPIN diagnosis among men in the highest relative to the lowest quartile of serum IGF-I level was 1.94 (95% confidence interval, 1.0-3.7; P = 0.04). The potential association between a high serum IGF-I level and the presence of HGPIN may represent an important clue to understanding the basis for the relationship between IGF-I physiology and prostate cancer risk. Larger studies will be required to confirm this relationship.
The ADH1C Polymorphism Modifies the Risk of Squamous Cell Carcinoma of the Head and Neck Associated with Alcohol and Tobacco Use
Authors: Peters Edward S. , McClean Michael D. , Liu Mei , Eisen Ellen A. , Mueller Nancy , Kelsey Karl T. 
Published: September 2005

Abstract
Alcohol consumption interacts with tobacco use to increase the risk of head and neck squamous cell carcinoma (HNSCC). Alcohol is eliminated through oxidation by alcohol dehydrogenase (ADH). The ADH1C gene is polymorphic and the ADH1C*1 allele metabolizes ethanol to acetaldehyde at a higher rate than the variant ADH1C*2 allele. This polymorphism has been reported to alter the risk of HNSCC associated with alcohol use, although the literature differs in the estimates of both the magnitude and direction of this effect modification. We have investigated the association between the established risk factors for HNSCC and variant genotypes of ADH1C in a case-control study in the greater Boston area. ADH1C genotypes were determined from 521 cases and 599 population-based controls. The odds ratio (OR) for HNSCC associated with &gt;26 drinks per week was 3.7 [95% confidence interval (95% CI), 2.4-5.7], whereas the OR for smoking &gt;58 pack-years was 5.6 (95% CI, 3.8-8.4). The combination of heavy smoking and heavy drinking significantly interacted to produce an OR of 17.3 (95% CI, 7.8-38.3). In cases and controls, respectively, 16% and 14% were ADH1C*1-1, 46% and 46% were ADH1C*1-2 and 38% and 40% were ADH1C*2-2. There was a significant interaction of alcohol use and genotype (P = 0.05), with an estimated oral cancer risk in heavy drinkers of 7.1 (95% CI, 2.3-22.0) for homozygous variants compared with an OR of 2.3 (95% CI, 1.4-3.8) for ADH1C homozygous wild type or heterozygous individuals (controlling for smoking, age, race, and gender). These findings suggest that the ADH1C*2-2 genotype is associated with susceptibility to smoking and drinking-related HNSCC by modifying the biologically effective dose of alcohol.