bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 2138: 6-Shogaol from dried ginger inhibits growth of prostate cancer cells both in vitro and in vivo
Authors: Saha Achinto , Blando Jorge , Silver Eric , Beltran Linda , Sessler Jonathan , DiGiovanni John 
Published: May 2015

Abstract
Prostate cancer (PCa) is the most common non-cutaneous neoplasm and is the second leading cause of cancer death in American men. Approximately 1 in 6 men will be diagnosed with PCa during their lifetime and about 1 in 36 will die of PCa. It is estimated that approximately 238,590 new cases of PCa will be diagnosed and 29,720 PCa-related deaths will occur in the United States in 2013. 6-Shogaol (6-SHO), a potent bioactive compound in ginger (Zingiber officinale Roscoe), has been shown to possess anti-inflammatory and anticancer activity. In the present study, the effect of 6-SHO on the growth of PCa cell lines was investigated. 6-SHO effectively reduced survival and induced apoptosis of cultured human (LNCaP, DU145 and PC3) and mouse (HMVP2) PCa cell lines. Mechanistic studies revealed that 6-SHO reduced constitutive and IL-6 induced STAT3 activation and inhibited both constitutive and TNF-α induced NF-κB activity in these cell lines. In addition, 6-SHO decreased the level of several STAT3 and NF-κB regulated target genes at the protein level (including cyclin D1, survivin and cMyc) and modulated mRNA levels of chemokine, cytokine, cell cycle and apoptosis regulatory genes (IL-7, CCL5, BAX, BCL2, p21 and p27). 6-SHO was more effective than two other compounds found in ginger, 6-gingerol and 6-paradol, at reducing survival of PCa cell lines and reducing STAT3 and NF-κB signaling. 6-SHO also showed significant tumor growth inhibitory activity in an allograft model using HMVP2 cells. Overall, the current results lead us to suggest that 6-SHO may have potential as a chemopreventive and/or therapeutic agent for PCa and that further study of this compound is warranted
Citation Format: Achinto Saha, Jorge Blando, Eric Silver, Linda Beltran, Jonathan Sessler, John DiGiovanni. 6-Shogaol from dried ginger inhibits growth of prostate cancer cells both in vitro and in vivo. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 2138. doi:10.1158/1538-7445.AM2014-2138
Abstract 2143: Inhibiting fatty acid synthase for chemoprevention of chemically induced colorectal tumors
Authors: Orita Hajime , Tanaka Sigekazu , Maekawa Hiroshi , Sakurada Mutsumi , Kushida Tomonori , Ito Tomoaki , Miyazaki Masahiro , Shiroishi Toshihiko , Sato Koichi 
Published: May 2015

Abstract
Purpose: Fatty acid synthase (FAS) is overexpressed in colorectal cancer, and we have investigated the potential use of FAS inhibitors for chemoprevention of colorectal cancer.
Experimental Design: Expression of FAS was evaluated in human colorectal lesions and in murine models of colorectal tumorigenesis [AOM and DSS induced colorectal tumors in mice]. Then, the ability of pharmacologic inhibitors of FAS to prevent development of the murine tumors was investigated.
Results: Immunohistochemical studies show that human colorectal cancers express high levels of FAS compared with normal tissues, suggesting that FAS might be a target for intervention in colorectal carcinogenesis. FAS is also expressed at high levels in chemically induced murine colorectal tumors, and the numbers and sizes of those murine tumors are significantly reduced by treating carcinogen-exposed mice with berberine include, Chinese traditional drug, Kampo.
Conclusions: We conclude that increased levels of FAS are common in human colorectal cancer. Based on studies in mouse models, it seems that inhibiting FAS is an effective strategy in preventing and retarding growth of colorectal tumors that have high expression of this enzyme.
Citation Format: Hajime Orita, Sigekazu Tanaka, Hiroshi Maekawa, Mutsumi Sakurada, Tomonori Kushida, Tomoaki Ito, Masahiro Miyazaki, Toshihiko Shiroishi, Koichi Sato. Inhibiting fatty acid synthase for chemoprevention of chemically induced colorectal tumors. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 2143. doi:10.1158/1538-7445.AM2014-2143
Abstract 2147: The effects of artemisinin, dihydroartemisinin and artemisinin-glycolipid on non-small cell lung cancer induced bone destruction
Authors: Ma Gwang-Taek , Park Kwang-Kyun , Chung Won-Yoon 
Published: May 2015

Abstract
Lung cancer is the major cause of cancer-related death in males worldwide. Non-small cell lung cancer (NSCLC) accounts for approximately 80% of entire lung cancer and largely metastasizes to bone. Bone consistently maintains the balance between osteoclasts and osteoblasts, but NSCLC metastasized to bone interacts with normal bone cells and abnormally enhances osteoclasts-mediated bone resorption. As a result, enhanced bone resorption results in the release of transforming growth factor-beta (TGF-β) and insulin-like growth factor -1 (IGF-1) which promote cancer progression. Plant-derived compounds have been received attention as therapeutic agents for many human diseases. Artemisinin (ART) which is isolated from chinese medicinal herb, Artemisia annua and its derivative dihydroartemisinin (DHA) have been known as outstanding anti-malarial agents and have also potent anti-cancer activities. ART-glycolipid is ART's derivative that combined ART with the glycolipid daumone in order to enhance anti-cancer activity. We found that cell viability was decreased in A549 cells treated with ART, DHA and ART-glycolipid. ART, DHA and ART-glycolipid decreased the migration of A549 cells treated with or without TGF- β1 and IGF-1 which are highly discovered in bone metastasis of NSCLC. In addition, they inhibited the receptor activator of nuclear factor kappa-B ligand (RANKL)-induced osteoclast formation in bone marrow macrophages (BMMs). In particular, ART-glycolipid showed the most potent inhibitory effect. Therefore, we expect that ART, DHA and ART-glycolipid can inhibit metastatic ability of A549 cells and bone resorbing activity of osteoclasts by reducing secretion of matrix metalloproteinases- 9 (MMP-9) and cathepsin K activities in BMM. These results indicate that ART, DHA and ART-glycolipid may serve as useful agents for attenuating NSCLC induced bone destruction.
Citation Format: Gwang-Taek Ma, Kwang-Kyun Park, Won-Yoon Chung. The effects of artemisinin, dihydroartemisinin and artemisinin-glycolipid on non-small cell lung cancer induced bone destruction. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 2147. doi:10.1158/1538-7445.AM2014-2147
Abstract 2148: Inhibitory effects of liensinine and nuciferine on breast cancer-associated bone loss
Authors: Kang Eun-Ji , Chung Won-Yoon , Park Kwang-Kyun 
Published: May 2015

Abstract
Breast cancer is the most common cause of cancer death in women and has a propensity to metastasize to bone. Once tumor cells become lodged in the skeleton, they interact with bone microenvironment establishing the “vicious cycle” that accelerates both tumor growth and bone destruction. Therefore, the vicious cycle between metastatic cancer cells and bone cells can be a possible target for cancer therapy.
Nelumbo nucifera (Lotus) has been used for various medicinal purposes in some parts of the world for treatment of several disorders including skin disease, cough, inflammation, fever. Liensinine and nuciferine are active components in Lotus but it is still unknown whether they can effectively inhibit breast cancer associated bone destruction.
In this study, we found that liensinine and nuciferine inhibited the receptor activator of nuclear factor kappa-B ligand (RANKL)-induced osteoclast formation in mouse bone marrow macrophage cells at non-cytotoxic concentrations. In addition, liensinine and nuciferine inhibited cell proliferation and induced apoptosis in MDA-MB-231 human breast cancer cells. Liensinine also displayed an inhibitory effect on the migration and invasion ability of MDA-MB-231 cells compared with nuciferine. Furthermore, liensinine and nuciferine may modulate cell cycle distribution and expression of apoptosis-related proteins in MDA-MB-231 cells and inhibit breast cancer-induced bone resorption in vivo. Therefore, liensinine and nuciferine can possess the potential to prevent breast cancer-mediated osteolysis.
Citation Format: Eun-Ji Kang, Won-Yoon Chung, Kwang-Kyun Park. Inhibitory effects of liensinine and nuciferine on breast cancer-associated bone loss. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 2148. doi:10.1158/1538-7445.AM2014-2148
Abstract 217: Salinomycin have antiproliferative and apoptotic effects on ovarian cancer stem-like cell
Authors: Shin So-Jin , Kim Jin-Young , Lee Hyun-Gyo , Nam Eun-Ji , Cho Chi-Heum 
Published: May 2015

Abstract
OBJECTIVE: Cancer stem cells (CSCs) represent a subpopulation of undifferentiated tumorigenic cells responsible for tumor initiation, maintenance, drug resistance and metastasis of tumors. CSCs involved in drug resistance and relapse of cancers can significantly affect ovarian cancer therapy. The antibiotics salinomycin has recently been shown to be a potent compound to deplete chemoresistant cells in adenocarcinoma. The objective of the present study was to evaluate the effect of salinomycin on ovarian CSC whereby salinomycin mono-and combination treatment with paclitaxol regimend were analyzed.
METHODS: The CD44+CD117+CSCs were isolated from the primary ovarian cancer cells derived from ascites fluids of patients with epithelial ovarian cancer by using immune magnetic-activated cell sorting system. To evaluate the effect of salinomycin on ovarian CSC, cells were treated in single and combined treatment. The expression was Nanog, Oct3/4, Sox2 and ABCG2 mRNA was determined by RT-PCR and protein expression was detected by Western blot analysis. The cell viability assay, gelatin zymography and apoptosis assay were applied to evaluate the effects of salinomycin compared with parental tumor cells and CSCs.
RESULTS: The combination of salinomycin with paclitaxel (PTX) was enhanced change cell viability or activating apoptosis in CD44+CD117+ cells, whereas the salinomycin monotreatment did not cause significant changes. Salinomycin treatment reduced stemness gene expression and suppressed invasion of CSCs.
CONCLUSIONS: Based on our findings, we concluded that anti-cancer effect of salinomycin with PTX reduced stemness and induced apoptosis in ovarian cancer and cancer stem cells.
Citation Format: So-Jin Shin, Jin-Young Kim, Hyun-Gyo Lee, Eun-Ji Nam, Chi-Heum Cho. Salinomycin have antiproliferative and apoptotic effects on ovarian cancer stem-like cell. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 217. doi:10.1158/1538-7445.AM2014-217
Abstract 2181: Association of sleep duration, daytime napping, and night shift work with breast cancer risk
Authors: Ren Zefang 
Published: May 2015

Abstract
Sleep habit is closely related to melatonin which protect against breast cancer (BC). Sleep duration, nap habit, and shift work have been separately investigated to associate with BC risk, but the combination has not been reported. In this study, we collected all the sleep habits data from 712 women with incident invasive BC before their treatments and 742 age-matched female controls between July 2010 and January 2012 in Guangzhou, China. We found that the women with either shorter or longer sleep duration had increased BC risk compared to the women with normal sleep time of 6.1-8.9h/day [OR (95%CI: 1.62 (1.18-2.24) and 1.55 (1.14-2.10), respectively]. Night shift work also increased the risk of BC [1.36 (1.07-1.73)] and nap habits marginally associated a decreased risk [0.83 (0.66-1.04)]. Women with night shift work and longer sleep duration had an increased risk of BC [3.80 (1.99-7.26)] compared to the women with normal sleep time and no night shift work. The interaction on BC risk was significant (P for interaction=0.009). We conclude that abnormal sleep increases BC risk and longer sleep duration may not compensate the effect of night shift work on risk of BC.
Table 1.Age-adjusted and multivariate-adjusted odds rations for the associations between sleep habits and breast cancer riskVariablesCases Controls OR#(95%CI)OR* (95%CI)OR^ (95%CI)(n=712) (%)(n=742)(%) Shift worknever443 (67.0)527 (73.8)1.00 (reference)1.00 (reference)1.00 (reference)ever218 (33.0)187 (26.2)1.39 (1.10-1.75)1.36 (1.07-1.73)1.34 (1.04-1.71)Napping statusnever293 (44.5)254 (37.7)1.00 (reference)1.00 (reference)1.00 (reference)ever365 (55.5)420 (62.3)0.75 (0.61-0.94)0.83 (0.66-1.04)0.83 (0.66-1.06)24-hour sleep duration≤6.0116 (17.7)85 (12.8)1.62 (1.18-2.21)1.62 (1.18-2.24)1.52 (1.10-2.11)6.1-8.9409 (62.6)485 (72.7)1.00 (reference)1.00 (reference)1.00 (reference)≥9.0129 (19.7)97 (14.5)1.58 (1.18-2.12)1.55 (1.14-2.10)1.59 (1.17-2.17)P-continuous0.6460.8830.451P-trend0.9090.9960.661OR#: Adjusted for age.OR*: Adjusted for age, education, BMI, marital status, age at menarche, menopausal status, parity, activity, breastfeeding and family history of breast cancer.OR^: Adjusted for age, education, BMI, marital status, age at menarche, menopausal status, parity, activity, breastfeeding, family history of breast cancer, and other sleep factors.
Citation Format: Zefang Ren. Association of sleep duration, daytime napping, and night shift work with breast cancer risk. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 2181. doi:10.1158/1538-7445.AM2014-2181
Abstract 2189: A rare copy number variant at chromosome 14q11 was associated with sporadic colorectal cancer risk in Singapore Chinese
Authors: Cheah Peh Yean , Thean Lai Fun , Teo Yik-Ying , Koh Woon-Puay , Yuan Jian-Min , Koh Poh Koon , Chew Min Hoe , Tang Choong Leong 
Published: May 2015

Abstract
Colorectal cancer (CRC) is one of the most frequent cancers and leading cause of cancer mortality in the developed world. Twin study has attributed about 35% of the etiology of sporadic CRC to genes. Structural variations in the human genome have recently been associated with complex neurological diseases. Their role in CRC, however, is unclear. We performed genome-wide association study (GWAS) on 2,000 ethnicity-, age-, and gender-matched Singapore Chinese CRC patients (aged 50 or more and with no dominant family history of CRC) and healthy controls. Genome-wide genotyping was performed using Affymetrix SNP 6 platform, and rare copy number variants (CNV) were interrogated in 1830 samples that passed the quality assurance tests. A 400 kb region at chromosome 14q11 was identified to be significantly associated (-log10 p-value = 11) with sporadic CRC risk. A chromatin modifier implicated in the β-catenin/Wnt signalling pathway is one of the candidate genes found in the region. Primers unique for this gene applied to an optimal real-time copy number assay verified the CNV region in an independent replication panel comprising another 1,000 sporadic CRC cases. About 6% of the cases exhibit copy number alterations at this region compared to 1% in the healthy controls. A second gene, a small guanosine triphosphatase (GTPase) involved in protein trafficking and preferentially up-regulated in colonic tumors , was shown by long-range polymerase chain reaction to have more structural variations in the cases compared to the controls. Furthermore, expression of the H1 binding domain of the chromatin modifier was positively correlated to the expressions of Cyclin D1 and C-myc. The data suggest that the rare CNV in 14q11 was dynamically associated with the activation of genes implicated in sporadic CRC in the Singapore Chinese.
Citation Format: Peh Yean Cheah, Lai Fun Thean, Yik-Ying Teo, Woon-Puay Koh, Jian-Min Yuan, Poh Koon Koh, Min Hoe Chew, Choong Leong Tang. A rare copy number variant at chromosome 14q11 was associated with sporadic colorectal cancer risk in Singapore Chinese. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 2189. doi:10.1158/1538-7445.AM2014-2189
Abstract 219: Inhibition of CD133 expression induce the chemoresistance to 5-fluorouracil in the colon cancer cell line
Authors: Lee Mi-Ra , Ji Sun-Young , Mia-Jan Khalilullah , Cho Mee-Yon 
Published: May 2015

Abstract
Background: The cancer stem cell (CSC) theory which postulates a small subset of tumor cells have the capacity in tumor initiation, progression and importantly resistance to chemotherapy. CD133 is a transmembrane glycoprotein that serves as a putative cancer stem cell (CSC) marker in colon cancer and its relationship with the chemoresistance has been on debate. In our previous clinical study, we found the patients with CD133+ colon cancer have better prognosis after 5 fluorouracil (5-FU) chemotherapy compared to CD133- tumors. Purpose: To understand the role of CSC marker expression in relation to chemoresistance in colon cancer, we evaluated the effect of CD133 inhibition in colorectal cancer (CRC) cell line on the genes expression which are related to chemoresistance or cell survival. Materials & Methods: CD133 siRNA transfection was performed on CD133+ colon cancer cell line (Caco-2). The proliferation assay used to detect the cytotoxic effect of 5-FU chemotherapy. The change in expression of chemoresistance related genes (AKT1, ABCG2 and MDR1) and cell survival related genes (survivin and beta-catenin) were evaluated by qRT-PCR and western blotting at 48hrs and 72hrs after CD133 siRNA transfection. Results: The proliferation assay demonstrated the increased chemoresistance of colon cancer cells after inhibition of CD133 expression when 5µM 5-FU was treated (p=0.0014). The mRNA expression of chemoresistance related genes (AKT1, ABCG2, MDR1) and cell survival related genes (survivin and β-catenin) were all significantly increased after transfection (p&lt;0.05) but there was no significant changes in expression at the protein level of all genes. Conclusions: The inhibition of CD133 expression in CD133+colon cancer cell line induce the chemoresistance to 5-FU chemotherapy through the increased expression of chemoresistance related genes. Therefore, CD133 expression seems to be related with the chemosensitivity to 5-FU in colon cancer despite the mechanism needs to be proven.
Citation Format: Mi-Ra Lee, Sun-Young Ji, Khalilullah Mia-Jan, Mee-Yon Cho. Inhibition of CD133 expression induce the chemoresistance to 5-fluorouracil in the colon cancer cell line. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 219. doi:10.1158/1538-7445.AM2014-219
Abstract 22: Interferon-γ produced by tumor-infiltrating NK cells and CD4+ T cells downregulates TNFSF15 expression in endothelial cells
Authors: Gu Xin , Cheng Tao , Li Luyuan 
Published: May 2015

Abstract
Endothelial cells in an established vasculature secrete tumor necrosis factor superfamily-15 (TNFSF15; VEGI; TL1A) that functions as a negative modulator of neovascularization to maintain blood vessel stability. TNFSF15 gene expression diminishes at angiogenesis and inflammation sites such as in cancers and wounds. Interferon-γ (IFNγ) is a pleiotropic cytokine expressed primarily by lymphocytes of T cell and NK cell lineages. IFNγ may mediate anti-tumor effects either directly on cancer cell growth or indirectly through immunomodulatory and antiangiogenic responses. However, it was also reported that IFNγ promotes angiogenesis under certain circumstances. Here we show that IFNγ suppresses TNFSF15 expression in human umbilical cord vein endothelial cells (HUVEC). This activity is mediated by IFNγ receptor and the transcription factor STAT1. Since tumor-infiltrating NK and CD4+ T cells are the main sources of IFNγ in tumor lesions, we isolated these cells from peripheral blood of healthy individuals, treated the cells with ovarian cancer OVCAR3 cell-conditioned media, and found a 1- and 10-fold increase of IFNγ production in NK and CD4+ T cells, respectively, compared with that in vehicle-treated cells. These findings support the view that tumor-infiltrating NK and CD4+ T cells under the influence of cancer cells significantly increase the production of IFNγ, which in turn inhibits TNFSF15 expression in tumor vascular endothelial cells, shifting the balance of pro- and anti-angiogenic factors toward escalated angiogenesis potential in the tumor.
Citation Format: Xin Gu, Tao Cheng, Luyuan Li. Interferon-γ produced by tumor-infiltrating NK cells and CD4+ T cells downregulates TNFSF15 expression in endothelial cells. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 22. doi:10.1158/1538-7445.AM2014-22
Abstract 2202: PIK3CA amplification was not associated with serrated polyps but tubular adenomas in colorectal lesions
Authors: Lee Jae-Ho , Kim Dae-Kwang , Choi In-Jang , Hwang IlSeon , Kang Yu-Na , Kim Shin 
Published: May 2015

Abstract
Colorectal cancer is a heterogeneous disorder than arises via multiple distinct pathways, from tubular adenomas (TAs) and serrated polyps (SPs), which are clinically, morphologically, and molecularly different. We examined PIK3CA amplification in colorectal precancerous legions, including TAs and SPs. DNA was isolated from paired normal and tumoral tissues in 64 TAs and 32 SPs. PIK3CA amplification, KRAS mutation, and BRAF mutation were analyzed by real-time PCR. PIK3CA amplification was found in 25% of TAs and 9.4% of SPs, respectively and low and high grade of TAs showed similar frequency of PIK3CA amplification. KRAS and BRAF mutations were mutually exclusive in both TAs and SPs. In TAs, PIK3CA amplification was associated with distal colon and it was mutually exclusive with KRAS mutation. These results suggest that PIK3CA amplification may be early and important event in colorectal carcinogenesis and may drive the development of TAs independently with KRAS mutation.
Keyword: colorectal cancer, PIK3CA amplification, serrated polyps, tubular adenomas
Note: This abstract was not presented at the meeting.
Citation Format: Jae-Ho Lee, Dae-Kwang Kim, In-Jang Choi, IlSeon Hwang, Yu-Na Kang, Shin Kim. PIK3CA amplification was not associated with serrated polyps but tubular adenomas in colorectal lesions. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 2202. doi:10.1158/1538-7445.AM2014-2202