bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 5531: Combination drug delivery using PBM nanoparticle to improve prostate cancer therapy
Authors: Singh Rajesh , Singh Shailesh , Sonpavde Guru P. , Lillard James W. 
Published: August 2015

Abstract
Docetaxel is the standard first-line chemotherapy for advanced prostate cancer (PCa). The key challenges in this treatment option are dose-limiting toxicities, acquired resistance, and lack of tumor cell specificity. Adjuvants and docetaxel encapsulation have been proposed to mitigate many of these hindrances. The proposed study evaluated a novel method for targeted delivery of resveratrol alone or in combination with docetaxel at desired rates. We described a proprietary planetary ball milling approach (PBM) that uses a natural polysaccharide (starch; FDA approved) to create a drug-polysaccharide nanoparticle as a core that is subsequently coated with novel folate-conjugated poly (ϵ-caprolactone) / poly (ethylene glycol) co-polymer, which allows binding to high affinity folate receptors present on PCa cells. The resulting PBM nanoparticles were shown to be rapidly internalized and induce significant cancer cell apoptosis at lower doses, than compared to unformulated resveratrol and/or docetaxel. Importantly, negative controls showed that PBM nanoparticles without resveratrol or docetaxel had no toxic effects on PCa cells. Furthermore, our data also suggests that resveratrol potently synergizes with docetaxel to inhibit proliferation and induce 60% cell death in PCa cell lines at concentrations lower than the IC50. Since docetaxel is associated with various debilitating toxicities, a synergistic combination of resveratrol-docetaxel with targeted delivery to tumor cells could provide a more potent therapeutic effect at lower drug concentrations and improve therapeutic index.
Citation Format: Rajesh Singh, Shailesh Singh, Guru P. Sonpavde, James W. Lillard. Combination drug delivery using PBM nanoparticle to improve prostate cancer therapy. [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 5531. doi:10.1158/1538-7445.AM2015-5531
Abstract 5543: Elucidating the cytotoxic effects of taxol,camptothecin and Lobostemon fruticosus extracts on non-small cell lung cancer
Authors: Motadi Lesetja Raymond , Ndlovu Lungile 
Published: August 2015

Abstract
Lung cancer is reportedly the most common form of cancer worldwide, with a 13-15% occurrence of all known cancers being reported daily. Lung cancer is also the most deadly form of cancer as it has been observed to be resistant to most therapeutic treatments and it demonstrates a metastasis within lymph nodes. An alternative approach is to identify the cytotoxic effects of non-invasive medicinal plant extracts on NSCLC. Thus the aim of the study was to compare the cytotoxic effects of the invasive anti-cancer drugs, taxol and camptothecin, with less invasive plant extracts of L. fruticosus on cell line A549. Cells seem to show a degree of cell death after treatment however some degree of cells still remain viable indicating usefulness in chemotherapy. The following techniques were used, exCELLigence RTCA, Cell cycle, Annexin V apoptosis analysis and LC-MS to identify the compound. Cells treated with camptothecin, Methanol and butanol extracts indicate some degree of early apoptosis which was indicative of little to no DNA fragmentation. Cell cycle arrest was observed in both camptothecin and taxol treated cells, however there was little evidence to suggest the same for L. Fruticosus extracts as there was a high degree of cell death that was observed during the cell cycle analysis. Apoptotic genes that were found in A549 treated cells upregulated in the absence of p53. Phytochemical screening of the L. Fruticosus plant extracts indicated that the plant possesses compounds that display apoptotic activity. These findings suggest that camptothecin, taxol and extract of L. fruticosus display cytotoxic activity on A549 cells. The upregulation of genes in absence of p53 seem to suggest that treatments induce apoptosis using an alternative apoptotic pathway.
Note: This abstract was not presented at the meeting.
Citation Format: Lesetja Raymond Motadi, Lungile Ndlovu. Elucidating the cytotoxic effects of taxol,camptothecin and Lobostemon fruticosus extracts on non-small cell lung 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 5543. doi:10.1158/1538-7445.AM2015-5543
Abstract 5553: In vivo and in vitro effect of Withania somnifera extract on the proliferation of side population (CD44HIGH /CD24LOW) cells sorted from MDA-MB-231 breast cancer cells
Authors: Khazal Kamel F. 
Published: August 2015

Abstract
Invasive breast cancer is considered a great challenge for treatment of cancer in women. In 2013, an estimated 232,340 new cases of invasive breast cancer were expected to be diagnosed in the U.S., along with 64,640 new cases of non-invasive breast cancer. For women under 45, breast cancer is more common in African-American women than white women, and, overall, African-American women are more likely to die of breast cancer. CD44high/CD24low cells have been associated with invasiveness of breast cancers, in particular basal-like breast cancers. In nude mice xenografted with MDA-MB-231 breast cancer cells, CD44high/CD24low cells are the side population associated with metastasis to the bones and are considered to be cancer stem cells. The side population cells are not only involved in invasiveness of breast cancer but are resistant to chemotherapeutic drugs such as mitoxantrone and doxorubicin.
The effects of an alcoholic extract of the roots of Withania somnifera (WS), a traditional herbal remedy, was tested in the sorted side population, CD44high/CD24low, of MDA-MB-231 breast cancer cells. WS caused a concentration-dependent inhibition of the sorted cells, with 95, 65, and 35% inhibition of the proliferation of cells after incubation with concentrations of 100, 50, and 25 μg/ml, respectively. Two groups of nude mice (10 mice ineach group) were xenografted with luciferase transfected CD44high/CD24low cells. Group1 served as control has been dosed with 10% DMSO via drinking water for 8 weeks. Group 2 has been given WS (300 mg/kg) via drinking water for 8 weeks. This experiment is on going and will end after 8 weeks. Tumoror size will be assessed each week using an in vivo imaging system. In conclusion, on, Withania somnifera extract showed a concentration-dependent inhibition of CD44high/CD24low cells and it is anticipated that the extract will be effective in inhibition of cell proliferation in treated mice. These findings serve as preliminary data for further preclinical studies evaluating the effects of WS.
Grant support: Research supported by NIH-NCI-U54-118948 at Tuskegee University and the University of Alabama at Birmingham.
Citation Format: Kamel F. Khazal. In vivo and in vitro effect of Withania somnifera extract on the proliferation of side population (CD44HIGH /CD24LOW) cells sorted from MDA-MB-231 breast cancer cells. [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 5553. doi:10.1158/1538-7445.AM2015-5553
Abstract 5556: Enhancing response of Ganoderma lucidum (Reishi) and lapatinib in HER2+ inflammatory breast cancer cells
Authors: Feliz-Mosquea Yismeilin , Suarez-Arroyo Ivette , Loperena Yaliz , Cubano Luis A. , Martinez-Montemayor Michelle M. 
Published: August 2015

Abstract
Inflammatory Breast Cancer (IBC) is an aggressive and unique form of breast cancer that develops rapidly. IBC, like non-IBC breast cancers, is a heterogeneous disease and can occur as any of the six molecular breast cancer subtypes. However, they are most commonly either triple negative; that is presenting with an absence of estrogen receptor (ER-), progesterone receptor (PR-) and the epidermal growth factor receptor 2 (HER2-) or ER-, PR- and HER2+ overexpressed. There is no specific IBC treatment; thus, it seems possible to find a therapeutic for this deadly disease. Our published data demonstrates that Ganoderma lucidum (Reishi) inhibits the viability of the triple negative IBC SUM149 cell line, but not of MCF10A noncancerous mammary epithelial cells. Subsequently, in this study, we aimed to investigate Reishi effects in the viability and molecular signaling of the ER-, PR-, HER2+ IBC cell lines SUM190, KPL-4 and IBC-3. Furthermore, we studied the effects of Reishi on IBC cells when treated in complement with the HER2 Tyrosine Kinase Inhibitor, lapatinib. The hypothesis for this study is that Reishi inhibits cancer cell viability and sensitizes IBC cells to lapatinib therapy and downregulates key proteins overexpressed in IBC. Herein, SUM190, KPL-4 and IBC-3 cells were treated with increasing concentrations of lapatinib and/or Reishi for 24 or 72h. The combination of lapatinib plus Reishi reduced cell viability of KPL-4 cells to 80% when treated with a concentration of 0.25 mg/mL of Reishi for 72h. Additionally, our data shows a reduction in cell viability of 70% in SUM190 cells treated with lapatinib plus Reishi for 72h. Also, Reishi and lapatinib downregulate the expression HER2 in KPL-4 cell after 72h of treatment. Our results provide evidence that Reishi inhibits cancer cell viability, highlighting the potential of Reishi as a natural anti-IBC-therapeutic. This project was sponsored by NIH/NCI #1F31 CA174307 to ISA, Title V PPOHA US Department of Education #P031M105050 to UCC/LAC, NIH/RCMI #G12 MD007583 to UCC/MMM, NIH/INBRE #5P20 GM103475 to UPR/UCC/MMM, NIH/NIMHD U54 MD008149 UH/MMM.
Citation Format: Yismeilin Feliz-Mosquea, Ivette Suarez-Arroyo, Yaliz Loperena, Luis A. Cubano, Michelle M. Martinez-Montemayor. Enhancing response of Ganoderma lucidum (Reishi) and lapatinib in HER2+ inflammatory breast cancer cells. [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 5556. doi:10.1158/1538-7445.AM2015-5556
Abstract 5566: Carnosic acid induces apoptosis through inhibition of STAT3 signaling and production of ROS in human colon cancer HCT116 cells
Authors: Chae In Gyeong , Yu Mi-Hee , Park Ki-Woong , Chun Kyung-Soo 
Published: August 2015

Abstract
Carnosic acid (CA), the main antioxidant compound of Rosmarinus officinalis L., has been shown to display anticancer activity. However, the molecular mechanisms underlying the anticancer effects of CA remain poorly understood. This study revealed that treatment with CA significantly reduced the cell viability and induced apoptosis in HCT116 cells as evidenced by the induction of p53 and Bax, release of cytochrome c, cleavage of caspase-9, -7 and -3 and PARP and the inhibition of Bcl-2 and Bcl-xl expression. CA inhibited the constitutive phosphorylation, the DNA binding and the reporter gene activity of signal transducer and activator of transcription-3 (STAT3) in HCT116 cells by blocking the phosphorylation of upstream Janus-activated kinase-2 (JAK2) and Src kinases. Moreover, CA attenuated the expression of STAT3 target gene products, such as survivin, cylcin D1, D2, and D3. Since ROS is a universal entity mediating apoptosis, we examined whether CA induced apoptosis via ROS formation. Treatment with CA generated ROS and pretreatment with ROS scavenger N-acetyl cysteine (NAC) rescued cells from apoptosis by abrogating the inhibitory effect of CA on the activation of JAK2-STAT3 and Src-STAT3 signaling pathways and rescued cells from CA-induced apoptosis by blocking the induction of p53, and the cleavage of caspase-3 and PARP. In conclusion, CA induced apoptosis in HCT116 cells via generation of ROS, induction of p53, activation of caspases and inhibition of STAT3 signaling pathway.
Citation Format: In Gyeong Chae, Mi-Hee Yu, Ki-Woong Park, Kyung-Soo Chun. Carnosic acid induces apoptosis through inhibition of STAT3 signaling and production of ROS in human colon cancer HCT116 cells. [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 5566. doi:10.1158/1538-7445.AM2015-5566
Abstract 5567: Anti-angiogenic activity of Thio-Cl-IB-MECA, a novel A3 adenosine receptor agonist, by regulating of PI3K/AKT/mTOR and ERK signaling pathways in endothelial cells
Authors: Oh Jedo , Kim Gi Dae , Jeong Lak Shin , Lee Sang Kook 
Published: August 2015

Abstract
Angiogenesis is a complex process that involves sprouting of new capillaries from pre-existing blood vessels. Angiogenesis is also involved in many pathological conditions including tumor growth, diabetic retinopathy, psoriasis, rheumatoid arthritis, and atherosclerosis. In cancer, newly formed vessels not only promote tumor growth but also cause the tumor cells to become more malignant and metastatic. Therefore, angiogenesis is an attractive target for the development of a wide variety of therapies, including antitumor agents. A3 adenosine receptor (A3AR) agonists have exhibited anti-proliferative activity against cancer cells. However, anti-angiogenic effects of A3AR agonists in endothelial cells have not been investigated yet. In the present study, the potential anti-angiogenic activity and precise mechanism of action of the A3AR agonist thio-Cl-IB-MECA (TCIM) were investigated in cultured HUVECs and mouse embryonic stem cells/embryonic body (mES/EB) derived endothelial cells. TCIM inhibited migration and tube formation of endothelial cells and markedly decreased ex vivo microvessel sprouting in cultured mouse aortic rings. TCIM also suppressed the expression of the endothelial biomarker platelet endothelial cell adhesion molecule (PECAM) via regulation of PI3K/AKT/mTOR and ERK signaling in mES/EB-derived endothelial cells.
Citation Format: Jedo Oh, Gi Dae Kim, Lak Shin Jeong, Sang Kook Lee. Anti-angiogenic activity of Thio-Cl-IB-MECA, a novel A3 adenosine receptor agonist, by regulating of PI3K/AKT/mTOR and ERK signaling pathways in endothelial cells. [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 5567. doi:10.1158/1538-7445.AM2015-5567
Abstract 5569: p73 dinucleotide polymorphism genotyping of human cancer cell lines
Authors: Carastro L. Michael , Hampton Kaia K. , Cordova Estupinan Ricardo A. , Park Hyun Y. , Kim Dongwha , Park Jong Y. 
Published: August 2015

Abstract
The p73 gene is a member of the p53 tumor suppressor family. The p73 dinucleotide polymorphism (DNP) (rs1801173) is a G4C14-to-A4T14 linked pair of transitions located in exon 2 between the P1 and P2 gene promoters. The P1 and P2 p73 gene promoters are the transcription initiation sites for mRNAs encoding TAp73 and ΔNp73 isoforms, respectively. Recently, we reported the p73 DNP allele was associated with (1) decreased risk [OR = 0.55, 95%CI = 0.31-0.99] for aggressive prostate cancer (PCa) and (2) increased TAp73/ΔNp73 protein isoform ratios in ten human cancer cell lines. We hypothesize the presence of the p73 DNP allele causes altered p73 promoter usage resulting in increased TAp73/ΔNp73 protein isoform ratios, which could explain the observed decreased risk for PCa aggressiveness. Our ultimate goal is to assess the potential of p73 DNP as a biomarker for lower aggressive PCa risk. Therefore, our initial aim in this study was to determine the p73 DNP genotype in ten additional human cancer cell lines (DU 145, JEG-3, K-562, LNCaP, MDA-MB-231, MDA-MB-468, MRC-5, PC-3, SW48 and U-2OS) not yet characterized for p73 DNP status. We previously reported the p73 DNP genotype of three human cancer cell lines that we used as genotyping controls: Caco-2 (homozygous polymorphic), NCI-H1299 (homozygous wild type), and HepG2 (heterozygous). Cell lines were cultured and genomic DNA was isolated and quantitated. Cell line genomic DNA samples were used in TaqMan Real Time-PCR allelic discrimination assays to determine the p73 DNP genotypes. Our data conclusively determined that DU 145, JEG-3, K-562, LNCaP, MDA-MB-468, MRC-5, SW48 and U-2OS were p73 DNP homozygous wild type, while PC-3 and MDA-MB-231 werw p73 DNP heterozygous.
Cell Line p73 DNP GenotypesCELL LINE NAMEP73 DNP GENOTYPEDU145CCJEG-3CCK-562CCLNCaPCCMDA-MB-231CTMDA-MB-468CCMRC-5CCPC-3CTSW48CCU-2OSCC
Citation Format: L. Michael Carastro, Kaia K. Hampton, Ricardo A. Cordova Estupinan, Hyun Y. Park, Dongwha Kim, Jong Y. Park. p73 dinucleotide polymorphism genotyping of human cancer cell lines. [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 5569. doi:10.1158/1538-7445.AM2015-5569
Abstract 5577: Text-mining methods applied to clinical records support an association between androgen deprivation therapy and subsequent cardiometabolic disease
Authors: Nead Kevin T. , Gaskin Gregory L. , Chester Cariad , Shah Nigam H. , Leeper Nicholas J. 
Published: August 2015

Abstract
We conducted this study to examine the association of androgen deprivation therapy in the treatment of prostate cancer with future metabolic and cardiovascular disease.
Here we utilize electronic medical record data from 1.8 million subjects in the Stanford Translational Research Integrated Database Environment. Specifically, we extracted ICD-9 diagnostic codes, patient medication lists and data from clinical notes using a previously validated text-analytics pipeline. Through this approach, we identified a cohort of 4,578 individuals with prostate cancer containing data on all defined covariates including Gleason score, age, race and use of antiplatelet, anticoagulant, antihypertensive and lipid lowering agents. We used multivariable logistic regression techniques to examine the association of androgen deprivation therapy use with diabetes, peripheral arterial disease, and stroke.
Following prostate cancer diagnosis, there were 80 new diagnoses of diabetes, 39 new diagnoses of peripheral arterial disease and 72 new diagnoses of stroke with 409 individuals receiving androgen deprivation therapy. The use of androgen deprivation therapy to treat prostate cancer was associated with an increased risk of diabetes (odds ratio [OR] = 2.37; 95% confidence interval [CI] 1.40-4.03; P = 0.001), peripheral arterial disease (OR = 2.15; 95% CI 1.07-4.32; P = 0.032) and stroke (OR = 2.88; 95% CI 1.72-4.80; P&lt;0.001).
Here we further demonstrate the utility of clinical data obtained during routine care to investigate clinical hypotheses. Additionally, we add evidence to the growing body of literature linking the use of androgen deprivation therapy to future cardiovascular and metabolic disease.
Citation Format: Kevin T. Nead, Gregory L. Gaskin, Cariad Chester, Nigam H. Shah, Nicholas J. Leeper. Text-mining methods applied to clinical records support an association between androgen deprivation therapy and subsequent cardiometabolic disease. [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 5577. doi:10.1158/1538-7445.AM2015-5577
Abstract 5582: Survey of oral cancer screening participants reveals widespread misconceptions about oral cancer risk factors, independent of educational background
Authors: Chester Cariad , Sabile Jean , Cho Grace , Hu Annie , Hamaguchi Ryoko , Ellis Lauren , Erdman Jonathan S. , Praharaj David , Golla Abhinav , Sunwoo John 
Published: August 2015

Abstract
Introduction: To develop more effective strategies to screen for oral cancer, we surveyed participants in a free oral cancer-screening event held at Stanford University to assess knowledge and understanding of oral cancer risk factors and behaviors.
Method: The survey was administered by trained members of the oral cancer screening team in accordance with guidelines approved by the Stanford Research Compliance Office.
Results: Participants (n = 51) were racially diverse with varied educational levels: approximately 43% of participants had completed high school only or attended some college, and 57% of participants had obtained a bachelor’s, master’s, or doctoral degree. A majority of the participants (62%) reported an annual income below $50,000, and a minority of participants (35%) had active dental insurance. Most of the participants (84%) had never previously been screened for oral cancer. All participants, regardless of educational level, demonstrated limited knowledge of the risk factors that contribute to oral cancer. Approximately 50% of the lower-education cohort and 31% of the higher-education cohort incorrectly believed that dental fillings increase the risk of developing oral cancer. Only 23% and 34% of the lower- and higher-education cohorts, respectively, correctly identified heavy alcohol consumption as a risk factor for oral cancer. Encouragingly, 85% of all participants recognized that behavioral changes can decrease one's risk of developing cancer.
Conclusions: Knowledge of oral cancer risk factors was low in all participants despite the majority of responders having obtained post-secondary degrees. Our work highlights the need to expand the target audience of oral cancer educational efforts to include community members from all educational backgrounds.
Note: This abstract was not presented at the meeting.
Citation Format: Cariad Chester, Jean Sabile, Grace Cho, Annie Hu, Ryoko Hamaguchi, Lauren Ellis, Jonathan S. Erdman, David Praharaj, Abhinav Golla, John Sunwoo. Survey of oral cancer screening participants reveals widespread misconceptions about oral cancer risk factors, independent of educational background. [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 5582. doi:10.1158/1538-7445.AM2015-5582