bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 5475: National survey of malignant mesothelioma and asbestos exposure in Japan
Authors: Fujimoto Nobukazu , Gemba Kenichi , Aoe Keisuke , Kato Katsuya , Takeshima Yukio , Inai Kouki , Kishimoto Takumi 
Published: August 2012

Abstract
A newspaper article published in June 2005 reported that 5 residents who lived near the now-closed asbestos cement pipe plant in Amagasaki developed pleural mesothelioma. The asbestos-related problems that the article described caused much social concern resulting in the so-called ‘Kubota shock.’ Patients who have a history of occupational asbestos exposure and have developed malignant mesothelioma are provided worker's compensation in Japan. However, among 878 cases of death due to mesothelioma in 2003, only 85 cases were actually compensated. Based on this, we initiated this retrospective survey and extracted 6,030 cases of death due to MM between 2003 and 2008 to clarify the clinical features of MM including the association with asbestos exposure (AE). Among them, clinical diagnosis of MM was confirmed in 929 cases. The origin of MM included the pleura in 794 (85.5%) cases, the peritoneum in 123 (13.2%) cases, the pericardium in 7 (0.8%) cases, and the testicular tunica vaginalis in 5(0.5%) cases. The histological subtype of MM included 396 (55.9%) epithelioid, 154(21.7%) sarcomatoid, 126 (17.8%) biphasic, and 33 (4.7%) cases classified as other types. AE was indicated in 76.8% and pleural plaques were detected in 34.2% of all MM cases. Asbestos particles were determined in 103 MM cases. More than 1,000 asbestos particles per gram dried lung tissue were detected in 74.8%, and more than 5,000 particles were detected in 43.7% of the cases. We compared the patient characteristics and the diagnostic procedures of MM before and after the ‘Kubota shock’. Compared to the early phase of this study (2003-2005), the median age at diagnosis of MM was higher, the number of cases without definite diagnosis of MM was lower, the proportion of cases diagnosed by thoracoscopy was higher, and the percentage of the cases in which the occupational history was described in the medical record was significantly higher in the late phase (2006-2008). Our study confirmed that more than 70% of MM cases in Japan are associated with AE. The ‘Kubota shock’ might affect some features pertaining to MM.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 5475. doi:1538-7445.AM2012-5475
Abstract 5478: Indoor coal smoke exposure, tobacco use, and lung cancer risk in Xuanwei, China
Authors: Kim Christopher , Chapman Robert , Hu Wei , He Xingzhou , Hosgood H. Dean , Liu Larry Z. , Lai Hong , Tian Linwei , Chen Wei , Rothman Nathaniel , Lan Qing 
Published: August 2012

Abstract
Introduction: Lung cancer rates in Xuanwei County, Yunnan Province are among the highest in China. We have previously reported that indoor combustion of smoky coal for home heating and cooking was associated with increased risk of lung cancer and that this effect varies markedly by coal type. Further, improved stove ventilation is followed by reduction in lung cancer risk. We explored the joint relationship between tobacco use and coal use in Xuanwei men. Methods: We analyzed data from a population-based case-control study of lung cancer in Xuanwei. Cases were identified from four Xuanwei hospitals and controls were selected from the general population by probability sampling. Controls were matched one-to-one with cases on age. In total, 260 cases and 260 controls were analyzed in this study. Tobacco, coal, and solid fuel exposures were tabulated from questionnaires and reported in cigarette pack-years, duration of smoking, and average tons of coal used annually. Odds ratios and 95% confidence intervals were estimated by conditional logistic regression with the main effects of coal, smoking, and coal-smoking interaction terms. Results: Overall, smoking was positively and significantly, although only modestly, associated with lung cancer risk (OR per pack-year: 1.02; 95% CI: 1.01-1.04). The risk of lung cancer per pack-year of smoking decreased as cumulative lifetime use of smoky coal increased (0-50 tons coal: OR: 1.07; 95% CI: 1.01-1.15; &gt;50-150 tons coal: OR: 1.05; 95% CI: 1.01-1.10; &gt;150 tons coal: OR: 1.00; 95% CI: 0.99-1.03; P-interaction: 0.041). Discussion: Our results suggest that the effect of tobacco on lung cancer risk was weaker in men exposed to higher amounts of coal. Results are consistent with previous cohort study findings in Xuanwei. Constituents of coal combustion, such as polycyclic aromatic hydrocarbons, could plausibly act to diminish the carcinogenicity of tobacco through metabolic competition or other possible mechanisms.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 5478. doi:1538-7445.AM2012-5478
Abstract 5489: Feasibility study of gut microbiome collection in randomly sampled women
Authors: Feigelson Heather Spencer , Bischoff Kimberly , Ravel Jacques , Gail Mitchell H. , Flores Roberto , Goedert James J. 
Published: August 2012

Abstract
Systemic estrogen level strongly determines risk for postmenopausal breast cancer (BC). We hypothesize that differences in hormone metabolism by the gut microbiota may contribute to BC risk by modulating enterohepatic circulation of estrogens. We conducted a study to determine the feasibility of enrolling healthy postmenopausal members of Kaiser Permanente Colorado (KPCO) in a fecal microbiome study. With electronic medical records, we created a pool of potentially eligible women aged 55-69 who recently had a negative screening mammogram. We excluded those with any hormone prescription in the prior 12 months, an antibiotic prescription in the prior 6 months, or history of cancer, inflammatory bowel disease or other conditions likely to affect fecal microbiota. A packet (invitation letter, informed consent form, information pamphlet, and opt-out postcard) was sent to 250 randomly sampled women. Women who have not returned the postcard are contacted by KPCO research staff to determine interest in participating, verify eligibility, and obtain verbal informed consent. Consented participants were mailed a second packet with a self-administered risk factor questionnaire, link to an on-line diet questionnaire, collection kit for urine (to measure 15 estrogens) and stool specimens, and shipping instructions to the laboratory. Enrollees have spent an estimated 1-2 hours completing all recruitment and data collection components. To date, 60 (24%) have enrolled, 70 (28%) refused (most via the opt-out card), and the remainder are pending phone contact. As shown in the table, the enrolled women are similar to the total sample; slightly more of them are non-Hispanic white, and they are more likely to have a history of breast biopsy. These data demonstrate that we can successfully recruit an apparently representative sample of women into a microbiome study.

Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 5489. doi:1538-7445.AM2012-5489
Abstract 5491: A history of allergies is associated with reduced risk of oral squamous cell carcinoma
Authors: Stott-Miller Marni , Chen Chu , Doody David R. , Schwartz Stephen M. 
Published: August 2012

Abstract
History of any type of allergy is associated with a decreased risk of multiple types of cancers, including colorectal, cervical, esophageal, pancreatic, stomach, leukemia and glioma. It is proposed that having a history of allergies may prevent cancer by enhancing immune surveillance against tumor cells early in disease development and/or against carcinogenic infectious agents. While a few prior studies suggest an inverse relationship between history of allergies and oral squamous cell carcinoma (OSCC); they did not distinguish between oropharyngeal cancer and oral cavity cancers, and did not account for HPV infection. We compared 400 OSCC cases newly diagnosed between 1985-1995 with 613 general population controls from the Seattle-Puget Sound metropolitan areas with respect to self-reported history of allergy to each of the following: dust, pollen, mold, dogs, cats, bee stings, drugs and food. We estimated odds ratios (OR) and 95% confidence intervals (CI), adjusted for age, education level, sex, race, pack years of cigarette smoking, and lifetime average alcoholic drinks per week. We observed a small inverse association between history of any allergy and OSCC (OR=0.81, 95% CI, 0.61-1.08). This inverse association was present only for dust (OR=0.70; 95% CI,0.43-1.13), pollen (OR=0.72; 95% CI,0.51-1.02) and mold (OR=0.34; 95% CI,0.14-0.83). Additional adjustment for HPV-16 seropositivity did not materially affect the estimates. In exploratory analyses, we examined associations with dust, pollen or mold more closely, and observed stronger associations with oropharyngeal cancer (OR=0.56; 95% CI, 0.35-0.90) than with oral cavity cancer (OR=0.71; 95% CI, 0.49-1.05); although a polytomous regression model did not suggest heterogeneity by site (p=0.5). There was no effect modification by sex, cigarette smoking, alcohol consumption, HPV-16 seropositivity (for all sites or oropharynx alone), or herpes simplex virus 1 seropositivity. The inverse association with dust/pollen/mold was near null for 30 cases of oncogenic HPV DNA-positive oropharyngeal cancer (OR=0.86; 95% CI, 0.38-1.94) and stronger for 46 cases of oncogenic HPV DNA-negative oropharyngeal cancer (OR=0.53; 95% CI, 0.24-1.19). These results suggest that a history of allergies to dust, pollen or mold may confer some protection against OSCC. That the inverse association was particularly apparent for oropharyngeal SCC would be consistent with heightened immune surveillance, due to the substantial amount of lymphatic tissue in this organ. Whether the inverse association involves an immune response to HPV or other antigen, or other carcinogenic mechanism, remains to be determined in more definitive studies.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 5491. doi:1538-7445.AM2012-5491
Abstract 5513: Treatment and mortality in men with localized prostate cancer: A population-based study in California
Authors: Sieh Weiva , Lichtensztajn Daphne Y. , Nelson David O. , Cockburn Myles , West Dee W. , Brooks James D. , Chang Ellen T. 
Published: August 2012

Abstract
Purpose: To provide patients and physicians with population-based estimates of mortality from prostate cancer or other causes depending upon the primary treatment modality, stratified by patient age, tumor stage and grade. Patients and Methods: We conducted a 10-year competing-risk analysis of 45,440 men diagnosed with clinically localized (T1 or T2) prostate cancer in California during 1995-1998. Information on patient demographics, tumor characteristics, primary treatment and causes of death was obtained from the California Cancer Registry. Results: In this population-based observational cohort, the most common primary treatment was surgery (40.4%), followed by radiotherapy (29.1%), active surveillance (20.8%), and androgen deprivation therapy (ADT) monotherapy (9.8%). Prostate cancer mortality differed significantly (p &lt; 0.0001) across treatment groups among patients &lt;80 years at diagnosis with moderately or poorly differentiated disease. In these patients, the 10-year disease-specific mortality rates were generally lowest for men treated with surgery, ranging from 1.2% (95% CI, 0.8-1.7%) to 11.0% (95% CI, 8.4-14.2%); and highest for men treated with ADT monotherapy, ranging from 3.3% (95% CI, 0.8-12.5%) to 53.8% (95% CI, 34.4-72.2%). Conclusion: Use of ADT monotherapy for localized prostate cancer is not uncommon and should be reconsidered in light of the poor outcomes found in this study, lack of supportive evidence from clinical trials, and potential side effects. Although comparisons of treatment effects based on observational data are subject to confounding by indication, the cause-specific mortality estimates provided in this population-based study can help patients and physicians make management decisions based upon expected outcomes and practice patterns in the general population.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 5513. doi:1538-7445.AM2012-5513
Abstract 5522: Analysis of recruitment of non small cell lung cancer patients into clinical trials
Authors: Joubert Richard , Bortini Stefanella , Raeth Ulrich , Moehler Thomas 
Published: August 2012

Abstract
Background: Clinical trials are a major step for the assessment of new molecules or novel treatments that may change the medical practice. Accurate estimation of patient recruitment plays a major role when planning clinical trials with new treatment modalities for non-small cell lung cancer (NSCLC) patients. Method: We performed a systematical review of all published results from NSCLC clinical studies in Journal of Clinical Oncology and Journal of Thoracic Oncology between January 2009 and December 2010 by focusing on the parameters considered to be relevant for patient recruitment: number of patients, sites and enrollment period, indication, Phase of trial, type of study sponsor, geographic region, type of drug and line of treatment. Results: Of 104 studies identified within PubMed, data from 51 studies could be integrated into the final analysis. Fifty-three studies were omitted from this analysis as recruitment data were missing. Most of trials were performed in the metastatic or advanced setting. Overall, a mean enrollment of 0.64 Patient/Month/Site (range, 0.02 to 7.14) was estimated and the highest mean recruitment rate estimated was 1.81 Patients/Month/Site corresponding to 9 single-center studies. The mean enrollment rates in Patient/Month/Site were 0.57 for Phase I trials, 0.78 for Phase II trials and 0.33 for Phase III trials. University-sponsored trials were able to enroll patients with the highest mean rate of 1.48 Patient/Month/Site. Trials conducted in only European sites recruited patients with the highest mean rate of 1.40 Patient/Month/Site (8 studies). The majority of the studies evaluated treatments based on targeted therapy alone or combined with cytotoxic chemotherapy. Thirty-five (69%) studies assessed first-line treatment but the highest recruitment rate of 1.02 Patient/Month/Site was estimated for second- and subsequent lines of treatment. The statistically significant differences were mainly found when comparing the mean recruitment rates for (i) the different types of sponsor and (ii) the number of sites involved in the study. These best recruitment rates were found for University driven studies and in single-center trials. Conclusions: Study design aspects as phase I dose escalation and randomization are systematic burden to patient recruitment. Thorough planning of the study to optimize and adapt the treatment concept used in the study and attract the interest of the investigators and patients are key to recruitment. In that respect, phase II trials on targeted agents as single agents or in combination with high potential to impact the standard treatment showed 2-fold higher than mean enrollment rate for multi-center trials.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 5522. doi:1538-7445.AM2012-5522
Abstract 5533: Imaging stromal recruitment during liver metastasis formation in the GFP-MUP-uPA mouse
Authors: Suetsugu Atsushi , Ogata Hisanobu , Moriwaki Hisataka , Saji Shigetoyo , Karin Michael , Hoffman Robert M. 
Published: August 2012

Abstract
Major urinary protein-urokinase type plasminogen activator (MUP-uPA) transgenic mice develop liver disease resembling that described for albumin promoter-uPA transgenic mice. We have developed the GFP-MUP-uPA mice, by crossing MUP-uPA mouse with transgenic C57/BL6 mouse expressing GFP. Hepatocyte fluorescence in this model is relatively weak. In contrast, GFP fluorescence of non-parenchymal cells such as stellate cells, Kupper cells and endotherial cells is very bright green more than parenchymal cells enabling the portal vein and sinusoid structure to be clearly visualized Huh7 liver cancer cells expressing red fluorescent protein (RFP) were injected in the spleen of MUP-uPA transgenic mice. By day 7, the Huh7-RFP celsl were visualized in the liver with the Olympus FV1000 conforcal microscope. The hepatoma cells grew around the sinusoids of the host liver. The liver-metastatic Huh7-RFP cells recruited bright GFP-expressing non-parenchymal cells. This model enables imaging the effects of uPA on liver metastasis and stromal recruitment enabling the metastasis to progress.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 5533. doi:1538-7445.AM2012-5533
Abstract 5535: Availability of a newly designed technique, triple-combination array analysis: Identification of estrogen receptor 1 gene in hepatocellular carcinoma using this method
Authors: Hishida Mitsuhiro , Nomoto Shuji , Inokawa Yoshikuni , Hayashi Masamichi , Kodera Yasuhiro 
Published: August 2012

Abstract
Background: Hepatocellular carcinoma (HCC) is one of the top five causes of cancer-related deaths worldwide. Recent developments in the treatment of HCC have failed to treat completely or prevent HCC. Genome-wide gene-expression profile analyses can now detect many candidate genes that are modified by HCC. We have developed a new technique to identify suppressor genes of HCC: triple-combination array analysis. Methods: Triple-combination array analysis, which combines gene expression profiles, single nucleotide polymorphism arrays and methylation arrays, was performed on each HCC tissue sample. Subsequently, samples from 48 HCC patients were subjected to quantitative real-time reverse-transcriptase polymerase chain reaction (PCR) and methylation-specific PCR. Results: Using this method, estrogen receptor 1 (ESR1) was detected as a candidate suppressor gene. Of the 48 clinical samples, 40 (83.3%) showed ESR1 promoter hypermethylation. In 24 (50%) HCC samples, the expression level of ESR1 gene was decreased by &gt;90%, which was significantly related to hepatitis B virus, high liver damage score, and pathological invasion of the intrahepatic portal vein. Conclusions: The present study indicates that triple-combination array is an available and convenient technique for detecting the genes with altered expression in disease, and we suggest that the ESR1 gene acts as a suppressor gene in HCC.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 5535. doi:1538-7445.AM2012-5535
Abstract 5540: Non malignant breast cancer tissue identification scoring system
Authors: Eppenberger-Castori Serenella , Sengstag Thierry , Delorenzi Mauro , Gueth Uwe , Wight Edward , Eppenberger Urs , Terracciano Luigi , Obermann Ellen , Obermann Ellen , Vuaroqueaux Vincent , Zanetti-Daellenbach Rosanna 
Published: August 2012

Abstract
Abstract: Introduction. Molecular pathology tools are increasingly important in routine diagnostic. Histological determination remains mandatory, while gene expression profiles (GEP) are successfully classifying breast cancer specimens also when minimal amount of tissue, such as core biopsies (CB), is available. The limit of this application resides however in the fact that the part of material used for RNA extraction could not represent the entire biopsy. To overcome this problem in the present work we calculated an algorithm for the identification of malignant cells in a giving CB. Patients and methods. The quantitative expression levels of 60 selected genes representative for relevant pathways in breast cancer (BC) oncogenesis were assessed by real time PCR in a total of 106 CB samples obtained from patients with neoplasia or invasive BC and in 12 biopsies with known good differentiation grade (Grade 1). The GEP of 48 CBs and of the 12 Grade 1 specimens were used as training set to build the scoring system based on the Welsh variant of t-test and best-fit logistic curves. The remaining GEPs were used as validation set. Results. A 15-genes classifier was built and cross-validated with 1000 iterations of a leave −10% out in which each of the 10 subset is used. The 15 genes were representative for proliferation (thymidine phosphorylase and E2F1), cell matrix degradation (CTSD, MMP1, MMP11, PLAU, PLAUR, SERPINE1), as well as angiogenesis (VEGFA, VEGFD, TGFbeta1). EGFR and GSTP1 were also part of this classifier able to discriminate non-malignant from malignant breast tissue with an accuracy of almost 90%. Discussion. The calculated classifier, which could also be reduced to only six genes, is robust and useful in the discrimination of malignant from non-malignant breast cancer tissue. Such an algorithm identifying normal proliferation rate and inability of invasion should be integrated in the evaluation of GEP data from microarrays before using them for other predictive purposes.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 5540. doi:1538-7445.AM2012-5540