bluuebunny/crossref_metadata_2025_split huggingface dataset:
Efficacy of Skin Self-Examination Practices for Early Melanoma Detection
Authors: Pollitt Ricardo A. , Geller Alan C. , Brooks Daniel R. , Johnson Timothy M. , Park Elyse R. , Swetter Susan M. 
Published: November 2009

Abstract
Although skin self-examination (SSE) may increase rates of early melanoma detection, the efficacy of different SSE practices has not been thoroughly studied. We examined associations between SSE practices and tumor thickness in patients with recently diagnosed melanoma.
Methods: 321 melanoma patients at three hospitals completed questionnaires on demographics and SSE practices. Patient-reported SSE was measured by routine examination of 13 specific body areas, frequency of mole examination, and use of a melanoma picture aid to assist with SSE. Histologic diagnoses and Breslow depth were confirmed by dermatopathologists. Regression analyses were used to calculate ratios of geometric mean tumor thickness and odds ratios for having thicker versus thinner tumors for different SSE behaviors.
Results: Rates of SSE varied considerably by SSE item. Patients routinely examining at least some of their skin had thinner melanomas [adjusted geometric mean tumor ratio, 0.73; 95% confidence interval (95% CI), 0.50-0.94]. Frequency of mole examination did not predict tumor thickness. Using a melanoma picture as a SSE aid was strongly associated with reduced tumor thickness (adjusted ratio, 0.75; 95% CI, 0.66-0.85 for ever versus never use). A composite measure of thoroughness of SSE was the best predictor of thickness (adjusted ratio, 0.58; 95% CI, 0.36-0.75) for high versus low thoroughness.
Conclusions: SSE was associated with decreased tumor thickness by most measures. However, the diverse rates of SSE practices and the distinct associations between these practices and melanoma thickness suggest a complexity in SSE that should be addressed in future studies. SSE should be evaluated by more than one measure. (Cancer Epidemiol Biomarkers Prev 2009;18(11):3018–23)
Evaluation of an ELISA for p16INK4a as a Screening Test for Cervical Cancer
Authors: Balasubramanian Akhila , Hughes James , Mao Constance , Ridder Ruediger , Herkert Matthias , Kiviat Nancy B. , Koutsky Laura A. 
Published: November 2009

AbstractBackground: The low sensitivity of cytology and low specificity of human papillomavirus testing prompts searching for more accurate cervical cancer screening strategies. Our goal was to evaluate an ELISA-based test for p16INK4a.Methods: 1,781 women undergoing routine screening provided cervical specimens for p16INK4a ELISA (original and enhanced versions of a prototype), liquid-based cytology, and Hybrid Capture II (hc2) testing. All women with a positive result and a random sample of those with negative results on all tests were referred for histologic diagnosis. Cervical intraepithelial neoplasia grade ≥3 (≥CIN3) was the main outcome. The original analysis included all ≥CIN3 outcomes (n = 28). The a posteriori analysis was used to represent clinically relevant results with ≥CIN3 as outcomes only when detected after a positive screening test (n = 27).Results: Participants had a median age of 23 years. The prevalence of high-risk human papillomavirus DNA was 30.6%. In a posteriori analyses, the sensitivity and specificity for p16INK4a ELISA (≥8 pg/mL cut-point), cytology, and hc2 were 50.9%, 58.1%, and 100.0%, respectively, and 90.4%, 89.3%, and 69.2%, respectively. Referral to colposcopy of women with positive results for hc2 and p16INK4a (enhanced ELISA, ≥6 pg/mL cut-point) had a sensitivity of 91.8% (95% confidence interval, 79.1-100.0%) and specificity of 86.0% (95% confidence interval, 82.0-89.0%). Results of the original analyses had similar specificity but substantially lower sensitivity due to the strong influence of the single CIN3 case with completely negative screening results.Conclusions: An enhanced version of this prototypic p16INK4a ELISA showed promise in screening, particularly when combined with hc2. (Cancer Epidemiol Biomarkers Prev 2009;18(11):3008–17)
Incidence of Cancer in Finnish Families with Clinically Aggressive and Nonaggressive Prostate Cancer
Authors: Pakkanen Sanna , Pukkala Eero , Kainulainen Heidi , Matikainen Mika P. , Koivisto Pasi A. , Tammela Teuvo L.J. , Schleutker Johanna 
Published: November 2009

Abstract
Background: Clinical features of familial prostate cancer (PCa) and other malignancies associated with PCa are poorly described. Using a large family-based data registry of histologically confirmed cancers with a 40-year follow-up, we sought to determine incidence of cancer in Finnish PCa families, separately for clinically aggressive and clinically nonaggressive PCa.
Methods: We calculated standardized incidence ratios (SIR) for 5,523 members of 202 families by dividing the number of observed cancers (altogether 497 cases) by the number of expected cancers. The number of expected cancers is based on the national cancer incidence rates.
Results: SIR for overall cancer risk, excluding PCa, for male relatives in clinically nonaggressive families was 0.7 [95% confidence interval (95% CI), 0.6-0.8] and in clinically aggressive families 0.8 (95% CI, 0.6-1.0). The respective SIRs for women were 1.0 (95% CI, 0.8-1.1) and 1.1 (95% CI, 0.8-1.3). The incidence of lung cancer among men was significantly lower than in the general population. The SIR for gastric cancer among women was 1.9 in both clinically nonaggressive and clinically aggressive families. In clinically aggressive families, there was borderline significant excess of cancer of the gallbladder in men and liver cancer in women.
Conclusions: The incidence of non-PCa cancers is not increased in clinically aggressive or clinically nonaggressive PCa families except for stomach cancer among women. (Cancer Epidemiol Biomarkers Prev 2009;18(11):3049–56)
Methylation Markers for CCNA1 and C13ORF18 Are Strongly Associated with High-Grade Cervical Intraepithelial Neoplasia and Cervical Cancer in Cervical Scrapings
Authors: Yang Nan , Eijsink Jasper J.H. , Lendvai Ágnes , Volders Haukeline H. , Klip Harry , Buikema Henk J. , van Hemel Bettien M. , Schuuring Ed , van der Zee Ate G.J. , Wisman G. Bea A. 
Published: November 2009

Abstract
Purpose: Recently, we reported 13 possible cervical cancer–specific methylated biomarkers identified by pharmacologic unmasking microarray in combination with large-genome computational screening. The aim of the present study was to perform an in-depth analysis of the methylation patterns of these 13 candidate genes in cervical neoplasia and to determine their diagnostic relevance.
Experimental Design and Results: Five of the 13 gene promoters (C13ORF18, CCNA1, TFPI2, C1ORF166, and NPTX1) were found to be more frequently methylated in frozen cervical cancer compared with normal cervix specimens. Quantitative methylation analysis for these five markers revealed that both CCNA1 and C13ORF18 were methylated in 68 of 97 cervical scrapings from cervical cancer patients and in only 5 and 3 scrapings, respectively, from 103 healthy controls (P &lt; 0.0005). In cervical scrapings from patients referred with an abnormal Pap smear, CCNA1 and C13ORF18 were methylated in 2 of 43 and 0 of 43 CIN 0 (no cervical intraepithelial neoplasia) and in 1 of 41 and 0 of 41 CIN I, respectively. Furthermore, 8 of 43 CIN II, 22 of 43 CIN III, and 3 of 3 microinvasive cancer patients were positive for both markers. Although sensitivity for CIN II or higher (for both markers 37%) was low, specificity (96% and 100%, respectively) and positive predictive value (92% and 100%, respectively) were high.
Conclusion: Methylation of CCNA1 and C13ORF18 in cervical scrapings is strongly associated with CIN II or higher-grade lesions. Therefore, these markers might be used for direct referral to gynecologists for patients with a methylation-positive scraping. (Cancer Epidemiol Biomarkers Prev 2009;18(11):3000–7)
An Admixture Scan in 1,484 African American Women with Breast Cancer
Authors: Fejerman Laura , Haiman Christopher A. , Reich David , Tandon Arti , Deo Rahul C. , John Esther M. , Ingles Sue A. , Ambrosone Christine B. , Bovbjerg Dana Howard , Jandorf Lina H. , Davis Warren , Ciupak Gregory , Whittemore Alice S. , Press Michael F. , Ursin Giske , Bernstein Leslie , Huntsman Scott , Henderson Brian E. , Ziv Elad , Freedman Matthew L. 
Published: November 2009

AbstractAfrican American women with breast cancer present more commonly with aggressive tumors that do not express the estrogen receptor (ER) and progesterone receptor (PR) compared with European American women. Whether this disparity is the result of inherited factors has not been established. We did an admixture-based genome-wide scan to search for risk alleles for breast cancer that are highly differentiated in frequency between African American and European American women, and may contribute to specific breast cancer phenotypes, such as ER-negative (ER−) disease. African American women with invasive breast cancer (n = 1,484) were pooled from six population-based studies and typed at ∼1,500 ancestry-informative markers. We investigated global genetic ancestry and did a whole genome admixture scan searching for breast cancer–predisposing loci in association with disease phenotypes. We found a significant difference in ancestry between ER+PR+ and ER−PR− women, with higher European ancestry among ER+PR+ individuals, after controlling for possible confounders (odds ratios for a 0 to 1 change in European ancestry proportion, 2.84; 95% confidence interval, 1.13-7.14; P = 0.026). Women with localized tumors had higher European ancestry than women with non–localized tumors (odds ratios, 2.65; 95% confidence interval, 1.11-6.35; P = 0.029). No genome-wide statistically significant associations were observed between European or African ancestry at any specific locus and breast cancer, or in analyses stratified by ER/PR status, stage, or grade. In summary, in African American women, genetic ancestry is associated with ER/PR status and disease stage. However, we found little evidence that genetic ancestry at any one region contributes significantly to breast cancer risk or hormone receptor status. (Cancer Epidemiol Biomarkers Prev 2009;18(11):3110–7)
Colorectal Mucosal Expression of MSH2 as a Potential Biomarker of Risk for Colorectal Neoplasms
Authors: Sidelnikov Eduard , Bostick Roberd M. , Flanders W. Dana , Long Qi , Seabrook March E. 
Published: November 2009

Abstract
To characterize the expression of the mismatch repair gene MSH2 in normal colorectal crypts in humans and assess parameters of its expression as a potential modifiable biomarker of risk for colorectal neoplasms, we conducted a pilot, colonoscopy-based case-control study (51 cases and 154 controls) of incident, sporadic colorectal adenoma. Biopsies of normal-appearing rectal, sigmoid, and ascending colon mucosa were procured, immunohistochemically processed for MSH2 protein, and analyzed using custom quantitative image analysis procedures. MSH2 expression in adenoma cases was lower than in controls by 49% (P = 0.01) and 23% (P = 0.06) in the ascending colon and rectum, respectively, but not in the sigmoid colon. MSH2 expression in the rectum was 39% (P = 0.04) higher in subjects who regularly took a nonsteroidal anti-inflammatory drug than in those who did not, and it tended to be lower in those with adenomas in the right colon and those who had an adenoma with more advanced characteristics. These preliminary data suggest that lower MSH2 expression in the normal colonic mucosa, at least in the ascending colon and rectum, may be associated with increased risk of incident, sporadic colorectal adenoma as well as with modifiable risk factors for colorectal neoplasms, thus supporting further investigation of MSH2 expression as a potential modifiable biomarker of risk for colorectal neoplasms. (Cancer Epidemiol Biomarkers Prev 2009;18(11):2965–73)
Selenium Supplementation Reduced Oxidative DNA Damage in Adnexectomized BRCA1 Mutations Carriers
Authors: Dziaman Tomasz , Huzarski Tomasz , Gackowski Daniel , Rozalski Rafal , Siomek Agnieszka , Szpila Anna , Guz Jolanta , Lubinski Jan , Wasowicz Wojciech , Roszkowski Krzysztof , Olinski Ryszard 
Published: November 2009

AbstractSome experimental evidence suggests that BRCA1 plays a role in repair of oxidative DNA damage. Selenium has anticancer properties that are linked with protection against oxidative stress. To assess whether supplementation of BRCA1 mutation carriers with selenium have a beneficial effect concerning oxidative stress/DNA damage in the present double-blinded placebo control study, we determined 8-oxodG level in cellular DNA and urinary excretion of 8-oxodG and 8-oxoGua in the mutation carriers. We found that 8-oxodG level in leukocytes DNA is significantly higher in BRCA1 mutation carriers. In the distinct subpopulation of BRCA1 mutation carriers without symptoms of cancer who underwent adnexectomy and were supplemented with selenium, the level of 8-oxodG in DNA decreased significantly in comparison with the subgroup without supplementation. Simultaneously in the same group, an increase of urinary 8-oxoGua, the product of base excision repair (hOGG1 glycosylase), was observed. Therefore, it is likely that the selenium supplementation of the patients is responsible for the increase of BER enzymes activities, which in turn may result in reduction of oxidative DNA damage. Importantly, in a double-blinded placebo control prospective study, it was shown that in the same patient groups, reduction in cancer incidents was observed. Altogether, these results suggest that BRCA1 deficiency contributes to 8-oxodG accumulation in cellular DNA, which in turn may be a factor responsible for cancer development in women with mutations, and that the risk to developed breast cancer in BRCA1 mutation carriers may be reduced in selenium-supplemented patients who underwent adnexectomy. (Cancer Epidemiol Biomarkers Prev 2009;18(11):2923–8)
Long-Term and Recent Recreational Physical Activity and Survival After Breast Cancer: The California Teachers Study
Authors: West-Wright Carmen Nicole , Henderson Katherine DeLellis , Sullivan-Halley Jane , Ursin Giske , Deapen Dennis , Neuhausen Susan , Reynolds Peggy , Chang Ellen , Ma Huiyan , Bernstein Leslie 
Published: November 2009

Abstract
Introduction: Long-term physical activity is associated with lower breast cancer risk. Little information exists on its association with subsequent survival.
Methods: California Teachers Study cohort members provided information in 1995-1996 on long-term (high school through age 54 years) and recent (past 3 years) participation in moderate and strenuous recreational physical activities. The 3,539 women diagnosed with invasive breast cancer after cohort entry and through December 31, 2004, were followed through December 31, 2005. Of these, 460 women died, 221 from breast cancer. Moderate and strenuous physical activities were combined into low (≤0.50 h/wk/y of any activity), intermediate (0.51-3.0 h/wk/y of moderate or strenuous activity but no activity &gt;3.0 h/wk/y), or high activity (&gt;3.0 h/wk/y of either activity type). Multivariable relative risks (RR) and 95% confidence intervals (95% CI) for mortality were estimated using Cox proportional hazards methods, adjusting for race/ethnicity, estrogen receptor status, disease stage, and baseline information on comorbidities, body mass index, and caloric intake.
Results: Women with high or intermediate levels of long-term physical activity had lower risk of breast cancer death (RR, 0.53; 95% CI, 0.35-0.80; and RR, 0.65; 95% CI, 0.45-0.93, respectively) than women with low activity levels. These associations were consistent across estrogen receptor status and disease stage, but were confined to overweight women. Deaths due to causes other than breast cancer were related only to recent activity.
Conclusions: Consistent long-term participation in physical activity before breast cancer diagnosis may lower risk of breast cancer death, providing further justification for public health strategies to increase physical activity throughout the lifespan. (Cancer Epidemiol Biomarkers Prev 2009;18(11):2851–9)
CYP1A2, GSTM1, andGSTT1Polymorphisms and Diet Effects on CYP1A2 Activity in a Crossover Feeding Trial
Authors: Peterson Sabrina , Schwarz Yvonne , Li Shuying S. , Li Lin , King Irena B. , Chen Chu , Eaton David L. , Potter John D. , Lampe Johanna W. 
Published: November 2009

AbstractCytochrome P-450 1A2 (CYP1A2) is a biotransformation enzyme that activates several procarcinogens. CYP1A2 is induced by cruciferous and inhibited by apiaceous vegetable intake. Using a randomized, crossover feeding trial in humans, we investigated the dose effects of cruciferous vegetables and the effects of any interaction between cruciferous and apiaceous vegetables on CYP1A2 activity. We also investigated whether response varied by CYP1A2*1F, GSTM1, and GSTT1 genotypes (glutathione S-transferases that metabolize crucifer constituents) and whether CYP1A2 activity rebounds after apiaceous vegetables are removed from the diet. Participants (N = 73), recruited based on genotypes, consumed four diets for two weeks each: low-phytochemical diet (basal), basal plus single dose of cruciferous (1C), basal plus double dose of cruciferous (2C), and basal plus single dose of cruciferous and apiaceous vegetables (1C+A). CYP1A2 activity was determined by urine caffeine tests administered at baseline and the end of each feeding period. Compared with basal diet, the 1C diet increased CYP1A2 activity (P &lt; 0.0001) and the 2C diet resulted in further increases (P &lt; 0.0001), with men experiencing greater dose-response than women. The 1C+A diet decreased CYP1A2 activity compared with the 1C and 2C diets (P &lt; 0.0001 for both). Although there was no overall effect of CYP1A2*1F or GSTM1-null/GSTT1-null genotypes or genotype-by-diet interactions, there were significant diet response differences within each genotype. Additionally, CYP1A2 activity recovered modestly one day after the removal of apiaceous vegetables. These results suggest complex interactions among dietary patterns, genetic variation, and modulation of biotransformation that may not be apparent in observational studies. (Cancer Epidemiol Biomarkers Prev 2009;18(11):3118–25)
Colorectal Cancer Incidence and Postmenopausal Hormone Use by Type, Recency, and Duration in Cancer Prevention Study II
Authors: Hildebrand Janet S. , Jacobs Eric J. , Campbell Peter T. , McCullough Marjorie L. , Teras Lauren R. , Thun Michael J. , Gapstur Susan M. 
Published: November 2009

Abstract
The Women's Health Initiative randomized trials showed a reduction in colorectal cancer risk with the use of estrogen plus progesterone (E + P), but not with estrogen alone (E-only), after intervention periods &lt;7 years. Using data from the Cancer Prevention Study II Nutrition Cohort, we examined associations of colorectal cancer risk with E-only and E + P, including analyses by recency and duration of hormone use. During 13.2 years of follow-up, 776 cases of invasive colorectal cancer occurred among 67,412 postmenopausal women participants. Cox proportional hazards models were used to estimate multivariate-adjusted relative risks (RR) and 95% confidence intervals (95% CI) of colorectal cancer for current and former hormone users according to hormone type and duration of use. Relative to women who never used postmenopausal hormones, current, but not former, use of E-only was associated with a reduced risk of colorectal cancer (RR 0.76; 95% CI, 0.59-0.97). Among current E-only users, duration of use was inversely and linearly associated with risk (Ptrend = 0.01). Use of E-only for &lt;5 years was not associated with reduced risk, whereas use for ≥20 years was associated with a 45% reduction in risk (RR, 0.55; 95% CI, 0.36-0.86). There were no statistically significant associations between E + P and colorectal cancer risk. Our results suggest a strong inverse association of long-term use of E-only with colorectal cancer risk, underscoring the importance of collecting data on duration of hormone use in epidemiologic studies of postmenopausal hormones and risk of disease. (Cancer Epidemiol Biomarkers Prev 2009;18(11):2835–41)
Breast Cancer Recurrence in Older Women Five to Ten Years after Diagnosis
Authors: Bosco Jaclyn L.F. , Lash Timothy L. , Prout Marianne N. , Buist Diana S.M. , Geiger Ann M. , Haque Reina , Wei Feifei , Silliman Rebecca A. ,   for the BOW Investigators
Published: November 2009

Abstract
Little is known about the risk of recurrence &gt;5 years after diagnosis among older breast cancer survivors. A community-based population of women ≥65 years diagnosed with early-stage breast cancer who survived disease free for 5 years was followed for 5 additional years or until a diagnosis of breast cancer recurrence, second primary, death, or loss to follow-up. These 5-year disease-free survivors (N = 1,277) had primary breast cancers that were node negative (77%) and estrogen receptor positive or unknown (86%). Five percent (n = 61) developed a recurrence between 5 and 10 years after diagnosis: 25% local, 9.8% regional, and 66% distant. Women who were node positive [hazard ratio (HR), 3.9; 95% confidence interval (95% CI), 1.5-10], had poorly differentiated tumors (HR, 2.5; 95% CI, 0.9-6.6), or who received breast conserving surgery without radiation therapy (HR, 2.4; 95% CI, 1.0-5.8) had higher recurrence rates compared with node negative, well differentiated, and receipt of mastectomy, respectively. Not receiving adjuvant tamoxifen, compared with receiving adjuvant tamoxifen, was also positively associated with late recurrence among women with estrogen receptor–positive/unknown tumors. Although relatively few women experience a late recurrence, most recurrences present as advanced disease, which is difficult to treat in older women. This study of late recurrence emphasizes that the risk, although small, is not negligible even in this group at high risk of death due to competing causes. (Cancer Epidemiol Biomarkers Prev 2009;18(11):2979–83)
Asbestos Exposure and Gestational Trophoblastic Disease: A Hypothesis
Authors: Reid Alison , Heyworth Jane , de Klerk Nick , Musk A.W. 
Published: November 2009

Abstract
Among 2,968 women and girls exposed to crocidolite (blue asbestos) at Wittenoom, three cases of choriocarcinoma and three cases of hydatidiform mole have been identified (crude incidence rate of 9.9 per 1000 women and 1.7 per 1000 deliveries for choriocarcinoma and hydatidiform mole, respectively). The women with choriocarcinoma were resident at Wittenoom at the time of disease development, whereas hydatidiform mole occurred much later in women who had first been exposed to asbestos as young girls. Four of the six cases were known to have lived with asbestos company workers who brought their dusty work-clothes home for washing. Asbestos fibers have been reported in the lung, the pleural and peritoneal mesothelium, and the human ovary. They have also been detected in placental digests of live and stillborn infants. This cluster of gestational trophoblastic diseases has some biological plausibility for asbestos causation. Taking an occupational and residential history and examining pathologic specimens for asbestos fibers or bodies may prove useful in patients with gestational trophoblastic disease. (Cancer Epidemiol Biomarkers Prev 2009;18(11):2895–8)