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  • American Association for Cancer Research (AACR)  (17)
  • 1
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 76, No. 20 ( 2016-10-15), p. 6076-6083
    Abstract: Incidence rates for liver cancer have increased 3-fold since the mid-1970s in the United States in parallel with increasing trends for obesity and type II diabetes mellitus. We conducted an analysis of baseline body mass index (BMI), waist circumference (WC), and type II diabetes mellitus with risk of liver cancer. The Liver Cancer Pooling Project maintains harmonized data from 1.57 million adults enrolled in 14 U.S.-based prospective studies. Cox regression estimated HRs and 95% confidence intervals (CI) adjusted for age, sex, study center, alcohol, smoking, race, and BMI (for WC and type II diabetes mellitus). Stratified analyses assessed whether the BMI–liver cancer associations differed by hepatitis sera-positivity in nested analyses for a subset of cases (n = 220) and controls (n = 547). After enrollment, 2,162 incident liver cancer diagnoses were identified. BMI, per 5 kg/m2, was associated with higher risks of liver cancer, more so for men (HR = 1.38; 95% CI, 1.30–1.46) than women (HR = 1.25; 95% CI, 1.17–1.35; Pinteraction = 0.02). WC, per 5 cm, was associated with higher risks of liver cancer, approximately equally by sex (overall, HR = 1.08; 95% CI, 1.04–1.13). Type II diabetes mellitus was associated with higher risk of liver cancer (HR = 2.61; 95% CI, 2.34–2.91). In stratified analyses, there was a null association between BMI and liver cancer risk for participants who were sera-positive for hepatitis. This study suggests that high BMI, high WC, and type II diabetes mellitus are associated with higher risks of liver cancer and that the association may differ by status of viral hepatitis infection. Cancer Res; 76(20); 6076–83. ©2016 AACR.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
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    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2016
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  • 2
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 77, No. 13_Supplement ( 2017-07-01), p. 3007-3007
    Abstract: Background: Since 1980, liver cancer has been among the most rapidly increasing cancer types in the United States (US), with 5-year survival rates of approximately 17%. While tobacco and alcohol are known to be associated with primary liver cancer, it is unclear whether they only increase the risk of hepatocellular carcinoma (HCC), the most common type of liver cancer, or whether they also increase risk of intrahepatic cholangiocarcinoma (ICC), second most common histologic type. Additionally, it is unclear what amount of alcohol consumption is associated with an increased risk of liver cancer. As liver cancer is a rare cancer type, we conducted a study of pooled data from the National Cancer Institute Cohort Consortium to examine the associations between smoking and alcohol use and liver cancer, stratified by histologic subtype. Methods: In the Liver Cancer Pooling Project, a consortium of US-based cohort studies, we pooled data from 1,518,741 individuals (HCC n=1,423, ICC n=410) in 14 cohorts. Multivariable-adjusted hazard ratios (HRs) and 95% confidence intervals (CI) were estimated using proportional hazards regression. Cubic splines were used to model the association between alcohol and liver cancer risk. Results: Compared to never smokers, both former and current smokers at study baseline had an increased risk of ICC (HR=1.32, 95% CI: 1.03-1.68 and HR=1.47, 95% CI: 1.07-2.02, respectively) and HCC (HR=1.24, 95% CI: 1.08-1.43 and HR=1.86, 95% CI: 1.57-2.20, respectively). This finding was consistent for heavier smoking intensity, longer duration of smoking, and more pack-years of smoking. Heavy alcohol consumption was associated with an 87% increased risk of HCC (HR≥7 drinks/day v. non-drinker=1.87, 95% CI: 1.41-2.47) and a non-significant 68% increased risk of ICC (HR≥5 drinks/day v. non-drinker=1.68, 95% CI: 0.99-2.86). Risk of HCC significantly increased at 4.5 alcoholic drinks per day, while risk of ICC was non-significantly increased with any amount of consumption. Conclusions: These findings suggest that, in a US population, cigarette smoking is associated with an increased risk of both histologic subtypes of primary liver cancer - HCC and ICC. In contrast, alcohol consumption was primarily associated with an increased risk of HCC. These results suggest that smoking cessation and alcohol reduction programs could be important intervention opportunities for these lethal cancer types. Citation Format: Jessica Leigh Petrick, Peter T. Campbell, Jill Koshiol, Jake E. Thistle, Gabriella Andreotti, Laura E. Beane-Freeman, Julie E. Buring, Andrew T. Chan, Dawn Q. Chong, Michele M. Doody, Susan M. Gapstur, John Michael Gaziano, Edward Giovannucci, Barry I. Graubard, I-Min Lee, Linda M. Liao, Martha S. Linet, Julie R. Palmer, Jenny N. Poynter, Mark P. Purdue, Kim Robien, Lynn Rosenberg, Catherine Schairer, Howard D. Sesso, Rashmi Sinha, Meir J. Stampfer, Marcia Stefanick, Jean Wactawski-Wende, Xuehong Zhang, Anne Zeleniuch-Jacquotte, Neal D. Freedman, Katherine A. McGlynn. Tobacco smoking, alcohol use and risk of hepatocellular carcinoma and intrahepatic cholangiocarcinoma: The Liver Cancer Pooling Project [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 3007. doi:10.1158/1538-7445.AM2017-3007
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
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    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2017
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  • 3
    In: Cancer Prevention Research, American Association for Cancer Research (AACR), Vol. 8, No. 12 ( 2015-12-01), p. 1156-1162
    Abstract: Chronic inflammation plays a pivotal role in the pathogenesis of hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (ICC), the two most common types of liver cancer. A number of prior experimental studies have suggested that nonsteroidal anti-inflammatory drugs (NSAIDs), including aspirin and ibuprofen, may potentially protect against liver cancer. However, no observational study has examined the association between aspirin duration and dose or other over-the-counter non-aspirin NSAIDs, such as ibuprofen, and liver cancer incidence. Furthermore, the association between NSAID use and risk of ICC is unclear. As part of the Liver Cancer Pooling Project, we harmonized data on 1,084,133 individuals (HCC = 679, ICC = 225) from 10 U.S.-based prospective cohort studies. Cox proportional hazards regression models were used to evaluate multivariable-adjusted HRs and 95% confidence intervals (CI). Current aspirin use, versus nonuse, was inversely associated with HCC (HR, 0.68; 95% CI, 0.57–0.81), which persisted when restricted to individuals not using non-aspirin NSAIDs and in a 5- and 10-year lag analysis. The association between aspirin use and HCC risk was stronger for users who reported daily use, longer duration use, and lower dosage. Ibuprofen use was not associated with HCC risk. Aspirin use was associated with a reduced ICC risk in men (HR, 0.64; 95% CI, 0.42–0.98) but not women (HR, 1.34; 95% CI, 0.89–2.01; Pinteraction = 0.01). The observed inverse association between aspirin use and liver cancer in our study, together with previous data, suggests the merit of future intervention studies of aspirin and other agents that affect chronic inflammatory pathways for HCC and possibly ICC. Cancer Prev Res; 8(12); 1156–62. ©2015 AACR.
    Type of Medium: Online Resource
    ISSN: 1940-6207 , 1940-6215
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2015
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  • 4
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 24, No. 9 ( 2015-09-01), p. 1398-1406
    Abstract: Background: Coffee consumption has been reported to be inversely associated with hepatocellular carcinoma (HCC), the most common type of liver cancer. Caffeine has chemopreventive properties, but whether caffeine is responsible for the coffee–HCC association is not well studied. In addition, few studies have examined the relationship by sex, and no studies have examined whether there is an association between coffee and intrahepatic cholangiocarcinoma (ICC), the second most common type of liver cancer. Methods: In the Liver Cancer Pooling Project, a consortium of U.S.-based cohort studies, data from 1,212,893 individuals (HCC, n = 860; ICC, n = 260) in nine cohorts were pooled. Multivariable-adjusted hazard ratios (HR) and 95% confidence intervals (CI) were estimated using proportional hazards regression. Results: Higher coffee consumption was associated with lower risk of HCC (HR & gt;3 cups/day vs. non-drinker, 0.73; 95% CI, 0.53–0.99; Ptrend cups/day = & lt;0.0001). More notable reduced risk was seen among women than men (Pinteraction = 0.07). Women who consumed more than three cups of coffee per day were at a 54% lower risk of HCC (HR, 0.46; 95% CI, 0.26–0.81), whereas men had more modest reduced risk of HCC (HR, 0.93; 95% CI, 0.63–1.37). The associations were stronger for caffeinated coffee (HR & gt;3 cups/day vs. non-drinker, 0.71; 95% CI, 0.50–1.01) than decaffeinated coffee (HR, 0.92; 95% CI, 0.55–1.54). There was no association between coffee consumption and ICC. Conclusions: These findings suggest that, in a U.S. population, coffee consumption is associated with reduced risk of HCC. Impact: Further research into specific coffee compounds and mechanisms that may account for these associations is needed. Cancer Epidemiol Biomarkers Prev; 24(9); 1398–406. ©2015 AACR.
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2015
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  • 5
    Online Resource
    Online Resource
    American Association for Cancer Research (AACR) ; 2009
    In:  Cancer Epidemiology, Biomarkers & Prevention Vol. 18, No. 1 ( 2009-01-01), p. 359-359
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 18, No. 1 ( 2009-01-01), p. 359-359
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2009
    detail.hit.zdb_id: 2036781-8
    detail.hit.zdb_id: 1153420-5
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  • 6
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    Online Resource
    American Association for Cancer Research (AACR) ; 2010
    In:  Cancer Epidemiology, Biomarkers & Prevention Vol. 19, No. 2 ( 2010-02-01), p. 443-446
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 19, No. 2 ( 2010-02-01), p. 443-446
    Abstract: Background: Tamoxifen can reduce the risk of developing invasive estrogen receptor–positive breast cancer by 49%, but it is unknown how many women in the United States are taking tamoxifen for primary prevention of breast cancer. Methods: Data from the years 2000 and 2005 National Health Interview Surveys were analyzed to estimate the prevalence of tamoxifen use among U.S. women for primary chemoprevention of breast cancer. Results: In 2000, ∼0.2% of U.S. women ages 40 to 79 years without a personal history of breast cancer took tamoxifen for chemoprevention (95% confidence interval, 0.13-0.31). In 2005, the prevalence was ∼0.08% (95% confidence interval, 0.03-0.17). Conclusion: The prevalence of tamoxifen use for primary prevention of breast cancer was very low in the years 2000 and 2005. Possible explanations for the low uptake are explored. Cancer Epidemiol Biomarkers Prev; 19(2); 443–6
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
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  • 7
    Online Resource
    Online Resource
    American Association for Cancer Research (AACR) ; 2013
    In:  Cancer Epidemiology, Biomarkers & Prevention Vol. 22, No. 3 ( 2013-03-01), p. 415-421
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 22, No. 3 ( 2013-03-01), p. 415-421
    Abstract: Background: Excessive alcohol consumption is a well-established risk factor for liver disease and hepatocellular carcinoma (HCC). Previous studies have found that increased alcohol consumption can lead to lower absorption of folate. Conversely, higher folate intake has been inversely associated with liver damage and HCC. In the current study, we investigate the effect of alcohol consumption and folate intake on HCC incidence and liver disease mortality in the NIH–American Association of Retired Persons Diet and Health Study. Methods: The study population included 494,743 participants who reported at baseline their dietary intake for the previous year. Alcohol and folate were analyzed with hazards ratios (HR) and 95% confidence intervals (CI) using multivariate Cox proportional hazards regression models adjusted for age, sex, race, education, smoking, body mass index, and diabetes. HCC incidence (n = 435) was determined through 2006 via linkage with cancer registries, and liver disease mortality (n = 789) was determined through 2008 via linkage to the U.S. Social Security Administration Death Master File and the National Death Index Plus by the National Center for Health Statistics. Results: Consumption of more than three drinks per day was positively associated with both HCC incidence (HR: 1.92; 95%CI: 1.42–2.60) and liver disease mortality (HR: 5.84; 95%CI: 4.81–7.10), whereas folate intake was associated with neither outcome. Folate, however, modified the relationship between alcohol and HCC incidence (Pinteraction = 0.03), but had no effect on the relationship between alcohol and liver disease mortality (Pinteraction = 0.54). Conclusions: These results suggest that higher folate intake may ameliorate the effect of alcohol consumption on the development of HCC. Impact: Folate intake may be beneficial in the prevention of alcohol-associated HCC. Cancer Epidemiol Biomarkers Prev; 22(3); 415–21. ©2013 AACR.
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2013
    detail.hit.zdb_id: 2036781-8
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  • 8
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 75, No. 15_Supplement ( 2015-08-01), p. 1880-1880
    Abstract: Background: Coffee drinking has been inversely associated with mortality as well as cancers of the endometrium, colon, skin and liver. Improved insulin sensitivity and reduced inflammation are among the hypothesized mechanisms by which coffee drinking may affect cancer risk. The association between coffee drinking and systemic levels of immune and inflammatory markers has not been well characterized. Objective: To explore the associations of coffee drinking with levels of a wide range of immune and inflammatory markers. Design: Luminex bead-based assays were used to measure serum levels of 77 immune and inflammatory markers in 1728 older non-Hispanic Whites from three case-control studies nested within the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. Usual coffee intake was self-reported using a semi-quantitative food frequency questionnaire. We used weighted multivariable logistic regression models to examine the associations between coffee drinking and dichotomized marker levels. We conducted statistical trend tests by assigning each coffee category its median value and modeling as a continuous variable. We applied a 20% false discovery rate criterion to the P-values for trend. Results: Ten of the 77 examined markers were nominally associated (P-value & lt;0.05) with coffee drinking. The five markers that withstood correction for multiple comparisons included various aspects of the host response namely chemotaxis of monocytes/macrophages (IFNγ, CX3CL1/fractalkine, CCL4/MIP-1β), pro-inflammatory cytokines (sTNFRII) and regulators of cell growth (FGF-2). Heavy coffee drinkers had lower circulating levels of IFNγ (OR = 0.35; 95% CI 0.16, 0.75; P-trend = 0.0003), CX3CL1/fractalkine (OR = 0.25; 95% CI 0.10, 0.64; P-trend = 0.0031), CCL4/MIP-1β (OR = 0.48; 95% CI 0.24, 0.99; P-trend = 0.0050), FGF-2 (OR = 0.62; 95% CI 0.28, 1.38; P-trend = 0.0080) and sTNFRII (OR = 0.34; 95% CI 0.15, 0.79; P-trend = 0.0112) than non-coffee drinkers. Conclusions: Coffee drinking was associated with lower circulating levels of inflammatory markers, which may partially mediate previously observed associations of coffee drinking with lower mortality and morbidity. Validation studies, ideally controlled feeding trials, and prospective studies, such as nested case-control studies, are needed to confirm these associations. Citation Format: Erikka Loftfield, Meredith S. Shiels, Barry I. Graubard, Hormuzd A. Katki, Anil Chaturvedi, Britton Trabert, Ligia Pinto, Troy Kemp, Fatma M. Shebl, Susan T. Mayne, Nicolas Wentzensen, Mark P. Purdue, Allan Hildesheim, Rashmi Sinha, Neal D. Freedman. Associations of coffee drinking with systemic immune and inflammatory markers. [abstract] . In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 1880. doi:10.1158/1538-7445.AM2015-1880
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
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    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2015
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  • 9
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    American Association for Cancer Research (AACR) ; 2010
    In:  Cancer Research Vol. 70, No. 8_Supplement ( 2010-04-15), p. 1834-1834
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 70, No. 8_Supplement ( 2010-04-15), p. 1834-1834
    Abstract: INTRODUCTION: Previous research has noted that cancer mortality rates are higher for males than females, but no extensive analysis of this has been conducted. We wanted to study the extent of sex disparities in cancer mortality and if these disparities persist after adjustment for characteristics of the person and cancer. METHODS: We extracted U.S. vital statistics mortality data and cancer incidence and survival data from the SEER*Stat system for 36 cancers and undertook age-adjusted mortality rates and survival analyses. For the age-adjusted mortality rate analyses we extracted mortality count, person-years, and mortality rate per 100,000 for each cancer, stratified by sex and age for the period 1977-2006. Male-to-female mortality rate ratios (MRRs) were calculated. For each cancer, we plotted sex-specific mortality rates and male-to-female MRRs. For the survival analyses, we extracted patient id, age and date of diagnosis, sex, primary site, stage, grade, survival time, vital status and cause of death. Relative hazards for the 5-year period following diagnosis were estimated from Cox proportional hazard models adjusted for age, stage, grade, and year of diagnosis. RESULTS: For the vast majority of cancers, age-adjusted mortality rates were higher among males than females; the 5 cancers with the highest male-to-female MRR were lip (5.51, 95% confidence interval (CI):5.05-6.03), larynx (5.37, 95%CI:5.29-5.45), hypopharynx (4.47, 95%CI:4.30-4.65), esophagus (4.08, 95%CI:4.05-4.11) and urinary bladder (3.36, 95%CI:3.34-3.39). Only 3 cancers had a higher mortality rate among females than males: peritoneum, omentum and mesentery (MRR=0.39, 95%CI:0.38-0.41); gallbladder (0.56, 95%CI:0.55-0.57); and anus, anal canal and anorectum (0.78, 95%CI:0.75-0.81). The survival analyses indicated that males had a significantly increased risk of death, relative to females, for the cancers: anus, anal canal and anorectum (hazard ratio: 1.21, 95%CI:1.03-1.44); colon and rectum (1.08, 95%CI:1.07-1.09); floor of mouth (1.29, 95%CI:1.04-1.59); larynx (1.09, 95%CI:1.01-1.18); liver and intrahepatic bile duct (1.20, 95%CI:1.14-1.26); lung and bronchus (1.19, 95%CI:1.17-1.20); pancreas (1.06, 95%CI:1.03-1.08); small intestine (1.16, 95%CI:1.04-1.29); and soft tissue including heart (1.12, 95%CI:1.03-1.21). Females had higher mortality risks for the cancers tongue (0.87, 95%CI:0.81-0.94) and urinary bladder (0.83, 95%CI:0.81-0.86). DISCUSSION: Male cancer mortality rates were higher than equivalent female rates for the majority of cancers studied. Moreover, males also had higher risk of cancer mortality following diagnosis, relative to females, for many cancers even after adjustment for age of diagnosis, stage, grade and year of diagnosis. These observations indicate that there are sex differences in exposure and/or endogenous metabolic processes which modify risk of both cancer incidence and cancer mortality following diagnosis. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 1834.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
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    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
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  • 10
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    Online Resource
    American Association for Cancer Research (AACR) ; 2010
    In:  Cancer Epidemiology, Biomarkers & Prevention Vol. 19, No. 10 ( 2010-10-01), p. 2430-2436
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 19, No. 10 ( 2010-10-01), p. 2430-2436
    Abstract: Background: Guidelines from the American Cancer Society recommend annual breast magnetic resonance imaging (MRI) screening for women with a projected lifetime risk of ≥20% based on risk models that use family history. Because MRI screening is costly and has limited specificity, estimates of the numbers of U.S. women with ≥20% breast cancer risk would be useful. Methods: We used data from the 2000 and 2005 National Health Interview Survey and the National Cancer Institute (NCI) Breast Cancer Risk Assessment Tool (i.e., Gail model 2 with a revision for African Americans) to calculate estimates of U.S. women by age and race/ethnicity categories with a lifetime absolute breast cancer risk of ≥20%. Distributions of 5-year and lifetime absolute risk of breast cancer were compared across demographic groups. Results: We estimated that 1.09% (95% confidence interval, 0.95-1.24%) of women age 30 to 84 years have a lifetime absolute breast cancer risk of ≥20%, which translates to 880,063 U.S. women eligible for MRI screening. The 5-year risks are highest for white non-Hispanics and lowest for Hispanics. The lifetime risks decrease with age and are generally highest for white non-Hispanics, lower for African American non-Hispanic, and lowest for Hispanics. Conclusion: We provide national estimates of the number of U.S. women who would be eligible for MRI breast screening and distributions of 5-year and lifetime risks of breast cancer using the NCI Breast Cancer Risk Assessment Tool. Impact: These estimates inform the potential resources and public health demand for MRI screening and chemopreventive interventions that might be required for U.S. women. Cancer Epidemiol Biomarkers Prev; 19(10); 2430–6. ©2010 AACR.
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
    detail.hit.zdb_id: 2036781-8
    detail.hit.zdb_id: 1153420-5
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