bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract B105: Inhibition of angiogenesis by oleanoleic acid-derived triterpenoids: mechanisms of action and potential prostate cancer prevention
Authors: Sogno Ilaria , Tosetti Francesca , Vene Roberta , Cammarota Rosaria , Generoso Luca , Noonan Douglas , Sporn Michael , Albini Adriana 
Published: May 2012

Abstract
B105
Angiogenesis is a limiting step for the switch from a dormant to malignant state in tumor progression. During tumor development tumor cells induce profound changes in the surrounding tissue, leading to the formation of an altered tumor microenvironment that is critical in permitting further tumor growth and tumor progression.. Angiogenesis and inflammation are common targets of many chemopreventive molecules that suppress the antiangiogenic switch in premalignant tumors.We evaluated in vitro and in vivo the antiangiogenic activity of two synthetic oleanoleic acid-derived triterpenoids under study for their chemopreventive and therapeutic potential, CDDO -Me and -Im. In vitro both compounds exhibited a strong inhibitory activity on endothelial cells isolated from umbilical veins (HUVEC). Futher, these compounds inhibited inflammatory cell chemotaxis towards specific chemokine stimului. The triterpenoids interfered with activation of the PI3K/Akt pathway following VEGF stimulation and activation of the NF-kappaB pathway subsequent to TNFalpha stimulation. Moreover CDDO-Me induces cell death in androgen-responsive and unresponsive human prostate cancer cell lines at very low concentrations, by acting agains GS3K pathway (Venè R, Larghero P, Arena G, Sporn MB, Albini A, Tosetti F. Cancer Res. 2008).In vivo CDDO-Im and especially CDDO-Me significantly inhibit neoangiogenesis in the matrigel sponge assay in C57BL mice, reducing both CD31+ cell number and Hb content in the sponges. We tested different schedules of treatment, by administering compounds as prevention before matrigel injection, as therapy after injection and as combination of prevention and therapy. All three protocols reduced angiogenesis when compared to controls the combinationof prevention and intervention was the most effective and at very low dosages. Since currently CDDO-Me is being assessed phase I trials in the US, the potential anti-angiogenic activity of these drugs should be taken into consideration in evaluating efficacy in these trials.
Citation Information: Cancer Prev Res 2008;1(7 Suppl):B105.
Abstract B115: Parity alters responses to ionizing radiation in the human mammary gland
Authors: Carter Matthew , Troester Melissa , Johnson Melissa , Jerry D. Joseph , Schneider Sallie 
Published: May 2012

Abstract
B115
Parity is associated with a significant reduction in breast cancer risk. Identification of key pathways, which are altered by parity, will provide important information for the development of chemoprotective agents against breast cancer. Radiation is a potent carcinogen in the mammary gland. It appears to have mutagenic effects through its ability to induce DNA damage, as well as through its ability to induce “bystander effects”. These effects have been shown to be tumor promoting in immortalized cells and involve modulation of various growth factor pathways for stem cell maintenance. We hypothesized that we would be able to obtain important information on parity-induced changes by examining gene expression responses to radiation exposure from the two types of tissue. Methods: Women undergoing elective breast reduction surgery were asked to enroll and donate their excised tissue. Portions of tissue were cultured and then either exposed or not to 5 Gy radiation. The tissue remained in culture for six hours to allow for changes in gene expression. Tissue was fixed for immunohistochemical analysis or RNA was isolated for microarray analysis. Results: A SAM analysis indicated a loose 200 gene signature, which responded to radiation differentially. The breast tissue from nulliparous women showed the most striking changes with increased expression of 80% genes in response to radiation whereas tissue from parous women illustrated no change or decreased expression of these same genes. The other 20% of the genes were strongly down regulated in tissue from nulliparous women in response to radiation, while they were up-regulated or not changed in parous tissue. The major pathways that appeared to be inversely affected in these tissues indicate parity-induced changes in signaling to tissue homeostasis and wound repair, as well as DNA replication and repair.
Citation Information: Cancer Prev Res 2008;1(7 Suppl):B115.
Abstract B116: Adjuvant-mediated DNA immunotherapy for cancer
Authors: Yang Ya-Wun , Ma Yi-Fan 
Published: May 2012

Abstract
B116
Cancer immunotherapy invokes immunity against cancerous cells by stimulating the immune response from the host. In an attempt to investigate the effect of adjuvant-mediated therapy, polyethyleneimine (PEI), a nonviral polycationic gene delivery vector, was employed in this study as an adjuvant to investigate the immunostimulatory effect on the murine bone marrow-derived dendritic cells (BMDCs) and in the tumor-bearing animals.
The physicochemical properties of the DNA-PEI complexes was characterized by the size and surface potential measurements. Murine bone-marrow-derived dendritic cells (BMDCs) at day 6 were treated with DNA-PEI complexes at various DNA/PEI ratios, followed by flow cytometric analysis of the expression of costimulatory molecules, including CD40, CD80, and CD86, at 24 h post-treatment. The production of the reactive oxygen species (ROS) after treatment with the PEI in the BMDCs was assessed with 2',7'-dichlorofluorescein diacetate (DCFH-DA) and hydroethidine (HE), followed by flow cytometry. To determine the effect of adjuvant on immunotherapeutic response, approximately 2 x 105 B16F10 melanoma cells were inoculated s.c. on the back of C57BL/6. Control groups were injected with PBS. When the tumor sizes reached 100 mm3 on day 6 after inoculation of B16F10 cells, animals were treated with the PEI-DNA complexes, containing the IL2 or caspase (fusion of caspase-2 prodomain and amino-terminal truncated caspase-3) plasmid DNA. Tumor sizes were measured with a caliper, and the volumes were determined using the formula of (length x width2)/2. Each group contained 4 animals.
Results obtained in this study demonstrated that treatment of BMDCs with PEI or LPS impaired the endocytic activity of BMDCs, and upregulated the expression of the costimulatory molecules, such as CD40 and CD86, suggesting the induction of maturation by PEI on the BMDCs. Treatment of BMDCs with the DNA-PEI complexes also lead to a concentration-dependent production of the reactive oxygen species (ROS), implicating the adjuvant function of PEI on immunostimulation. Injection of the animals with IL-2 or caspase plasmid DNA, complexed with PEI, was able to induce significant inhibition of the growth of tumors in the tumor-bearing animals. These results demonstrated the prevention and therapeutic effect of adjuvant-mediated DNA immunotherapy in the murine melanoma model.
Citation Information: Cancer Prev Res 2008;1(7 Suppl):B116.
Abstract B12: Variations in cancer incidence rate sex ratios
Authors: Cook Michael , Dawsey Sanford , Devesa Susan , McGlynn Katherine 
Published: May 2012

Abstract
B12
Cancer epidemiology manuscripts often make passing reference to the fact that cancer rates are often higher among males than females, yet rarely is this theme the subject of investigation. In a hypothesis-generating exercise, we used the Surveillance, Epidemiology, and End Results (SEER) program data to compute age-adjusted (2000 US standard population) sex-specific incidence rates and male-to-female incidence rate ratios (IRR) for specific cancer sites/histologies for the period 1975-2004. The ten most frequent cancers among males were lung and bronchus (81.6 per 100,000 man-years), colon and rectum (60.2), urinary bladder (31.8), non-Hodgkin lymphoma (18.9), skin excluding basal and squamous (17.0), stomach (12.6), kidney and renal pelvis (12.4), pancreas (12.1), lymphocytic leukemia (7.8) and larynx (7.6). The respective cancers for females were breast (115.1 per 100,000 woman-years), colon and rectum (45.4), lung and bronchus (40.2), non-Hodgkin lymphoma (13.2), skin excluding basal and squamous (12.7), pancreas (9.4), thyroid (8.5), urinary bladder (8.4), kidney and renal pelvis (6.3) and stomach (5.9). The ten cancers with the largest male-to-female IRR during 1975-2004 were Kaposi sarcoma (32.00), lip (7.24), larynx (5.14), mesothelioma (4.64), hypopharynx (4.10), urinary bladder (3.78), esophagus (3.49), tonsil (3.05), oropharynx (2.93), and other oral cavity and pharynx (2.72). Only five cancer sites had a higher incidence in females compared to males: breast (0.01), peritoneum, omentum and mesentery (0.29), thyroid (0.37), gallbladder (0.56), and anus, anal canal and anorectum (0.77). Of the 47 cancers analyzed, 19 had a male-to-female IRR higher than 2. The largest, consistent increases in male-to-female IRR during 1975-2004 were for cancers of the tonsil, oropharynx and esophagus. Cancers for which the male-to-female IRR has been decreasing include: pancreas, gum and other mouth, retroperitoneum, larynx, ureter, lip, nose, nasal cavity and middle ear, Hodgkin lymphoma, cranial nerves and other nervous system, peritoneum, omentum and mesentery, kidney and renal pelvis, thyroid, and lung and bronchus. Male-to-female IRRs may be informative because they are likely not to be subject to artifactual trends attributable to changes in diagnostics, prevention, tumor definitions and coding practices. In addition, male-to-female IRRs may be indicative of differential exposures and/or responses important in the pathogenesis of cancer. Higher levels of tobacco use and alcohol consumption among males have likely contributed to many of the elevated IRRs, but other exposures have also certainly played a role. These observations should serve as a foundation for further studies of sex differences in cancer etiopathogenesis.
Citation Information: Cancer Prev Res 2008;1(7 Suppl):B12.
Abstract B120: Capturing connection between aging and aging-associated diseases: The case of cancer
Authors: Yashin Anatoli , Akushevich Igor , Arbeev Konstantin , Akushevich Lucy , Kulminski Alexander , Ukraintseva Svetlana 
Published: May 2012

Abstract
B120
Traditional epidemiological studies of cancer often approximate age patterns of the incidence and mortality rates by appropriate parametric functions. Although such formal description is certainly convenient from the demographic point of view it does not allow for biological interpretation of the respective parameters, and, therefore, has limited use beyond demographic applications. The idea to describe cancer hazard rates in terms of biologically interpretable parameters resulted in the development of the research area called the “mathematical modeling of cancer” or “cancer modeling.” These models, however, do not allow for studying either connection between health history events, or links between cancer and aging, detected in a number of recent molecular biological and experimental studies. To take such connections into account, the new models of cancer are needed.
In this paper, we suggest a new approach to modeling health history events associated with cancer and aging. The events include the onset of cancer, death from causes different from cancer, and death of individuals with and without cancer. Besides, this approach allows for taking into account unobservable precancerous changes in tissues, as well as deterioration in individuals’ health associated with the aging related processes. An attractive feature of this model is that all functional forms for the population characteristics can be derived analytically. The model also allows for studying a possible trade-off between two lines of organisms’ defense against a disease. The first is responsible for its vulnerability (robustness) and affects the age of disease onset. The second deals with organism’s resilience, i.e., its ability of coping with disease when it strikes. It affects chances of recovery, as well as duration of staying in an unhealthy state. The model allows for testing hypotheses about possibility of trade-off between these two defense strategies.
The derived model was tested by fitting it to the combined data set consisting of the Surveillance, Epidemiology and End Results (SEER) dataset on cancer incidence and case-fatality data in the U.S. for different types of cancer and the U.S. overall mortality data taken from the Human Mortality Database (HMD). The results of the analyses show that the approach captures non-monotonic age patterns of cancer incidence and case fatality rates. The developed approach is capable of explaining links among health history data and provides useful insights on mechanisms of cancer occurrence, disease progression, other aging related changes, and mortality. The results also indicate that parameters, characterizing individual aging rate, may depend on type of cancer developing in body. Further developments of this approach are discussed.
Citation Information: Cancer Prev Res 2008;1(7 Suppl):B120.
Abstract B123: Stopping a silent killer in the underserved Asian community: A novel liver cancer prevention clinic
Authors: Lin Steven , Kang Hyunseung , Aguilar Phillip , Chan Elton , Jeong Monica , Thieu William , Trinh Frank 
Published: May 2012

Abstract
B123
Asian and Pacific Islanders bear a disproportionate burden of liver disease caused by chronic hepatitis B virus (HBV) infection, which is associated with a 25% risk of death from cirrhosis or liver cancer. However, few community based programs exist to tackle this serious public health problem among low income, uninsured Asian and Pacific Islander immigrants. The Hep B Free Clinic is a student-run grassroots organization that focuses on HBV and liver cancer prevention in one of the nation’s largest immigrant communities: San Jose, California. From 2007-2008, we provided free HBV serological screening to 510 patients. For chronically infected patients who elected to undergo follow up monitoring, a series of blood tests were given to evaluate for liver damage (alanine transaminase, ALT), a liver cancer marker (alpha-fetoprotein, AFP), and HBV replication (HBV DNA levels). Of those screened, 17% were chronically infected. Remarkably, one-third (33%) of infected patients were unaware that they were infected. Of those chronically infected, 100% showed signs of active liver damage as measured by elevated ALT, and 9% had elevated AFP tumor markers for hepatocellular carcinoma. Nearly one-quarter (24%) of those chronically infected carried HBV DNA levels that met the criteria for treatment. Patients who were candidates for antiviral therapy were signed up for free drug assistance programs, and those requiring triphasic CT scans for possible liver cancer were referred. Uninfected patients lacking protective HBV antibodies were provided free vaccinations. Our striking findings call for more aggressive liver cancer prevention in this community, including universal screening for HBV.
Citation Information: Cancer Prev Res 2008;1(7 Suppl):B123.
Abstract B125: Adipose tissue accumulation of d-limonene with the consumption of a lemonade preparation rich in d-limonene content.
Authors: Miller Jessica , Hakim Iman , Chew Wade , Thompson Patricia , Thomson Cynthia , Chow H-H. Sherry 
Published: May 2012

Abstract
B125

Purpose
d-Limonene is a bioactive food component commonly found in high concentration in citrus peel. It has demonstrated anti-cancer effects in preclinical studies with the most compelling results in mammary carcinogenesis models. Information on the oral bioavailability and tissue disposition of d-limonene in humans is rather limited for extrapolation of preclinical data to human situations. As a fat-soluble compound, d-limonene is more likely to deposit in fatty tissues such as the breast where we hypothesize that biologic activity may be greatest. We conducted a clinical study to determine the systemic and adipose tissue disposition of d-limonene with the consumption of a lemonade preparation rich in d-limonene content.

Methods
Seven healthy adults underwent a one-week washout period during which their diets were void of all citrus. At entry, participants consumed a breakfast that included the freshly prepared lemonade (40 oz containing 0.6 gm d-limonene) in the clinic. Serum and needle fat biopsies of the buttocks were collected 6 hours post-feeding. Participants then consumed 40 oz of freshly prepared lemonade daily for 4 weeks. At completion of the 4-week feeding period, participants repeated the controlled breakfast with high d-limonene lemonade prepared in the clinic followed by repeat serum and fat sampling. Matched pre- and post-intervention fat biopsies (n = 7) and serum samples (n = 6) were analyzed for d-limonene levels using gas chromatography-mass spectrometry.

Results
The d-limonene levels in the initial fat biopsies ranged from non-detectable to 0.79 μM (median = 2.55 μM) concentration. The adipose d-limonene levels increased significantly (p &lt; 0.01) after 4 weeks of intervention with levels ranging from 53.56 to 293 μM (median = 99.68 μM). There was a slight but statistically significant increase (p &lt; 0.05) in serum d-limonene levels after 4 weeks of intervention; initial levels ranged from 0.35 - 0.72 μM (median = 0.46 μM) and post intervention levels ranged from 0.54 - 1.65 μM (median = 1.20 μM). The adipose d-limonene levels were significantly higher than the serum d-limonene levels (p &lt; 0.05).

Conclusions
Oral consumption of high d-limonene lemonade results in d-limonene deposition in adipose tissue in levels much higher than levels in the systemic circulation. Assessing the serum d-limonene levels is not likely to reflect d-limonene exposure in the adipose tissue. In addition, given d-limonene’s anticarcinogenic properties, and because breast tissue is mostly composed of adipose, the data suggests that d-limonene could also accumulate at this site, thus potentially modulating breast cancer risk.
Citation Information: Cancer Prev Res 2008;1(7 Suppl):B125.
Abstract B127: Alcohol consumption and risk of testicular germ cell carcinoma
Authors: Biggs Mary , Starr Jacqueline , Doody David , Schwartz Stephen 
Published: May 2012

Abstract
B127
The incidence of testicular germ cell carcinoma (TGCC), the most common malignancy among men aged 20-34, has increased several-fold during the past several decades. The etiology of TGCC is poorly understood and the cause of the increased incidence is unknown. Established risk factors include age, race, personal history of undescended testes, and family history of TGCC, none of which is modifiable.
Alcohol is an established testicular toxicant, causing testicular atrophy, gynecomastia, and disrupted sexual function in alcoholic men. In both alcoholics and non-alcoholic men with moderate intake, alcohol depresses levels of circulating testosterone and luteinizing hormone. We hypothesized that alcohol consumption, particularly during adolescence, increases the risk of TGCC. A single previous epidemiologic analysis of alcohol intake and TGCC found no association.
We conducted a population-based case-control study among 18-44 year-old male residents of three Washington State counties. Cases (n=400) were diagnosed during 1999-2006 with a first, primary TGCC. Controls (n=1,020) were men of similar age with no history of TGCC from the same population identified through random-digit telephone dialing. Questionnaires elicited information on demographic, medical, and lifestyle factors, including usual consumption of beer, wine, and liquor during the 5 years prior to reference date and during grades 7-12. We used logistic regression models to compute odds ratio (OR) estimates and 95% confidence intervals (CI) for TGCC in men that consumed 1-6, 7-13, and 14+ alcoholic beverages per week compared to those that consumed none, adjusting for age, education, smoking, and current marijuana use.
A higher proportion of cases than controls (73% vs. 66%) reported drinking 1 or more alcoholic beverages per week during the five years prior to reference date, and during grades 9-12 (44% vs. 37%). Consumption of 14+ alcoholic drinks/week was associated with an approximately 60% increased risk of TGCC (OR=1.62; 95% CI: 1.02-2.58) for consumption during the 5 years prior to reference date, and for consumption during grades 9-12 (OR=1.56; 95% CI: 0.99-2.47). The risk of TGCC appeared to be similar for consumption of beer, wine, or liquor, and for consumption of alcoholic beverages during adolescence versus consumption during adulthood. The risk of TGCC associated with 14+ alcoholic drinks/week was higher among men diagnosed with nonseminomas (OR=2.28; 95% CI: 1.08-4.82) than among men diagnosed with seminomas (OR=1.40 95%CI: 0.80-2.42).
Our results indicate that consumption of 14 or more alcoholic beverages per week during adolescence or adulthood may be associated with a doubling of the risk of non-seminomatous TGCC. This is the first study to report an association between alcohol consumption and an increased risk of TGCC. Additional studies are needed to clarify the relationship between alcohol intake and TGCC.
Citation Information: Cancer Prev Res 2008;1(7 Suppl):B127.
Abstract B130: Fruit, vegetables, and colorectal cancer risk: The European Prospective Investigation into Cancer and Nutrition
Authors: van Duijnhoven Franzel , Bueno-de-Mesquita H. , Ferrari Pietro , Jenab Mazda , Boshuizen Hendriek , Ros Martine , Casagrande Corinne , the EPIC study group for 
Published: May 2012

Abstract
B130

Background
Higher consumption of fruit and vegetables is possibly associated with a decreased risk of colorectal cancer (CRC). However, the findings to date are inconsistent. We examined the relation between self-reported, usual consumption of fruit and vegetables and the incidence of CRC.

Methods
In the European Prospective Investigation into Cancer and Nutrition (EPIC), 452,755 subjects (131,985 men and 320,770 women) in 9 European countries, participated, completed a dietary questionnaire in 1993-2000, and were followed up for cancer incidence and mortality until 2006. A multivariate Cox proportional hazard model was used to estimate adjusted hazard ratios (HRs) and 95% confidence intervals (95%CI) for EPIC-wide quintiles of intake.

Results
After an average follow-up of 8.8 years 2,819 incident CRC cases were reported. Consumption of fruit and vegetables was inversely associated with CRC (highest versus lowest quintile of intake, HR (95%CI) = 0.86 (0.75-1.00); ptrend=0.04) and in particular with colon cancer risk (HR (95%CI) = 0.76 (0.63-0.91); ptrend&lt;0.01). Only after exclusion of the first 2 years of follow-up, this was corroborated by calibrated continuous analyses (HR for 100 g increase in intake (95%CI) = 0.95 (0.91-1.00); p=0.04 and 0.94 (0.89-0.99); p=0.02, respectively).
The association between fruit and vegetable consumption and CRC risk was inverse in never and former smokers, but positive in current smokers. This modifying effect was present for fruit and vegetables combined as well as for vegetables alone (both pinteraction&lt;0.01).

Conclusions
These findings suggest that regular consumption of fruit and vegetables is associated with a reduced CRC and especially colon cancer risk. This effect may depend on smoking status.
Citation Information: Cancer Prev Res 2008;1(7 Suppl):B130.