bluuebunny/crossref_metadata_2025_split huggingface dataset:
A Tailored Smoking, Alcohol, and Depression Intervention for Head and Neck Cancer Patients
Authors: Duffy Sonia A. , Ronis David L. , Valenstein Marcia , Lambert Michael T. , Fowler Karen E. , Gregory Lynn , Bishop Carol , Myers Larry L. , Blow Frederic C. , Terrell Jeffrey E. 
Published: November 2006

Abstract
Background: Smoking, alcohol use, and depression are interrelated and highly prevalent in patients with head and neck cancer, adversely affecting quality of life and survival. Smoking, alcohol, and depression share common treatments, such as cognitive behavioral therapy and antidepressants. Consequently, we developed and tested a tailored smoking, alcohol, and depression intervention for patients with head and neck cancer.
Methods: Patients with head and neck cancer with at least one of these disorders were recruited from the University of Michigan and three Veterans Affairs medical centers. Subjects were randomized to usual care or nurse-administered intervention consisting of cognitive behavioral therapy and medications. Data collected included smoking, alcohol use, and depressive symptoms at baseline and at 6 months.
Results: The mean age was 57 years. Most participants were male (84%) and White (90%). About half (52%) were married, 46% had a high school education or less, and 52% were recruited from Veterans Affairs sites. The sample was fairly evenly distributed across three major head and neck cancer sites and over half (61%) had stage III/IV cancers. Significant differences in 6-month smoking cessation rates were noted with 47% quitting in the intervention compared with 31% in usual care (P &lt; 0.05). Alcohol and depression rates improved in both groups, with no significant differences in 6-month depression and alcohol outcomes.
Conclusion: Treating comorbid smoking, problem drinking, and depression may increase smoking cessation rates above that of usual care and may be more practical than treating these disorders separately. (Cancer Epidemiol Biomarkers Prev 2006;15(11):2203–8)
New Marker of Colon Cancer Risk Associated with Heme Intake: 1,4-Dihydroxynonane Mercapturic Acid
Authors: Pierre Fabrice , Peiro Géraldine , Taché Sylviane , Cross Amanda J. , Bingham Sheila A. , Gasc Nicole , Gottardi Gaëlle , Corpet Denis E. , Guéraud Françoise 
Published: November 2006

Abstract
Background: Red meat consumption is associated with an increased risk of colon cancer. Animal studies show that heme, found in red meat, promotes preneoplastic lesions in the colon, probably due to the oxidative properties of this compound. End products of lipid peroxidation, such as 4-hydroxynonenal metabolites or 8-iso-prostaglandin-F2α (8-iso-PGF2α), could reflect this oxidative process and could be used as biomarkers of colon cancer risk associated with heme intake.
Methods: We measured urinary excretion of 8-iso-PGF2α and 1,4-dihydroxynonane mercapturic acid (DHN-MA), the major urinary metabolite of 4-hydroxynonenal, in three studies. In a short-term and a carcinogenesis long-term animal study, we fed rats four different diets (control, chicken, beef, and blood sausage as a high heme diet). In a randomized crossover human study, four different diets were fed (a 60 g/d red meat baseline diet, 120 g/d red meat, baseline diet supplemented with heme iron, and baseline diet supplemented with non-heme iron).
Results: DHN-MA excretion increased dramatically in rats fed high heme diets, and the excretion paralleled the number of preneoplastic lesions in azoxymethane initiated rats (P &lt; 0.0001). In the human study, the heme supplemented diet resulted in a 2-fold increase in DHN-MA (P &lt; 0.001). Urinary 8-iso-PGF2α increased moderately in rats fed a high heme diet (P &lt; 0.0001), but not in humans.
Conclusion: Urinary DHN-MA is a useful noninvasive biomarker for determining the risk of preneoplastic lesions associated with heme iron consumption and should be further investigated as a potential biomarker of colon cancer risk. (Cancer Epidemiol Biomarkers Prev 2006;15(11):2274–9)
Association between Nonsteroidal Anti-inflammatory Drug Use and the Incidence of Lung Cancer in the Iowa Women's Health Study
Authors: Hayes Jennifer H. , Anderson Kristin E. , Folsom Aaron R. 
Published: November 2006

Abstract
Background: Previous studies have suggested that use of aspirin or other nonsteroidal anti-inflammatory drugs (NSAIDs) may be associated with reduced risk of lung cancer, but the data are inconsistent and are limited particularly with respect to the effects of aspirin, separate from other NSAIDs.
Methods: The Iowa Women's Health Study is a prospective cohort of 41,836 Iowa women ages 55 to 69 years old at baseline in 1986. NSAID use was assessed in 1992. Over 10 years of follow-up, 403 incident cases of lung cancer were identified. The association of incident lung cancer with current use of aspirin or non-aspirin NSAIDs was analyzed after adjustment for lung cancer risk factors. Hazard ratios (HR) were estimated using multivariate COX proportional hazards regression.
Results: There were 27,162 women in the analytic cohort. After controlling for age, education, alcohol intake, pack-years, smoking status, body mass index, and total fruit intake, the RR of women taking six or more aspirin weekly was 1.21 (95% confidence interval, 0.92-1.59). The HR was 1.23 for women taking six or more non-aspirin NSAIDs weekly (95% confidence interval, 0.92-1.65). There was no statistically significant trend by frequency of use for either aspirin (Ptrend = 0.22) or non-aspirin NSAIDs (Ptrend = 0.53). Analyses by histologic type and smoking status yielded similar null results. Information on dosage and duration of use were not available for this analysis.
Conclusion: These findings do not suggest that aspirin or other NSAIDs reduce risk of lung cancer in this cohort of postmenopausal women. (Cancer Epidemiol Biomarkers Prev 2006;15(11):2226–31)
Effect of Mammography on Breast Cancer Risk in Women with Mutations in BRCA1 or BRCA2
Authors: Goldfrank Deborah , Chuai Shannon , Bernstein Jonine L. , Ramon y Cajal Teresa , Lee Johanna B. , Alonso M. Carmen , Diez Orland , Baiget Monserrat , Kauff Noah D. , Offit Kenneth , Robson Mark 
Published: November 2006

Abstract
Women who carry mutations in either the BRCA1 or BRCA2 genes are at risk for early-onset breast cancer and are recommended to begin screening mammography at age 25 to 30 years. Results of in vitro and animal studies suggest that BRCA1/BRCA2 mutation carriers are hypersensitive to ionizing radiation and possibly to radiation-induced breast cancer. This study was undertaken to investigate the association of low-dose radiation exposure from mammograms with breast cancer status in BRCA mutation carriers. One hundred sixty-two female mutation carriers provided information at time of genetic testing about exposure to mammograms before enrollment. Using unconditional logistic regression, breast cancer status was not associated with number of mammograms received before diagnosis (affected women) or ascertainment [unaffected women; adjusted odds ratio (OR), 0.94; P = not significant]. A larger group of 213 women provided information about lifetime number of mammograms. There was no association between mammogram exposure and risk in the group as a whole (adjusted OR, 1.04; P = not significant), although there was a modest association in BRCA1 carriers (adjusted OR, 1.08; P = 0.03). These findings indicate that screening mammography is unlikely to be associated with a large increase in breast cancer risk in this population. (Cancer Epidemiol Biomarkers Prev 2006;15(11):2311–3)
Malignant Lymphomas in Autoimmunity and Inflammation: A Review of Risks, Risk Factors, and Lymphoma Characteristics
Authors: Smedby Karin Ekström , Baecklund Eva , Askling Johan 
Published: November 2006

Abstract
Certain autoimmune and chronic inflammatory conditions, such as Sjögren's syndrome and rheumatoid arthritis (RA), have consistently been associated with an increased risk of malignant lymphomas, but it is unclear whether elevated lymphoma risk is a phenomenon that accompanies inflammatory conditions in general. Likewise, it is debated whether the increased risk identified in association with some disorders pertains equally to all individuals or whether it varies among groups of patients with different phenotypic or treatment-related characteristics. It is similarly unclear to what extent the increased lymphoma occurrence is mediated through specific lymphoma subtypes. This update reviews the many findings on risks, risk levels, and lymphoma characteristics that have been presented recently in relation to a broad range of chronic inflammatory, including autoimmune, conditions. Recent results clearly indicate an association between severity of chronic inflammation and lymphoma risk in RA and Sjögren's syndrome. Thus, the average risk of lymphoma in RA may be composed of a markedly increased risk in those with most severe disease and little or no increase in those with mild or moderate disease. The roles of immunosuppressive therapy and EBV infection seem to be limited. Furthermore, RA, Sjögren's syndrome, systemic lupus erythematosus, and possibly celiac disease may share an association with risk of diffuse large B-cell lymphoma, in addition to well-established links of Sjögren's syndrome with risk of mucosa-associated lymphoid tissue lymphoma and of celiac disease with risk of small intestinal lymphoma. However, there is also obvious heterogeneity in risk and risk mediators among different inflammatory diseases. (Cancer Epidemiol Biomarkers Prev 2006;15(11):2069–77)
Hepatitis C Virus and Risk of Lymphoma and Other Lymphoid Neoplasms: A Meta-analysis of Epidemiologic Studies
Authors: Dal Maso Luigino , Franceschi Silvia 
Published: November 2006

Abstract
The present meta-analysis was conducted to evaluate the strength and the consistency of the association between hepatitis C virus (HCV) infection and non–Hodgkin lymphoma (NHL) and other lymphoid neoplasms. Only studies with ≥100 cases which were also adjusted for sex and age were included. Fifteen case-control studies and three prospective studies contributed to present analysis, nine of which had not been included in previous meta-analyses. We calculated the pooled relative risks (RR) with corresponding 95% confidence intervals (95% CI), as a weighted average of the estimated RRs by random-effect models. The pooled RR of all NHL among HCV-positive individuals was 2.5 (95% CI, 2.1-3.0), but substantial heterogeneity was found between studies and by study design. Pooled RRs were 2.5 (95% CI, 2.1-3.1) in case-control studies and 2.0 (95% CI, 1.8-2.2) in cohort ones. The strongest source of heterogeneity seemed to be the prevalence of HCV among NHL-free study subjects (RR for NHL among HCV-positive individuals 3.0 and 1.9, respectively, for ≥5% and &lt;5% HCV prevalence). RRs were consistently increased for all major B-NHL subtypes, T-NHL, and primary sites of NHL presentation. Thus, previous suggestions that the RRs for HCV differed by NHL subtype were not confirmed in our meta-analysis. Associations weaker than with NHL were found between HCV infection and Hodgkin's lymphoma (RR, 1.5; 95% CI, 1.0-2.1) and multiple myeloma (RR, 1.6; 95% CI, 0.7-3.6), but they were based on much fewer studies than NHL. The etiologic fraction of NHL attributable to HCV varies greatly by country, and may be upward of 10% in areas where HCV prevalence is high. (Cancer Epidemiol Biomarkers Prev 2006;15(11):2078–85)
Coexpression of Fragile Histidine Triad and c-kit Is Relevant for Prediction of Survival in Patients with Small Cell Lung Cancer
Authors: Rehfeld Nina , Geddert Helene , Atamna Abedelsalam , Gabbert Helmut E. , Steidl Ulrich , Fenk Roland , Kronenwett Ralf , Haas Rainer , Rohr Ulrich-Peter 
Published: November 2006

AbstractBackground: In a retrospective analysis of 195 patients with small cell lung cancer (SCLC), we examined the prognostic value of a coexpression of fragile histidine triad (FHIT) protein and c-kit on patient's survival.Methods: As assessed by immunohistochemistry using formalin-fixed, paraffin-embedded tissue sections, tumors of 195 patients with SCLC were evaluated for FHIT and c-kit coexpression.Results: Coexpression of FHIT and c-kit was observed in 53.3%; a positive expression of either FHIT or c-kit was found in 40.5%. Complete lack of FHIT and c-kit (6.2%) was associated with a significantly shorter survival time for the patients with a mean of 122 ± 45 days compared with 468 ± 89 days for patients with lung cancer coexpressing FHIT and c-kit (P = 0.0011). The proportion of FHIT- and c-kit-positive cells within a tumor was also related to survival time. Patients with tumors with a proportion between 0% to 25% of FHIT- and c-kit-positive cells had the worst survival of 157 ± 34 days compared with 496 ± 95 days for patients showing &gt;25% FHIT- and c-kit-positive cells (P = 0.0002). Further, variables associated with shorter survival times were low performance status, elevated lactate dehydrogenase level, and advanced tumor stage according to tumor-node-metastasis classification. Multivariate analysis using Cox regression model, including 11 variables, confirmed the prognostic significance of a combined expression of FHIT and c-kit next to tumor stage, performance status, and lactate dehydrogenase level.Conclusions: Differential FHIT and c-kit expression was of prognostic relevance for survival in patients with SCLC and therefore provide useful variables for therapeutic decisions. (Cancer Epidemiol Biomarkers Prev 2006;15(11):2232–8)
Body Size, Mammographic Density, and Breast Cancer Risk
Authors: Boyd Norman F. , Martin Lisa J. , Sun Limei , Guo Helen , Chiarelli Anna , Hislop Greg , Yaffe Martin , Minkin Salomon 
Published: November 2006

AbstractBackground: Greater weight and body mass index (BMI) are negatively correlated with mammographic density, a strong risk factor for breast cancer, and are associated with an increased risk of breast cancer in postmenopausal women, but with a reduced risk in premenopausal women. We have examined the associations of body size and mammographic density on breast cancer risk.Method: We examined the associations of body size and the percentage of mammographic density at baseline with subsequent risk of breast cancer among 1,114 matched case-control pairs identified from three screening programs. The effect of each factor on risk of breast cancer was examined before and after adjustment for the other, using logistic regression.Results: In all subjects, before adjustment for mammographic density, breast cancer risk in the highest quintile of BMI, compared with the lowest, was 1.04 [95% confidence interval (CI), 0.8-1.4]. BMI was associated positively with breast cancer risk in postmenopausal women, and negatively in premenopausal women. After adjustment for density, the risk associated with BMI in all subjects increased to 1.60 (95% CI, 1.2-2.2), and was positive in both menopausal groups. Adjustment for BMI increased breast cancer risk in women with 75% or greater density, compared with 0%, increased from 4.25 (95% CI, 1.6-11.1) to 5.86 (95% CI, 2.2-15.6).Conclusion: BMI and mammographic density are independent risk factors for breast cancer, and likely to operate through different pathways. The strong negative correlated between them will lead to underestimation of the effects on risk of either pathway if confounding is not controlled. (Cancer Epidemiol Biomarkers Prev 2006;15(11):2086–92)
Prognostic Value of PAI1 in Invasive Breast Cancer: Evidence That Tumor-Specific Factors Are More Important Than Genetic Variation in Regulating PAI1 Expression
Authors: Sternlicht Mark D. , Dunning Alison M. , Moore Dan H. , Pharoah Paul D.P. , Ginzinger David G. , Chin Koei , Gray Joe W. , Waldman Frederic M. , Ponder Bruce A.J. , Werb Zena 
Published: November 2006

Abstract
Plasminogen activator inhibitor-1 (PAI1) can promote cancer progression, and its protein expression in tumors is an independent indicator of poor prognosis in many forms of cancer. Here, we show that high PAI1 mRNA levels also predict for shorter overall survival in two independent breast cancer data sets, highlighting the importance of its transcriptional regulation. The −675insG (4G/5G) single-nucleotide polymorphism in the PAI1 gene promoter has been shown to influence PAI1 transcription, with the 4G allele eliciting higher reporter gene expression in vitro and higher levels of circulating PAI1 in vivo. Nevertheless, its genotypic distribution in 2,539 British women with invasive breast cancer was virtually identical to that seen in 1,832 matched controls (P = 0.72), and annual mortality rates for 4G4G, 4G5G, and 5G5G cases were 2.6%, 2.8%, and 3.1% per year, respectively (P = 0.10). Thus, there was no association with breast cancer incidence or outcome, and in a separate set of breast cancers, the 4G/5G single-nucleotide polymorphism showed no association with PAI1 mRNA expression (P = 0.85). By contrast, connective tissue growth factor (CTGF), which can regulate PAI1 expression in culture, was associated with PAI1 expression in three independent cohorts (P ≪ 0.0001). In addition, PAI1 gene copy number differences in the tumors were correlated with PAI1 mRNA expression (P = 0.0005) and seemed to affect expression independently of CTGF. Thus, local factors, such as CTGF and genomic amplification, seem to be more important than germ line genetic variation in influencing PAI1 expression and its untoward effects in breast cancer. (Cancer Epidemiol Biomarkers Prev 2006;15(11):2107–14)
Synergy between Cigarette Smoking and Human Papillomavirus Type 16 in Cervical Cancer In situ Development
Authors: Gunnell Anthony S. , Tran Trung N. , Torrång Anna , Dickman Paul W. , Sparén Pär , Palmgren Juni , Ylitalo Nathalie 
Published: November 2006

Abstract
Background: A majority of studies have implicated the involvement of cigarette smoking in cervical cancer development, although its mechanism of action remains unclear. We conducted a large population-based case-control study to address the potential interaction between smoking and human papillomavirus type 16 (HPV-16) in development of cervical cancer in situ (CIS).
Methods: Information on risk factors for CIS was collected via interview, and archival cervical smears were tested for HPV-16 DNA presence in cases (n = 375) and controls (n = 363). Adjusted odds ratios (OR) for the effects of smoking, HPV-16 presence/absence, and load at first smear (taken, on average, 9 years before diagnosis) were calculated.
Results: The risk for CIS among current smokers who were HPV-16 positive at time of first smear was &gt;14-fold [adjusted OR, 14.4; confidence interval (95% CI), 5.6-36.8] compared with HPV-16-negative current smokers. In contrast, the risk for CIS among HPV-16-positive nonsmokers was only 6-fold (adjusted OR, 5.6; 95% CI, 2.7-11.5), compared with HPV-16-negative nonsmokers. HPV-16-positive smokers with high viral load at time of first smear exhibited a high risk for CIS (adjusted OR, 27.0; 95% CI, 6.5-114.2) compared with HPV-16-negative smokers. Within nonsmokers, however, high HPV-16 load contributed only a 6-fold increased risk compared with HPV-16-negative nonsmokers (adjusted OR, 5.9; 95% CI, 2.4-14.6). Interaction was observed (P = 0.03) between duration of smoking and HPV-16 presence in CIS development.
Conclusion: Results suggest a synergistic effect between smoking and both HPV-16 status and HPV-16 viral load, which may occur almost a decade before CIS detection. (Cancer Epidemiol Biomarkers Prev 2006;15(11):2141–7)
Identifying and Screening Patients at Risk of Second Cancers
Authors: Vogel Victor G. 
Published: November 2006

Abstract
Background: The average age of the U.S. population is increasing, and cancer incidence increases with age. Both improved early detection of first malignancies and effective primary oncologic therapy have led to prolonged survival, and the risk of secondary malignancies has consequently increased. A few anatomic sites are at increased risk for second malignancies within the same organ: breast, colon and rectum, lung, head and neck (or upper aerodigestive malignancies), prostate, and the uterine cervix. Some of the cancers also incur a risk for a second malignancy at another anatomic site. In addition, there are well-described clinical genetic syndromes that, as unique clinical entities, predispose to second malignant tumors.
Methods/Results: In this review, we focus on issues related to the risk of second malignancies among patients with primary breast, colon, lung and head and neck, prostate, and cervical cancers that comprise the most common sites of primary malignancy among patients in the United States. We review recent data related to both established and new screening strategies at these sites.
Conclusions: There is some evidence that screening will improve outcomes among patients who may develop second malignancies, although the data are limited. The optimal screening modalities and strategies to reduce mortality from second malignancies remain to be defined for most tumor sites. (Cancer Epidemiol Biomarkers Prev 2006;15(11):2027–32)
Risk of Squamous Cell Carcinoma of the Upper Aerodigestive Tract in Cancer-Free Alcoholic Japanese Men: An Endoscopic Follow-up Study
Authors: Yokoyama Akira , Omori Tai , Yokoyama Tetsuji , Sato Yasuo , Mizukami Takeshi , Matsushita Sachio , Higuchi Susumu , Maruyama Katsuya , Ishii Hiromasa , Hibi Toshifumi 
Published: November 2006

Abstract
Asian case-control studies have shown a strong relationship between the development of squamous cell carcinoma (SCC) of the esophagus and alcohol consumption combined with inactive aldehyde dehydrogenase-2 (ALDH2*1/*2), less-active alcohol dehydrogenase-1B (ADH1B*1/*1), high mean corpuscular volume (MCV), and self-reported facial flushing in response to alcohol. However, little is known about whether these risk factors prospectively influence cancer development in cancer-free alcoholics. Between 1993 and 2005, 808 Japanese alcoholic men diagnosed as cancer-free by an initial endoscopic screening examination received follow-up examinations ranging from 1 to 148 months (median, 31 months) later, and SCC of the upper aerodigestive tract was diagnosed in 53 of them (esophagus in 33 and oropharyngolarynx in 30). Cox proportional hazards analysis showed that the age-adjusted relative hazard for SCC was 11.55 [95% confidence interval (95% CI), 5.73-23.3] in ALDH2*1/*2 heterozygotes compared with ALDH2*1/*1 homozygotes, 2.02 (95% CI, 1.02-4.02) in ADH1B*1/*1 homozygotes compared with ADH1B*1/*2 heterozygotes or *2/*2 homozygotes, 2.64 (95% CI, 1.49-4.67) in patients with flushing compared with those who had never experienced flushing, 2.91 (95% CI, 1.63-5.20) in those with an MCV ≥ 106 compared with those with an MCV &lt; 106, 2.52 (95% CI, 1.22-5.22) in those who smoked ≥30 cigarettes per day compared with those who smoked 0 to 19 cigarettes per day, 7.26 (95% CI, 3.99-13.23) in those with esophageal dysplasia compared with those without distinct iodine-unstained lesions ≥5 mm, and 0.28 (95% CI, 0.09-0.85) in those with body mass index ≥ 23.2 (highest quartile) compared with those with body mass index &lt; 19.0 (lowest quartile). These predictors are useful for selecting appropriately patients for careful follow-up examinations. (Cancer Epidemiol Biomarkers Prev 2006;15(11):2209–15)