bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 4575: Açaí intake reduces the aberrant crypt foci development in a colitis-associated carcinogenesis model in male Wistar rats
Authors: FRAGOSO MARIANA F. , ROMUALDO GUILHERME R. , PELLIZZON CLAUDIA H. , BARBISAN LUIS F. 
Published: August 2015

Abstract
Colorectal cancer is a main cause of cancer death in the western world. In Brazil, it is the third more common neoplasia in both men and women (INCA, 2014). In our previous study (Fragoso et al., Food Chem Toxicol., 2013), we showed that spray-dried açaí (Euterpe oleraceae Mart.) pulp intake retarded the development of colon cancer in male Wistar rats. Therefore, the objective of this research was to evaluate the potential protection of dietary freeze-dried açaí pulp using a chemically-induced colon carcinogenesis and colitis-associated model in male Wistar rats. The animals were randomly distributed into four groups: G1, DMH [dimethylhydrazine] + TNBS [2,4,6-trinitrobenzene sulfonic acid] + basal diet; G2, DMH + TNBS + basal diet with 5% açai pulp; G3, DMH + TNBS + basal diet with 7.5% açai pulp; G4, DMH + TNBS + basal diet with 0.2% of NAC [N-acetylcysteine]. The acute colitis was induced with the administration of 10 mg of TNBS dissolved in 0.25 ml 50% ethanol (v/v) by means of a Teflon cannula inserted 8 cm into the anus. At the end of the 25th week, animals were sacrificed for evaluation of Aberrant Crypt Foci (ACF) in the colon. Unsenctioned and fixed colons were analyzed for total aberrant crypt (AC) and total ACF and ACF multiplicity under methylene blue staining. The results were analyzed by ANOVA followed by post hoc Tukey test. A significant reduction in total ACF and AC for G2 when compared to G1 (p ≤0.001) was seen. Regarding the ACF multiplicity, it was observed a significant reduction in ACF with 4-10 aberrant crypts for G2 and G4 and for ACF with &gt;10 aberrant crypts for G2-G4 groups in relation to the G1 group (p = ≤0.001, respectively). Also, it was observed a significant reduction in the number of total AC in the distal colon from the G2 and G4 groups compared to G1 group (p = 0.003) and in the medial colon from the G2 group compared to G1 group (p = 0.016). These results suggest that açaí intake may reduce the number of AC and ACF and the number of ACF with more than four aberrant crypts in this chemically-induced colon carcinogenesis and colitis-associated model in rats.
Citation Format: MARIANA F. FRAGOSO, GUILHERME R. ROMUALDO, CLAUDIA H. PELLIZZON, LUIS F. BARBISAN. Açaí intake reduces the aberrant crypt foci development in a colitis-associated carcinogenesis model in male Wistar rats. [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 4575. doi:10.1158/1538-7445.AM2015-4575
Abstract 4579: The role of carnosol in reducing skin cancer development and progression
Authors: Tong Lingying , Wu Shiyong 
Published: August 2015

Abstract
Carnosol is a natural compound extracted from rosemary and sage, which are commonly used in traditional Mediterranean cuisine. Among all the compounds extracted from Mediterranean herbs, carnosol, first isolated from sage in 1941, has been demonstrated to be beneficial to health for its anti-inflammation, anti-oxidation and anti-cancer properties. Because of its structure similarity to sex hormones, research has been done on the effect of carnosol mainly on breast and prostate cancers. However, very little is known on the effect of carnosol on UV-induced skin cancer. In this report, we studied the effect of carnosol on UV-induced skin cancer formation and progression. Our data showed that carnosol could partially reduce UVB-induced reactive oxygen species (ROS) elevation and thus protect UV-induced DNA damage in normal skin cells. We also showed that carnosol could inhibit the UVB-induced NF-κB activation. As a result, the normal cell apoptosis induced by UV radiation was partially protected. Moreover, it could also prohibit skin cancer cell progression with or without UV radiation. Therefore, we propose that carnosol could be a potential therapeutic for chemoprevention and treatment of UVB-induced skin cancers.
Citation Format: Lingying Tong, Shiyong Wu. The role of carnosol in reducing skin cancer development and progression. [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 4579. doi:10.1158/1538-7445.AM2015-4579
Abstract 4581: Genetic variations in CDKN1A and RHPN2 associated with prognosis for patients with colorectal cancer
Authors: Kang Byung Woog , Kim Jong Gwang , Chae Yee Soo , Lee Shin Yup , Lee Soo Jung , Yoon Shinkyo 
Published: August 2015

Abstract
Genome-wide association studies (GWASs) have already identified at least 22 common susceptibility loci associated with an increased risk of colorectal cancer (CRC). This study examined the relationship between these single nucleotide polymorphisms (SNPs) and the clinical outcomes of patients with colorectal cancer. Seven hundred seventy-six patients with surgically resected colorectal adenocarcinoma were enrolled in the present study. Twenty-two of the GWAS-identified SNPs were genotyped using a Sequenom MassARRAY. Among the 22 SNPs, two (rs1321311G&gt;T in CDKN1A and rs10411210C&gt;T in RHPN2) were significantly associated with the survival outcomes of CRC in a multivariate survival analysis. In a recessive model, the rs1321311 TT genotype (vs. GG + GT) and rs10411210 TT genotype (vs. CC + CT) were associated with a worse prognosis for disease-free survival (adjusted HR = 1.90; 95% confidence interval = 1.00-3.60; P = 0.050, adjusted HR = 1.94; 95% confidence interval = 1.05-3.57; P = 0.034, respectively) and overall survival (adjusted HR = 2.05; 95% confidence interval = 1.00-4.20; P = 0.049, adjusted HR = 2.06; 95% confidence interval = 1.05-4.05; P = 0.036, respectively). None of the other SNPs was significantly associated with any clinicopathologic features or survival. The present results suggest that the genetic variants of the CDKN1A (rs1321311) and RHPN2 (rs10411210) genes can be used as prognostic biomarkers for patients with surgically resected colorectal cancer.
Citation Format: Byung Woog Kang, Jong Gwang Kim, Yee Soo Chae, Shin Yup Lee, Soo Jung Lee, Shinkyo Yoon. Genetic variations in CDKN1A and RHPN2 associated with prognosis for patients with colorectal cancer. [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 4581. doi:10.1158/1538-7445.AM2015-4581
Abstract 4591: Differential expression of tight junction polarity genes in human colon cancer
Authors: Royse Kathryn E. , Chen Liang , Uriostegui Jocelyn , Ittmann Michael , Graham David Y. , El-Serag Hashem , Jiao Li 
Published: August 2015

Abstract
Tight junctions perform significant and multifactorial functions in cellular polarity maintenance and paracellular transport. A number of studies have found structural disruption of epithelial colon cells can significantly impact early tumorigenesis and progression. However, little is known about the direct contribution of polarity gene expression in human colon cancer development. We compared the expression of tight junction genes in colon cancer with normal control mucosa. Total RNA was extracted from fresh frozen tissue biopsies of six white male patients (N = 3 for early stage tumore, N = 3 for late stage tumor, and N = 2 for normal adjacent controls) and four unrelated normal colon mucosa from polyp-free individuals. We used the Qiagen RT2 Profiler PCR array to determine the expression of 84 genes in the tight junction pathway. Student's t test was used to compare the expression levels between different groups (control vs. early-stage tumor and late-stage tumor) using normalized gene expression data. Functional annotation clustering of statistically significant genes by group was conducted using DAVID. Significant (P&lt;0.05) down regulation of claudin (CLDN5, CLDN6, CLDN7) expression was seen in both early and late-stage tumor compared with controls, all with fold change (FC)&gt; 2; while CLDN1 (FC = 15) was only significantly upregulated (P = 0.0007) in early-stage tumor. Down regulation (FC&gt;2) of polarity complex gene PARD6A (P&lt;.001) and associated genes (JAM2, P&lt;.001 and JAM3, P &lt;.001) were present in both early and late-stage tumors along with associated down-regulation of tumor suppressor PTEN (P&lt;.0001). We found differential expression of tight junction genes in normal versus colon tumor. Down regulation of polarity genes is likely to affect apico-basal polarity and promote random non-coordinated migration which can lead to disruption of epithelial structure and to carcinogenic tissue infiltration. Further larger studies are warranted to investigate the role of tight junction proteins in the progression of human colon tumor.
Citation Format: Kathryn E. Royse, Liang Chen, Jocelyn Uriostegui, Michael Ittmann, David Y. Graham, Hashem El-Serag, Li Jiao. Differential expression of tight junction polarity genes in human colon cancer. [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 4591. doi:10.1158/1538-7445.AM2015-4591
Abstract 4598: Low-frequency coding variants in BAT2, HIST1H1E and BPIFB1 are associated with lung cancer risk in Chinese populations
Authors: Jin Guangfu , Zhu Meng , Yin Rong , Shen Wei , Xu Lin , Hu Zhibin , Lin Dongxin , Shen Hongbing 
Published: August 2015

Abstract
Objective: Genome-wide association studies have successfully identified a subset of common variants associated with lung cancer risk. However, these variants explain only a fraction of lung cancer heritability. Alternatively, it is proposed that uncommon variants may have strong effects and contribute to the missing heritability. The aim of the study was to evaluate the role of low-frequency or rare variants in lung cancer development.
Methods: We analyzed exome chips with a total of 247,870 variants in 1,348 lung cancer cases and 1,998 controls in discovery stage and subsequently validated promising associations in additional 3,581 cases and 3,669 controls in replication stages. Single-variant and gene-based analyses were carried out in coding variants with minor allele frequency less than 0.05.
Results: We identified three low-frequency missense variants in BAT2 (OR = 0.54, P = 1.02×10-9), HIST1H1E (OR = 0.49, P = 5.66×10-7) and BPIFB1 genes (OR = 1.79, P = 3.99×10-7) significantly associated with lung cancer risk. The risk allele of variant in BPIFB1 was also associated with early onset of lung cancer. BAT2 and HIST1H1E located at MHC III region across 6p22.2-6p21.31 and BPIFB1 at 20q11.21 were frequently associated with inflammation/immune-related diseases, and were found to be differentially expressed between lung tumors and paired normal tissues. In addition, down-regulation of BPIFB1 was significantly associated with poor prognosis of lung cancer patients.
Conclusions: Our results highlight importance of uncommon variants in lung cancer susceptibility, and indicate potential biology of candidate genes at 6p22.2-6p21.31 and 20q11.21 in the process of lung carcinogenesis.
Citation Format: Guangfu Jin, Meng Zhu, Rong Yin, Wei Shen, Lin Xu, Zhibin Hu, Dongxin Lin, Hongbing Shen. Low-frequency coding variants in BAT2, HIST1H1E and BPIFB1 are associated with lung cancer risk in Chinese populations. [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 4598. doi:10.1158/1538-7445.AM2015-4598
Abstract 4601: Genetic polymorphisms in the vitamin D pathway in relation to lung cancer risk and survival
Authors: Kong Jinyu , Xu Fangxiu , Qu Jinli , Wang Yu , Gao Ming , Yu Herbert , Qian Biyun 
Published: August 2015

Abstract
Studies have suggested that vitamin D may have protective effects against cancer development or tumor progression. To search for additional evidence, we investigated the role of genetic polymorphisms involved in the vitamin D pathway in non-small cell lung cancer (NSCLC). We evaluated common genetic polymorphisms associated with the vitamin D pathway in relation to NSCLC in a case-control study of 603 newly diagnosed NSCLC patients and 661 matched healthy controls. Seven single nucleotide polymorphisms (SNPs) were genotyped, the expression of CYP27B1 and CYP24A1 were measured in 153 tumor samples and their associations with genotypes and patient survival were also analyzed. In the case-control comparison, we found SNP rs3782130 (CYP27B1), rs7041 (GC), rs6068816 and rs4809957 (CYP24A1) associated with NSCLC risk. The risk of NSCLC was increased with the number of risk alleles. CYP27B1 and CYP24A1 expression were significantly different between tumor and normal tissues in NSCLC. High CYP27B1 expression was associated with better overall survival, and the expression was different by the rs3782130 genotype. The study suggests that some genetic polymorphisms involved in the vitamin D pathway may associate with NSCLC risk, and one of the polymorphisms (rs3782130) may affect gene expression and patient survival.
Note: This abstract was not presented at the meeting.
Citation Format: Jinyu Kong, Fangxiu Xu, Jinli Qu, Yu Wang, Ming Gao, Herbert Yu, Biyun Qian. Genetic polymorphisms in the vitamin D pathway in relation to lung cancer risk and survival. [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 4601. doi:10.1158/1538-7445.AM2015-4601
Abstract 4603: Male pattern baldness in relation to prostate cancer-specific mortality: A prospective analysis in the NHANES I Epidemiologic Followup Study (NHEFS)
Authors: Zhou Cindy Ke , Levine Paul H. , Cleary Sean D. , Hoffman Heather J. , Graubard Barry I. , Cook Michael B. 
Published: August 2015

Abstract
Background: Androgenic action underlies prostate gland development and prostate cancer progression. However, the role of such in prostate carcinogenesis remains unclear. Results from studies that have quantitated pre-diagnostic, circulating androgens at a single time-point in relation to prostate cancer are inconsistent, possibly due to the failure to capture cumulative or relevant age-specific hormone exposure. Therefore, we used male pattern baldness as a proxy of long-term androgen exposure, and investigated the association between dermatologist-assessed male pattern baldness and prostate cancer-specific mortality in the NHANES-I Epidemiologic Followup Study (NHEFS).
Methods: We included 4,316 men from NHEFS, who were 25-74 years, received dermatologic exams, and had no prior cancer diagnosis at baseline. Hazard ratios (HRs) and 95% confidence intervals (95%CIs) were estimated using Cox proportional hazards regression with age as the time-metric and baseline hazard stratified by age at baseline. A hybrid model was used to account for stratification and clustering of the survey design, while adjusting for variables used to calculate sample weights.
Results: During follow-up (median = 21 years), 3,284 deaths occurred, 107 of which had the underlying cause of prostate cancer. Any degree of baldness was associated with a 56% increased risk of prostate cancer-specific mortality (HR = 1.56; 95%CI = 1.02, 2.37) and, specifically, moderate balding was associated with an 83% increased risk of the outcome (HR = 1.83; 95%CI = 1.15, 2.92), each compared with no balding. Conversely, male pattern baldness was not statistically significantly associated with all-cause mortality.
Conclusion: Our analysis suggests that male pattern baldness is associated with an increased risk of fatal prostate cancer, and supports the hypothesis of overlapping pathophysiological mechanisms.
Impact: If the association between male pattern baldness and fatal prostate cancer is substantiated in future studies, male pattern baldness may contribute to predictive algorithms of prostate cancer risk, helping guide individuals as to whether they should opt to undergo cancer screening.
Citation Format: Cindy Ke Zhou, Paul H. Levine, Sean D. Cleary, Heather J. Hoffman, Barry I. Graubard, Michael B. Cook. Male pattern baldness in relation to prostate cancer-specific mortality: A prospective analysis in the NHANES I Epidemiologic Followup Study (NHEFS). [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 4603. doi:10.1158/1538-7445.AM2015-4603
Abstract 4608: Racial differences in the distribution of prostate tumor biomarkers and treatment failure: The SCORE study
Authors: Lal* Priti , Yamoah* Kosj , Ziober Amy , Walker Amy , Zhou Wenting , Spangler Elaine , Zeigler-Johnson Charnita , Feldman Michael , Rebbeck Timothy R. 
Published: August 2015

Abstract
Prostate cancer exhibits the greatest disparity in mortality between African American (AA) and European American (EA) men of any cancer in the US. The reasons for this disparity include access to care, screening patterns, and behavior. Biological differences may lead some AA men to have biologically aggressive tumors. Using the Study of Clinical Outcomes, Risk, and Ethnicity (SCORE) study, we identified prostate tumor tissues from men undergoing prostatectomy at the Hospital of the University of Pennsylvania between 1991-2008. Immunohistochemistry was undertaken on the FFPE tumors of 45 EA and 55 AA men (mean age: 59.1 years, range: 41-71). No statistically significant difference in marker phenotypes was observed for prevalence of TMPRSS2/ERG fusion proteins, or in staining intensity for PSMA or Rb. We observed statistically significant differences in marker phenotype for RACEMASE (EA Mean: 188.1 vs. AA Mean: 144.7, p = 0.004), c-myc (EA Mean: 54.7 vs. AA Mean: 21.6, p = 0.005), and AR (EA Mean: 192.1 vs. AA Mean: 136.5, p = 0.002). These data suggest that markers that have been reported to be associated with tumor aggressiveness differ between EA and AA men.
We further evaluated whether these markers were associated with clinical outcome as measured by biochemical (PSA) failure (BF) after radical prostatectomy (RP). We observed 41 BF with a mean follow up of 32.6 months post-RP, compared with 68 non-BF with a mean follow up of 53.7 months post-RP. After adjusting for pathology tumor grade, only the presence of a TMPRSS2-ERG fusion protein was significantly associated with BF. We observed a significant interaction (p = 0.031) by race suggesting TMPRSS2-ERG fusions were less likely to be associated with BF in AA than in EA. These data suggest that TMPRSS2-ERG fusions may not be important predictors of prostate cancer outcomes in AA men as has been suggested in EA men.
*These authors contributed equally to the work.
Citation Format: Priti Lal*, Kosj Yamoah*, Amy Ziober, Amy Walker, Wenting Zhou, Elaine Spangler, Charnita Zeigler-Johnson, Michael Feldman, Timothy R. Rebbeck. Racial differences in the distribution of prostate tumor biomarkers and treatment failure: The SCORE study. [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 4608. doi:10.1158/1538-7445.AM2015-4608
Abstract 4639: Metformin decreases cellular ceramides in MCF-7 and MDA-MB 231 breast cancer cell lines by inhibition of ceramide synthetic enzymes
Authors: Wann Daniel , Palau Victoria , Lightner Janet , Brannon Marianne , Stone William , Krishnan Koyamangalath 
Published: August 2015

Abstract
Metformin, an anti-diabetic biguanide, has been shown to have cytotoxic and chemopreventive properties in in vitro and epidemiological studies, respectively. Metformin's predominant cytotoxic functions may be through activation of 5′ adenosine monophosphate-activated protein kinase (AMPK) with subsequent cell apoptosis. Ceramides, a group of waxy lipids found in the cellular membrane, are key players in many elements of cell signaling, including the regulation of cell differentiation, proliferation, and apoptosis. While traditionally thought of as being pro-apoptotic, this notion has been questioned with the discovery of pro-survival ceramides, as well as the demonstration that certain species of ceramides are increased in breast cancer cells. Metformin reduces ceramides in insulin-resistant mouse myoblasts and may reduce the vascular complications of diabetes mellitus.
MCF-7 and MDA-MB-231 breast cancer cell lines were treated with increasing concentrations of metformin and cytotoxicity was determined by MTT cell culture experiments after 72 hours of drug exposure. Metformin induces cytotoxicity in these breast cancer cells at a lowest concentration of 1.25 mM, and percentage cytotoxicity increases in a dose-dependent manner. We then determined the effect of metformin on cell ceramide synthesis by analyzing key ceramide synthetic enzymes. Using western immunoblot and polymerase chain reaction (PCR) analysis, we determined that metformin induces a reduction in serine palmitoyl transferase, ceramide synthase, dihydroceramide desaturase, and neutral sphingomyelinase in MCF-7 and MDA-MB-231 breast cancer cells. We also analyzed the distribution of ceramides in treated breast cancer cells using polyclonal antibodies against ceramides. By confocal microscopy, ceramides are globally decreased in MCF-7 and MDA-MB-231 cells treated with metformin.
This data suggests that the pro-apoptotic effect of metformin may be partly mediated through its disruption of the balance of ceramides and/or through the reduction of pro-survival ceramides within breast cancer cells. It is also possible that the predominant ceramides in MCF-7 and MDA-MB-231 breast cancer cells are pro-survival and metformin suppresses these ceramides. Further work is necessary to characterize the ceramide content of MCF-7 and MDA-MB-231 cancer cells before and after metformin treatment.
Citation Format: Daniel Wann, Victoria Palau, Janet Lightner, Marianne Brannon, William Stone, Koyamangalath Krishnan. Metformin decreases cellular ceramides in MCF-7 and MDA-MB 231 breast cancer cell lines by inhibition of ceramide synthetic enzymes. [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 4639. doi:10.1158/1538-7445.AM2015-4639