bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract A90: Anthropometry, cigarette smoking, alcohol consumption, and the risk of thyroid cancer in the U.S. Radiologic Technologists Study
Authors: Meinhold Cari , Ron Elaine , Schonfeld Sara , Alexander Bruce , Freedman D. Michal , Linet Martha , Berrington de Gonzalez Amy 
Published: May 2012

Abstract
A90
Several case-control studies suggest that BMI may increase and cigarette smoking may reduce the risk of thyroid cancer, but results from prospective studies are limited. We investigated the associations between anthropometric factors, cigarette smoking, alcohol consumption and thyroid cancer risk by following a cohort of 67,055 female and 20,557 male radiologic technologists in the United States from 1983 through 2006. Hazards ratios (HRs) and 95% confidence intervals (CIs) were calculated using proportional hazards models adjusted for age, sex, smoking status, and benign thyroid conditions, and where appropriate, height or BMI. After a mean follow-up of 15.8 years, 268 (229 female and 39 male) incident thyroid cancer cases were ascertained. Obesity (BMI ≥30.0 kg/m2) was associated with an increased risk of thyroid cancer (HR for women= 1.74, 95% CI 1.22, 2.49; HR for men= 2.27, 95% CI 1.00, 5.13) compared to BMI in the normal range (18.5-24.9 kg/m2). Compared to never smokers, current but not former smokers had a reduced risk of thyroid cancer (HR for women= 0.52, 95% CI 0.34, 0.79; HR for men= 0.28, 95% CI 0.08, 0.94). Alcohol consumption and smoking duration and intensity were not associated with thyroid cancer after adjustment for current smoking. The results were similar after restricting to confirmed (N=223, 83%) or papillary (N=191, 86%) thyroid cancers. We estimate that obesity may account for 9% of thyroid cancers in this cohort and 22% of incident thyroid cancers in the United States currently. In this prospective study, obesity increases and current cigarette smoking decreases the risk of thyroid cancer in both women and men.
Citation Information: Cancer Prev Res 2008;1(7 Suppl):A90.
Abstract A91: Obesity and the TMPRSS2:ERG translocation in prostate cancer
Authors: Mucci Lorelei , Ma Jing , Perner Sven , Stampfer Meir , Kurth Tobias , Rubin Mark , Kantoff Philip 
Published: May 2012

Abstract
A91

Background
The recently identified TMPRSS2:ERG translocation is an early and common somatic event in prostate cancer pathogenesis involving the TMPRSS2 promotor, which is androgen regulated, and ERG, a member of the ETS family of transcriptional factors. Regulation of TMPRSS2 by androgens is intriguing and suggests both a potential mechanism whereby a man’s hormonal milieu could drive the progression of prostate tumor cells and also a mechanism by which androgen deprivation therapy may work. We explored the relationship of obesity, with its known relation with lower circulating testosterone and higher estradiol, on prostate cancer risk according to TMPRSS2:ERG fusion status.

Methods
The study was nested among 29,067 men in the prospective Physicians’ Health Study (PHS) during 1982 to 2008. Information on obesity was collected through structured questionnaires at baseline and follow-up, and included total obesity (weight and body mass index, BMI) and central obesity (waist circumference) measures. We characterized the TMPRSS2:ERG fusion by fluorescence in situ hybridization on archival tumor tissue from 305 men diagnosed with incident prostate cancer during 25 years of follow-up. We applied logistic regression models to compare the association of obesity on relative risk of fusion positive and fusion negative prostate cancer.

Results
Almost half the men in PHS were overweight (BMI 25-26.9 kg/m2) or very overweight/obese (BMI 27 kg/m2 or greater) at the start of follow-up. Prevalence of the TMPRSS2:ERG translocation among the men with prostate cancer was 40.0%, in line with other studies. The association of obesity on prostate cancer risk differed in relation to the translocation. Men with a higher BMI at baseline had a reduced risk of developing fusion positive prostate cancer (7% lower risk per increase in BMI, p for trend ~ 0.0021). Compared to healthy weight men, those who were very overweight/obese had a 60% lower risk of fusion positive prostate cancer (RR=0.43, 95% CI 0.22-0.83). Moreover, men with a larger waist circumference were at lower risk of developing fusion positive cancer (p for trend ~0.0017). In contrast, there was no association between total or central adiposity measures at baseline and risk of fusion-negative prostate cancer.

Discussion
Obesity appears to reduce the risk of prostate tumors that carry the TMPRSS2:ERG fusion, but is unrelated to risk of prostate cancers that occur via fusion-independent mechanisms. These preliminary data provide insight into the link between the hormonal milieu and the heterogeneity of prostate cancer.
Citation Information: Cancer Prev Res 2008;1(7 Suppl):A91.
Abstract A95: Genetic variability in energy metabolism and pancreatic cancer risk: A population-based case-control study in Minnesota
Authors: Zhang Jianjun , Dhakal Ishwori , Gross Myron , Lang Nicholas , Kadlubar Fred , Kadlubar Susan , Anderson Kristin 
Published: May 2012

Abstract
A95
Pancreatic cancer is one of the leading causes of cancer death in developed countries. Although the etiology of pancreatic cancer remains elusive, based on epidemiologic studies, obesity and type-2 diabetes appear to increase risk of this fatal disease. Therefore, it is possible that polymorphisms in genes involved in energy metabolism modulate pancreatic cancer risk. We investigated this hypothesis using a case-control study conducted during 1994-1998 in Minnesota. Cases (n=189), aged 20 years or older, were ascertained from all hospitals in the metropolitan area of the Twin Cities and the Mayo Clinic; from the later, only cases residing in the Upper Midwest of the US were recruited. Controls (n=486) were randomly selected from the general population and frequency matched to cases by age (within 5 years) and sex. Polymorphisms in four genes were genotyped: leptin (LEP, -2548G&gt;A, rs7799039), leptin receptor (LEPR, Gln223Arg, rs1137101), and neuropeptide Y (NPY, Leu7Pro, rs16139) (regulating energy intake), and β2-adrenoceptor (ADRB2, Gly16Arg, rs1042713) (regulating energy expenditure). Odds ratios (OR) and 95% confidence intervals (95% CI) were estimated using unconditional logistic regression. After adjustment for age, sex, race, education, cigarette smoking, and alcohol use, a statistically significantly reduced risk of pancreatic cancer was observed in subjects who were heterozygous or homozygous for the NPY7Pro allele as compared with those who were homozygous for the NPY7Leu allele) [OR (95%CI): 0.39 (0.15-0.89)]. The variant allele (16Arg) of ADRB2 was associated with a borderline significantly increased risk [OR (95%CI): 1.47 (0.99-2.21)]. No appreciable effects were detected for the LEP and LEPR sequence variants examined. The genetic associations described above were not markedly modified by physical activity or dietary intake of energy, fat, or fiber. This study offers novel data suggesting that genetic variability in the regulation of energy intake and expenditure influences pancreatic cancer risk.
Citation Information: Cancer Prev Res 2008;1(7 Suppl):A95.
Abstract A96: Association of leptin with sex steroid hormones, insulin, and CRP among adult men in NHANES III
Authors: Lai Gabriel , Rohrmann Sabine , Rifai Nader , Platz Elizabeth 
Published: May 2012

Abstract
A96

Objective
We previously observed an inverse association between leptin concentration and risk of prostate cancer, which was contrary to our hypothesis (AACR 2008). It is possible that the association between leptin - a hormone secreted by adipocytes - and prostate cancer or other cancers may be explained by confounding by other hormone and metabolic biomarkers. To address this issue, we evaluated the association of leptin with sex steroid hormones, insulin, and C-reactive protein (CRP) among a nationally representative sample of US men in the Third National Health and Nutrition Survey (NHANES III).

Methods
1149 men aged 20+ years and who attended the morning examination session of Phase I of NHANES III (1988-1991) were included. We measured serum concentrations of testosterone, androstanediol glucuronide (AAG) (a metabolite of dihydrotestosterone), estradiol, and sex hormone binding globulin (SHBG) by immunoassay. Insulin, CRP, and leptin were measured previously. Free hormones were estimated from measured total hormones, albumin, and SHBG. Height, weight and waist circumference were measured. Percent body fat was calculated from bioelectrical impedance and anthropometric data. Data on alcohol, smoking, and physical activity were obtained by interview. Using linear regression, we estimated geometric mean concentrations of hormones, insulin, and CRP by quartiles of leptin, applying sampling weights and adjusting for age, alcohol, smoking, physical activity, waist circumference, percent body fat and race/ethnicity.

Results
Men who had higher leptin concentrations had lower testosterone (Q1: 5.7, Q2: 5.3, Q3: 4.8, Q4: 4.7 ng/mL; p-trend = 0.02). Although the trend was not statistically significant, men who had higher leptin had lower free testosterone (0.109, 0.106, 0.098, 0.096 ng/mL; p-trend = 0.10). Men who had higher leptin had higher estradiol (34.7, 34.8, 36.4, 38.5 pg/mL; p-trend = 0.03), free estradiol (0.86, 0.89, 0.94, 1.01 pg/mL; p-trend = 0.007), and insulin (43.7, 50.1, 56.3, 60.0 pmol/L; p-trend = 0.0006) levels. Men in the lowest quartile of leptin had the highest SHBG; levels were the same in the upper 3 quartiles (37.7, 34.0, 33.1, 32.5 nmol/mL; p-trend = 0.14). Leptin did not appear to be associated with AAG or CRP. These patterns were similar within age strata.

Conclusions
Even after taking into account extent of body fat and other factors, leptin appears to be inversely associated with total and free testosterone but positively associated with estradiol, free estradiol, and insulin. In analysis of the independent association of leptin and prostate and other cancers, whether overall or by stage/grade, in addition to adiposity, adjustment for other hormonal and metabolic correlates of leptin may also be necessary.
Citation Information: Cancer Prev Res 2008;1(7 Suppl):A96.
Abstract A98: Cigarette smoking, environmental tobacco smoke exposure, and pancreatic cancer risk in the European Prospective Investigation into Cancer and Nutrition
Authors: Vrieling Alina , Bueno-de-Mesquita H. Bas , Boshuizen Hendriek , the EPIC study group For 
Published: May 2012

Abstract
A98
Cigarette smoking is an established risk factor for pancreatic cancer. However, prospective data for most European countries are lacking, and epidemiologic studies on exposure to environmental tobacco smoke (ETS) in relation to pancreatic cancer risk are scarce.
We examined the association of cigarette smoking (current and lifetime intensity, duration, pack-years, time since quitting) and exposure to ETS with pancreatic cancer risk within the European Prospective Investigation into Cancer and Nutrition (EPIC). This analysis was based on 465,910 participants, including 524 first incident pancreatic cancer cases diagnosed after a median follow-up of 8.9 years. Estimates of risk were obtained by Cox proportional hazard models and adjusted for weight, height, and history of diabetes mellitus.
Current cigarette smokers had an elevated risk of pancreatic cancer compared to never smokers (hazard ratio (HR) = 1.71, 95% confidence interval (CI): 1.36, 2.15), and risk increased with greater intensity and pack-years. Former cigarette smokers who quit for less than 10 years were also at greater risk of pancreatic cancer (HR = 1.44, 95% CI: 1.06, 1.95), but risk was comparable to never smokers after quitting for 10 years or more. Further, pancreatic cancer risk was increased among never smokers daily exposed to ETS (for many hours) during childhood (HR = 2.60, 95% CI: 0.95, 7.06) and exposed to ETS at home and/or work (HR = 1.54, 95% CI: 1.00, 2.39).
These results from a large European prospective cohort suggest that both active cigarette smoking, as well as exposure to ETS, is associated with increased risk of pancreatic cancer.
Citation Information: Cancer Prev Res 2008;1(7 Suppl):A98.
Abstract B10: Development and pilot testing of a brochure to increase awareness of inherited breast cancer in black women
Authors: Vadaparampil Susan , Quinn Gwendolyn , Giyishi Anxhela , Pal Tuya 
Published: May 2012

Abstract
B10

Background
Due to low levels of awareness about hereditary breast cancer and underutilization of genetic counseling and testing services in the Black community, there is an urgent need to provide information about these topics to Black women. Existing genetic education materials have generally been developed by and for White women and thus may have reduced relevance for Black women. Objective: To create a culturally tailored, educationally relevant brochure to increase awareness about hereditary breast cancer within the Black community. Methods: Three focus groups were conducted with female members of Black community based organizations representing a diverse set of sociodemographic (e.g., age, education) and clinical (e.g., breast cancer status) characteristics. Discussions were led using a standardized guide with probes to assess the creative and educational aspects of a mock brochure (n=46). Trained, race-concordant moderators with previous experience discussing preventive health behaviors were used for each focus group. Each focus group was audio-taped and handwritten notes were taken by at least 3 members of the research team. Summaries of each focus group were created using these data sources. Content analysis based on Grounded Theory was conducted using an iterative process, and each summary was independently coded by three members of the research team.

Results
The majority of participants were over age 41 (67%) and married (43%). Thirty-seven percent were college graduates or beyond and 72% had children. The key content areas related to improvement of the brochure were to: (1) Include additional information about aspects of breast cancer specific to Black women; (2) Use the term Black rather than African American or Women of Color; (3) Provide more details about the process of genetic counseling and testing; and (4) Include a color scheme representative of the Black community. Positive aspects of the brochure that were well received included: (1) Using patient photos and personal vignettes; (2) Targeting Black women with the race specific information about risk; and 3) Acknowledgment of common misperceptions about hereditary breast cancer.

Conclusion
Black women in this study expressed a strong desire for culturally relevant information related to genetic counseling and testing for hereditary breast cancer. When provided an opportunity to offer feedback prior to finalizing a brochure, women identified important areas for improvement that are likely to lead to more culturally tailored and acceptable educational materials. By implementing these suggestions, the study team expects the brochure will provide meaningful information about inherited breast cancer that is appropriate for widespread dissemination to Black women.
Citation Information: Cancer Prev Res 2008;1(7 Suppl):B10.
Abstract B100: Chemopreventive efficacy of Spirulina in precancerous lesions of cervix.
Authors: Sharma Nidhi , Kumar Ashok 
Published: May 2012

Abstract
B100

Objectives
Gynaecological malignancies represent approximately 13 % of cancers in women and accounts for 9.8% of all cancers deaths. India accounts for one-fifth of the world burden of cervical cancer, which is a good example of disease with a preclinical phase that can be detected in a pre-invasive stage, using Papanicolaou Smear. In the present study attempt has been made to prevent or delay the development of cancer in ostensibly healthy females with specified risk factors or precancerous conditions through chemoprevention. Extensive work has been done on the chemopreventive efficacy of the Spirulina in oral cancer patients, which is a tiny bluish algae and is the highest source of vitamin b12 in addition with iron, vit-A, C, E, zinc and selenium.

Method
78 females above the age of 35, with eroded cervix were identified with precancerous lesions in Zanana Hospital (in between 2002-2005) who were questioned about their habits, habitat, dietary habits, economic status, reproductive history and other related conditions. The female were divided into two groups, the first group with eroded cervix was treated with Monalina (a product of Spirulina)and the other group served as control and both the groups were screened at 4 to 6 month intervals for two years annually thereafter.

Results
The results in the first group demonstrated significantly reduction in the progression of dysplasia incidence, while in some cases the moderate condition was arrested as such without transformation into hyperplasia as compared to the control group.

Conclusions
There is a lot of research potential in analyzing the cervical cancer patients with Spirulina, by screening them with Pap smear, before the onset of invasive cervical carcinoma.
Citation Information: Cancer Prev Res 2008;1(7 Suppl):B100.
Abstract B101: Caspase-dependent induction of apoptosis by novel lupane-type pentacyclic triterpenoids
Authors: Koohang Ali , Mar Aye Aye , Szotek Erika , Eiznhamer David , Flavin Michael , Xu Ze-Qi 
Published: May 2012

Abstract
B101

Background
Betulinic acid is a naturally occurring lupane-type pentacyclic triterpenoid with great activity in the treatment and prevention of cancer. As an apoptosis inducer, it inhibits cancer cell growth in human melanoma, glioblastoma, neuroblastoma, leukemia, prostate and ovarian carcinomas. Several studies have linked the anticancer property of betulinic acid to its ability to induce apoptosis in cancer cells by targeting the mitochondrial pathway of apoptosis. We have been interested in the structure -activity studies of modified lupane-type pentacyclic triterpenoids to develop new cancer preventive drugs with enhanced pro-apoptotic activities.

Methods
New compounds were prepared in five to seven synthetic steps. The panel of cell lines used in our investigation included SK-MEL-2 and A-375 from malignant melanoma of the skin, Daoy and LN-229 from cerebellar medulloblastoma, OVCAR-3 from ovarian, HT-29 from colorectal adenocarcinoma and MCF-7 from breast adenocarcenoma clinical samples. Cell growth inhibitory activity was measured by tetrazolium-based MTS assay and reported as IC50 values. Homogeneous caspase activation was quantified by a fluorimetric assay and apoptosis induction was characterized by an annexin-type flow cytometry assay and measured as ratio of early-mid apoptotic to necrotic cells.

Results
The structure -activity relationship analysis reveals that amino group incorporation has significant impact on the cytotoxicty of triterpenes. Mono-amino derivatives inhibited cancer cell growth with potency 2-6 times higher than betulinic acid, whereas bis-amino analogues exhibited inhibitory effect with IC50 values of 10-100 times lower. Further mechanism of action studies revealed that these new amino pentacyclic triterpenoids induced apoptosis and activated caspases. In SK-MEL-2 (melanoma) cells, apoptosis was induced as early as 2 h at 15 μM and a similar amount of apoptosis induction was observed at 16 h in Daoy (glioblastoma) cells.

Conclusions
Our results show that incorporation of amino groups into the structure of lupane-type pentacyclic triterpenoids at various positions markedly improves cytotoxicity of these molecules with unique apoptosis induction ability. Further pharmacological evaluation on this new class of modified natural products is warranted to develop promising agents for cancer treatment and prevention.
Citation Information: Cancer Prev Res 2008;1(7 Suppl):B101.
Abstract B102: Fenretinide induces lethal autophagy via a novel ensemble of life and death regulators: dihydroceramide and sphinganine versus sphinganine 1-phosphate
Authors: Sims Kacee , Fluke Katie , Symolon Holly , Zheng Wenjing , Munter Elizabeth , Momin Amin , Pack Carrie , Haynes Chris , Kelly Samuel , Allegood Jeremy , Wang Elaine , Merrill Alfred 
Published: May 2012

Abstract
B102
Fenretinide (4-hydroxyphenylretinamide, 4HPR) is a promising anticancer agent that is being evaluated in human clinical trials. One of the proposed mechanisms of action for 4HPR is to increase the biosynthesis of ceramide, an inducer of apoptosis. Using liquid chromatography, electrospray ionization tandem mass spectrometry (LC ESI MS/MS) for “sphingolipidomic” analysis, we have found (H Wang et al., Mol. Cancer Ther. 7: 2967-2976, 2008) that 4HPR elevates dihydroceramides instead of ceramides due to the inhibition of dihydroceramide desaturase, and also increases the amounts of sphinganine and sphinganine 1-phosphate. In exploring how these metabolites could mediate 4HPR cytotoxicity, we have additionally discovered that dihydroceramides induce autophagy, and whether this is cytotoxic depends on the relative amounts of sphinganine 1-phosphate versus sphinganine--a highly toxic compound due to its effects on multiple signaling pathways as well as being lysosomotrophic. These findings reveal new facets of sphingolipid biology and autophagy, and suggest that the efficacy of 4HPR_and presumably other inhibitors of dihydroceramide desaturase--might be increased by concomitant inhibition of sphingosine kinase. (Acknowledgement: Some of these studies were conducted in collaboration with Dr. Myles Cabot of the John Wayne Cancer Institute, and funded by the Lipid MAPS Consortium grant GM069338.)
Citation Information: Cancer Prev Res 2008;1(7 Suppl):B102.
Abstract B103: Aquaporin 5 (AQP5) is expressed in primary human leukemic cells.
Authors: Chae Young Kwang , Kim Myungshin , Han Kyungja , Jung Chan Kwon , Kim Yonggoo , Sidransky David , Moon Chulso 
Published: May 2012

Abstract
B103
Aquaporins (AQPs) are water channel proteins that facilitate transcellular water movements. H        uman AQPs have previously been associated with increased expression in solid tumors. Recent reports suggest the role of AQP5 in promoting cancer progression,         providing a potential basis for designing a novel therapy targeting AQP5        . However, its expression pattern in hematologic malignancies has not been described yet. Thus, here, we have performed flow cytometry analysis with bone marrow samples of human leukemic patients (n=47). We have found that AQP5 is expressed in human leukemia (57.4%, 27/47) including acute myeloid leukemia (13/22), acute lymphoblastic leukemia (6/10), and chronic myelogenous leukemia (7/14) and chronic lymphocytic leukemia (1/1). However, normal bone marrow samples (n=5) did not show any expression of AQP5. Among 47 samples, cells with only surface expression of AQP5 were 8 (17.0%), cells with only cytoplasmic expression were 12 (25.5%), and cells with both surface and cytoplasmic expression were 7 (14.9%). Of interest, the association between AQP5 expression and resistance in chemotherapy was suggestive (chi square test, p=0.059). 7 out of 8 relapse cases expressed AQP5. Intriguingly, the odds of developing relapse in patients with AQP5 expression (7/20) was 6.7 times that in patients without AQP5 expression (1/19).
In summary, our report demonstrates for the first time that human AQP5 is expressed in all types of primary human leukemic cells. It also provides a basis for pursuing its possible role in the progression of human blood cancers as in solid tumors.
Citation Information: Cancer Prev Res 2008;1(7 Suppl):B103.