bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract ED08-01: How should we optimize technology to allow personalized medicine?
Authors: Meyskens Frank 
Published: May 2012

Abstract
ED08-01
TECHNOLOGY AND PREVENTION. What type of strategies should be followed to develop useful high technology in the service of preventing cancer in the individual?
There are many useful recommendations that have been suggested : screening, early detection, chemoprevention, but usage is relatively low, expensive in many cases, not without risk and with significant false positive and false negatives . This talk will explore a futuristic paradign that may lead to better results for the individual.
For those who want to be in the right mood for this presentation bring along a glass of red wine(preferably pinor noir) and beforehand read:
Meyskens FL.Jr. Cancer Prevention in the Year 2025: an anticipation. European J Cancer 36:1737-1740,2000.
Citation Information: Cancer Prev Res 2008;1(7 Suppl):ED08-01.
Abstract ED09-01: Prevention of non-melanoma skin cancer with celecoxib
Authors: Elmets Craig 
Published: May 2012

Abstract
ED09-01
Cutaneous squamous cell and basal cell carcinomas are particularly common malignancies, the most common cause of which is overexposure to solar ultraviolet radiation. While physicians advise patients to apply sunscreens to prevent their occurrence, sunscreens are only modestly effective. In vitro studies and in vivo studies in animal models have suggested that prostaglandins and cyclooxygenase-2 (COX-2) play an important role in the development of non-melanoma skin cancers. In Skh-1 hairless mice, the cyclooxygenase inhibitor celecoxib has been reported to prevent UV-induced skin tumors. In addition, immunohistochemical examination of human actinic keratoses and squamous cell carcinomas has shown that COX-2 expression is increased, whereas expression of this enzyme is not observed in normal skin. In order to determine whether these experimental findings are applicable to humans, we have conducted a phase II/III double blind multicenter placebo controlled clinical trial examining the efficacy and safety of celecoxib in adult patients at risk for actinic keratoses and non-melanoma skin cancers. The studies offer the possibility of additional options for the prevention of this common malignancy.
Citation Information: Cancer Prev Res 2008;1(7 Suppl):ED09-01.
Abstract PL01-04: The role of regulatory T cells in K-Ras driven lung cancer
Authors: Dennis Phillip 
Published: May 2012

Abstract
PL01-04

Background
K-Ras mutations occur in up to 30% of human lung adenocarcinomas (Salgia and Skarin 1998) and occur almost exclusively in patients with a history of smoking. These mutations confer resistance to commonly used cytotoxic chemotherapies as well as targeted agents (Eberhard, Johnson et al. 2005). In preclinical mouse models of lung cancer, K-Ras mutations are necessary for tobacco carcinogen-driven lung tumorigenesis and are sufficient to cause lung adenocarcinomas in transgenic mice (Johnson, Mercer et al. 2001). Inflammation is characteristic of smoking-related lung cancer and preclinical models of K-Ras-driven lung tumorigenesis. Specific components of the inflammatory response such as regulatory T cells (Treg) regulate inflammation and are thought to contribute to tumorigenesis. Because inhibitors of mTOR such as the immunosuppressant rapamycin can prevent K-Ras mediated murine lung tumorigenesis (Wislez, Spencer et al. 2005; Granville, Warfel et al. 2007), we hypothesized that the anti-tumor effects of rapamycin might be related to alterations in lung-associated inflammation.

Methods and Findings
Lung tumorigenesis was studied in three different murine models that depend on mutant K-Ras; a tobacco carcinogen-driven model, a syngeneic inoculation model and a transgenic model. Splenic and lung-associated T cells were studied using flow cytometry and immunohistochemistry. Exposure of A/J mice to the tobacco-carcinogen NNK that causes K-Ras mutations (Belinsky, Devereux et al. 1989) tripled the fraction of lung-associated Treg prior to tumor development. Induction of lung tumors and induction of lung associated Foxp3+ cells by NNK was dose dependent. When administered to achieve trough levels comparable to that in humans, rapamycin prevented the induction of lung associated Foxp3+ cells by NNK, coincident with a 90% decrease in lung tumors. In A/J mice inoculated with syngeneic lung adenocarcinoma cells that were resistant to the anti-proliferative effects of rapamycin, rapamycin neither inhibited tumor growth nor decreased Treg. In contrast, depletion of Treg in inoculated mice using an anti-CD25 antibody prevented lung tumorigenesis by 80%. Transgenic mice that express mutant K-Ras (K-RasLA2) also develop lung tumors with infiltrating Foxp3+ cells, and when K-RasLA2 mice were crossed to genetically engineered mice that bear a loss of function mutation in Foxp3, lung tumorigenesis was inhibited by 75%.

Conclusions
These studies show that Treg are required for K-Ras-mediated lung tumorigenesis, and provide a strong rationale to clinically evaluate rapamycin or other agents that decrease Treg, to determine if decreasing Treg will inhibit K-Ras driven lung cancer.
Citation Information: Cancer Prev Res 2008;1(7 Suppl):PL01-04.
Abstract PL03-02: Inflammation-driven myeloid-derived suppressor cells: co-opting anti-tumor immunity to promote tumor progression
Authors: Ostrand-Rosenberg Suzanne , Sinha Pratima , Clements Virginia , Bunt Stephanie , Srivastava Minu 
Published: May 2012

Abstract
PL03-02
Inflammation facilitates tumor onset and promotes tumor progression through a variety of mechanisms. One of these mechanisms is by activating myeloid-derived suppressor cells (MDSC), a population of cells that block anti-tumor immunity. MDSC are present in most patients and experimental animals with primary and/or metastatic cancer. They inhibit adaptive anti-tumor immunity by preventing the activation of CD4+ and CD8+ T cells, and by blocking innate immunity by inhibiting natural killer cell cytotoxicity and polarizing immunity towards a tumor-promoting type 2 phenotype. Because of their extreme immune suppressive activity, MDSC will be a significant impediment to active immunotherapy in patients with established malignancies. The accumulation and retention of MDSC are driven by multiple pro-inflammatory factors that arise from chronic inflammation and that are produced by malignant cells and by the tumor microenvironment. Multiple pro-inflammatory mediators, including IL-1β, IL-6, prostaglandin E2 (PGE-2), and the S100A8/A9 proteins, accentuate the accumulation and retention of MDSC in tumor-bearing individuals. IL-1β mediates its effects indirectly, while IL-6, PGE-2, and S100A8/A9 proteins appear to directly interact with MDSC through their respective receptors. In addition to increasing the T cell suppressive activity of MDSC, IL-1β increases the cross-talk between MDSC and macrophages. This cross-talk enhances a type 2 immune response that favors tumor progression by increasing MDSC production of IL-10 and decreasing macrophage production of IL-12. MDSC not only respond to these pro-inflammatory molecules, but they also exacerbate an inflammatory tumor microenvironment by synthesizing and secreting proinflammatory mediators, including the S100A8/A9 proteins. As a result, once induced and activated, MDSC maintain an autocrine feedback loop that sustains their levels in the blood, lymph nodes, and at tumor sites. Multiple approaches are being developed to block the induction/activation of MDSC. Since both IL-1β and S100A8/A9 activate MDSC through the NF-κB signaling pathway, drugs that target this pathway may reduce MDSC levels and be useful therapeutic agents in conjunction with active immunotherapy in cancer patients. (Supported by NIH R01CA84232, RO1CA115880)
Citation Information: Cancer Prev Res 2008;1(7 Suppl):PL03-02.
Abstract PR-1: A randomized factorial trial of vitamins E and C in the prevention of cancer in men: the Physicians' Health Study II
Authors: Buring Julie , Sesso Howard , Gaziano J , the Physicians' Health Study Research Group for 
Published: May 2012

Abstract
PR-1

Background
Basic science and observational studies support a potential role of antioxidants, including vitamins E and C, in the prevention of cancer. Previous trials have suggested a possible benefit of vitamin E, in particular on prostate cancer. Few long-term trials have evaluated vitamin C alone in the prevention of cancer. Despite uncertainty regarding long-term effects, use of vitamin supplementation remains highly prevalent in the US.

Methods
The Physicians’ Health Study II (PHS II) evaluated the roles of supplementation with vitamin E (400 IU every other day) and vitamin C (500 mg daily) on risk of cancer in a randomized, double-blind, placebo-controlled trial of 14,641 U.S. male physicians initially aged ≥50 years. The trial included 1,274 (8.7%) men with prevalent cancer at randomization. The randomized vitamin E and C trial components terminated as scheduled on August 31, 2007, and identification of cancer endpoints that occurred prior to that date will continue through September 30, 2008. The primary endpoint of the vitamin E component was prostate cancer, with total cancer (defined as excluding non-melanoma skin cancer) as a secondary endpoint. For vitamin C, the primary endpoint was total cancer. All endpoints were reviewed and confirmed by an Endpoints Committee of physicians blinded to randomized treatment assignment. High rates of morbidity and mortality follow-up have been maintained in the PHS II.

Results
During a median (interquartile range) follow-up of 7.6 (7.1 to 9.6) years among men with a mean baseline age of 64.3 years, there have been 1,929 cases of cancer, including 1,013 cases of prostate cancer. Based upon preliminary results, those randomized to vitamin E had a relative risk of prostate cancer of 0.95 (490 events in the active group vs. 523 in the placebo group; 95% CI, 0.84-1.07; p=0.39), and a relative risk of total cancer of 1.04 (978 vs 951; 95% confidence interval, 0.95-1.14; p=0.38). For those randomized to vitamin C, the relative risk of total cancer was 1.00 (964 events in the active group, 965 in placebo; 95% CI, 0.92-1.10; p=0.95).
In addition to updating the results above, we will also present the results for other site-specific cancers, as well as analyses that consider the effects of compliance, effect modification by baseline risk factors and baseline cancer, and potential adverse effects.

Conclusion
These preliminary data from a large-scale prevention trial of long duration indicate no beneficial effect of vitamin E supplementation on either prostate or total cancer, nor a beneficial effect of vitamin C supplementation on total cancer. These data will help inform clinical and public health recommendations regarding effects of vitamin E or vitamin C supplementation on risks of total and site-specific cancers.
Citation Information: Cancer Prev Res 2008;1(7 Suppl):PR-1.
Abstract PR-13: Inhibition of chronic colitis-induced carcinogenesis in IL-10 knockout mice by dietary supplementation of black raspberries
Authors: Liao Jie , Chung Yeon Tae , Wang Li-Shu , Yang Allison , Stoner Gary , Yang Guang-Yu 
Published: May 2012

Abstract
PR-13
Epidemiological and experimental studies indicate that inflammation is associated with the development of colon cancer. For example, it is known that patients with ulcerative colitis have an increased incidence of colon cancer, and anti-inflammatory drugs and bioactive food components that suppress colonic inflammation reduce the risk of colon cancer. IL-10 is an important regulatory anti-inflammatory cytokine associated with the development of colonic colitis. 100% of IL-10 knockout (KO) mice develop colitis after 3 months of age; histopathology reveals transmural inflammation, predominantly in the cecum. We have shown that the administration of a diet containing twice the recommended amount of iron leads to the development of colonic adenocarcinoma in more than 80% of IL-10 KO mice within 5 months. In the present study, we evaluated the effects of a dietary supplementation of black raspberries on spontaneous colitis-induced carcinogenesis in IL-10 KO mice. Beginning at 4 weeks of age, mice were administered black raspberry powder in AIN-93G diet at concentrations of 5% and 10% until termination of the experiment at 23 weeks. The colorectal tumor incidence in IL-10 KO mice fed control AIN-93G diet was 71.4% (10/14 mice with tumors). Significant reductions in colonic tumor incidence [38% (5/13 mice) and 30.8% (4/13 mice)] were observed in mice receiving 5% and 10% black raspberry diets, respectively. Histopathologic analysis of chronic inflammatory activity in the colon showed that the berries significantly inhibited the overall inflammatory index, including the extent of inflammation, ulcer formation and epithelial hyperplasia. Mechanistic studies suggest that inhibition of colitis-associated carcinogenesis by dietary berries might relate to their effects on modulation of myeloperoxidase-labeled inflammatory cells, nitro-oxidative stress, and cell proliferation. We conclude that black raspberries, as a food-based prevention agent, have potential for the prevention of inflammation-related carcinogenesis in the colon. (Supported by NIH grants R01-CA104741 and -CA103180).
Citation Information: Cancer Prev Res 2008;1(7 Suppl):PR-13.
Abstract PR-7: A European genome-wide association study of urinary bladder cancer
Authors: Kiemeney Lambertus , Thorlacius Steinunn , Sulem Patrick , Geller Frank , Aben Katja , Kiltie Anne , Bishop Timothy , Matullo Giuseppe , Vineis Paolo , Porru Stefano , Zeegers Maurice , Buntinx Frank , Kumar Rajiv , Fletcher Tony , Koppova Kvetoslava , Rudnai Peter , Gurzau Eugene , Steineck Gunnar , Mayordomo Jose , Gulcher Jeffrey , Thorsteinsdottir Unnur , Kong Augustine , Rafnar Thorunn , Stefansson Kari 
Published: May 2012

Abstract
PR-7
We conducted a genome-wide SNP association study on 1,803
urinary bladder cancer (UBC) cases and 34,336 controls from
Iceland and the Netherlands using Illumina HumanHap300 and HumanCNV370-duo Beadchips. The 10 most significant SNPs were genotyped using Centaurus single track assays in 7 follow up case-control groups (2,165 cases and 3,800 controls) from Italy (Torino and Brescia), the UK, Belgium, Eastern Europe (Hungary, Romania and Slovakia), Sweden and Spain.
The strongest association was observed with allele T of rs9642880 on chromosome 8q24, 30 kb upstream of MYC (allele-specific odds ratio (OR) = 1.22; P = 9.34 x 10-12). Approximately 20% of individuals of European ancestry are homozygous for rs9642880[T], and their estimated risk of developing UBC is 1.49 times that of noncarriers. A weaker signal, but nonetheless of genome-wide significance, was captured by rs710521[A] located near TP63 on 3q28 (allele-specific OR = 1.19; P = 1.15 x 10-7).
No association was observed between UBC and the four 8q24 variants previously associated with prostate, colorectal and breast cancers, nor did rs9642880 associate with any of these three cancers. Individuals with low risk tumors (i.e. confined to the bladder mucosa and not poorly differentiated) had a higher frequency of rs9642880[T] than individuals with high risk tumors (OR = 1.15, P = 0.011). No difference was found in the frequencies of rs9642880[T] between ever-smoking and never-smoking cases.
Citation Information: Cancer Prev Res 2008;1(7 Suppl):PR-7.
Abstract A109: Intake of polyunsaturated fatty acids and distal large bowel cancer risk in whites and African Americans
Authors: Kim Sangmi , Sandler Dale P. , Galanko Joseph A. , Martin Christopher , Sandler Robert S. 
Published: May 2012

Abstract
Experimental and clinical data suggest anti-neoplastic properties of long-chain ω-3 polyunsaturated fatty acids in the colon. Epidemiologic evidence is inconclusive. We examined the association between intakes of different polyunsaturated fatty acids and distal large bowel cancer in a population-based case-control study of 1,509 whites (716 cases and 787 controls) and 369 African Americans (213 cases and 156 controls) in North Carolina (2001–2006). Dietary intake of 19 different polyunsaturated fatty acids was assessed using a validated food frequency questionnaire. Unconditional logistic regression was used to estimate odds ratios (OR) and 95% confidence intervals (CI) for distal large bowel cancer risk in relation to quartiles of polyunsaturated fatty acid intake. Increased consumption of long-chain ω-3 fatty acids was associated with reduced risk of distal large bowel cancer. Compared to the lowest quartile, the multivariable odds ratios for the second, third and highest quartile were: OR=0.96 (95% CI: 0.71–1.31), OR=0.75 (95% CI: 0.54–1.04), and OR=0.61 (95% CI: 0.44–0.86), respectively; P for trend&lt;0.01). Intake of individual eicosapentanoic acids and docosahexanoic acids was similarly inversely related to distal large bowel cancer risk, whereas the ratio of ω-6 to long-chain ω-3 fatty acids was associated with increased risk of distal large bowel cancer. These associations were limited to whites, and not observed among African Americans (likelihood ratio test for interaction p&lt;0.01). There was no evidence of effect measure modification by nonsteroidal anti-inflammatory drug use, obesity, or tumor location. Our results support the hypothesis that long-chain ω-3 polyunsaturated fatty acids have beneficial effects in colorectal carcinogenesis. Whether or not the possible benefit of long-chain ω-3 fatty acids varies by race warrants further evaluation.
Citation Information: Cancer Prev Res 2010;3(1 Suppl):A109.
Abstract A118: The impact of participating in a team sport versus a group physical activity program on group cohesion in cancer survivors
Authors: Carter Cindy L. , Onicescu Georgiana , Cartmell Kathleen B. , Sterba Katherine R. , Tomsic Jim , Dunmeyer Erica , Taylor Chrissy , Fox Todd , Alberg Anthony J. 
Published: May 2012

Abstract
Objectives: Being a member of a cohesive group could provide a source of high-quality social support that could positively impact the quality of life in cancer survivors. In a nonrandomized trial, we compared group cohesion in a team-oriented (dragon boat paddling team) and non-team-oriented (group walking program) group physical activity intervention. We hypothesized that group cohesion would be stronger among those who participated in the team-oriented dragon boat paddling team compared to the group walking program.
Participants and Methods: 122/134 (91%) of participants who enrolled in the study completed the eight-week physical activity programs, dragon boat paddling team (n=68) or group walking program (n=54). Group cohesion was measured post-intervention using a modified 11 item version of the Group Environment Questionnaire. We tested differences in median cohesion scores between paddlers and walkers using the Wilcoxon Rank Sum test, a nonparametric equivalent of the t-test which is robust to deviations from the normality assumption.
Results: Following completion of the group physical activity program, the median group cohesion score for paddlers was statistically significantly higher than for walkers (paddlers=4.36, walkers=3.73, p=0.004).
Conclusions: Participating in a team sport was associated with significantly higher group cohesion even in comparison to a group physical activity program that was not team oriented. These novel findings suggest that team-oriented physical activity programs such as dragon boat paddling may provide a greater opportunity for social support through increased group cohesion than a group-based walking program. Future studies should examine the mechanisms underlying these differences and the outcomes associated with increased cohesion. Among cancer survivors, team membership may provide a natural source of social support.
Citation Information: Cancer Prev Res 2010;3(1 Suppl):A118.
Abstract A124: Genome-wide association identified susceptibility loci as modifiers of colorectal cancer risk in Lynch syndrome
Authors: Pande Mala , Frazier Marsha L. , Lynch Patrick M. , Broaddus Russell , Reuther Jacquelyn , Jiang Wenxiao , Amos Chistopher I. 
Published: May 2012

Abstract
Purpose: The purpose of this study was to determine whether 5 common low-penetrance variants identified in recent genome-wide association studies (GWAS) for colorectal cancer modify colorectal cancer risk in people with Lynch syndrome. People with Lynch syndrome are genetically predisposed to colorectal cancer owing to an inherited DNA mismatch repair (MMR) gene mutation; however, disease expression varies, pointing to the role of modifying factors. A study of Dutch Lynch syndrome families (Wijnen et al., 2009) examined 6 GWAS-identified markers and found that 2 of them—rs16892766 (8q23.3) and rs3802842 (11q23.1)—were associated with colorectal cancer risk. However, other risk variants have yet to be characterized in Lynch syndrome. A replication study of 3 markers in subjects enrolled irrespective of whether they were MMR gene mutation carriers (Poynter et al., 2007) found that 2 risk variants in the 8q24 region (rs10505477 and rs6983267) and 1 variant in the 9p24 region (rs719725) were associated with colorectal cancer risk.
Methods: In a retrospective cohort study, we analyzed 278 people with Lynch syndrome and a confirmed MMR gene mutation from the M. D. Anderson Lynch syndrome registry. We genotyped the 5 aforementioned risk variants—rs16892766, rs3802842, rs10505477, rs6983267, and rs719725—and analyzed the association between each risk variant and colorectal cancer using Cox proportional hazards regression while adjusting for sex, MMR gene mutation status, and familial correlation.
Results: Of the 278 subjects from 128 families with 11,702 person years of follow-up, 146 subjects had colorectal cancer, and the remaining subjects were unaffected. In a codominant model, rs16892766 was significantly associated with colorectal cancer (hazard ratio [HR]: 1.61; 95% confidence interval [CI]: 1.10–2.35). Similarly, rs3802842 exhibited a marginally significant trend in an additive model (Ptrend = 0.07), and the association was most clearly evident among carriers of mutations in the MLH1 MMR gene in a codominant model (HR: 1.98; 95% CI: 1.18–3.33).
Conclusion: Our study replicates the previous finding of an association between 2 GWAS-identified susceptibility loci and risk of colorectal cancer in people with Lynch syndrome. Although people with Lynch syndrome have a strong predisposition to colorectal cancer due to the underlying MMR mutation, these common genetic variants may further modify their colorectal cancer risk, particularly in carriers of multiple risk alleles. These and other low-penetrance susceptibility loci are likely to have future application in personalized risk prediction in identifying individuals who are most susceptible so that they can be provided more rigorous cancer-prevention strategies.
Citation Information: Cancer Prev Res 2010;3(1 Suppl):A124.