tbuckley/cabot-search huggingface dataset:
Abstract 131: Chemotherapeutic effects of naturally occurringcolossolactonesagainst solid tumor cells in-vitro
Authors: Mohammed A. Baghdadi, Fahad A. Al-Abbasi, Ali M. El-Halawany, Ahmed M. Al-Abd
Journal: Cancer Research (2017)

Abstract Colossolactones were isolated previously from the Vietnamese mushroom ganoderma colossum, such triterpenoids. The different colossolactone compounds (schisanalactonoe a, colossolactone I, ergosterol, colossolactone III, colossolactone II, colossolactone IV, colossolactone E) characterized by the presence of a six-membered lactone ring (ring D) with or without a seven-membered lactone rings (ring A) were isolated. In the current study, using DPPH free radical scavenging assay, all colossolactone compounds showed weak antioxidant activity with EC50’s of 99.46, 220.32, 219.65, 100.81, 238.54, 116.57 and 131.94 µM, respectively. Isolated compounds were examined for their potential anticancer activity against breast (MCF-7), cervix (HeLa), colorectal (HCT-116) and liver (HepG2) cancer cells. Cytotoxicity of the isolated compounds was assessed in the aforementioned cell lines using SRB assay after 72 h of exposure and fitted using Emax model. Amongst colossolactones, schisanalactonoe-A and colossolactone-IV showed the best cytotoxic profile in all cell lines under investigation with IC50’s ranged from 4.9 to 64.2 µM; and R-fraction less than 47.5%. Further mechanistic studies for the detailed mechanism of cytotoxicity of schisanalactonoe-A and colossolactone-IV are currently carried out. Citation Format: Mohammed A. Baghdadi, Fahad A. Al-Abbasi, Ali M. El-Halawany, Ahmed M. Al-Abd. Chemotherapeutic effects of naturally occurring colossolactones against solid tumor cells in-vitro [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 131. doi:10.1158/1538-7445.AM2017-131
Abstract 2322: Antitumor activity of spicatoside A, a steroidal saponin, via induction of switch from autophagy to apoptotic cell death
Authors: Won Kyung Kim, Yuna Pyee, Hyen Joo Park, Ji-Young Hong, Sang Kook Lee
Journal: Cancer Research (2017)

Abstract The antitumor activity of spicatoside A (SA), a steroidal saponin isolated from the tuber of Liriope platyphylla (Liliaceae), and its underlying mechanisms were investigated in HCT116 human colorectal cancer cells. SA induced autophagy and apoptotic cell death and inhibited tumor growth in a nude mouse xenograft model implanted with HCT116 cells. Treatment with SA for 24 h enhanced the formation of acidic vesicular organelles in the cytoplasm, indicating the induction of the onset of autophagy. This event was associated with the regulation of autophagic markers including microtubule-associated protein 1 light chain 3 (LC3)-II, p62, beclin 1, lysosomal-associated membrane protein 1, and cathepsin D by inhibiting the PI3K/Akt/mTOR signaling pathway, regulating mitogen-activated protein kinase signaling, and increasing p53 levels. However, a prolonged exposure to SA resulted in apoptosis characterized by the accumulation of a sub-G1 cell population and an annexin V/propidium iodide-positive cell population. Apoptosis induced by SA was associated with the regulation of apoptotic proteins including Bcl-2, Bax, and Bid, the release of cytochrome c into the cytosol, and the accumulation of cleaved poly ADP-ribose polymerase (PARP). Further study revealed that cleavage of beclin 1 by caspase-8 plays a critical role in the SA-mediated switch from autophagy to apoptosis. Taken together, these findings highlight the significance of SA in the modulation of crosstalk between autophagy and apoptosis, as well as the potential use of SA as a novel candidate in the treatment of human colorectal cancer cells. Acknowledgement: This work was supported by a National Research Foundation of Korea (NRF) grant funded by the Korean Government (MEST) (No. 2009-0083533) Citation Format: Won Kyung Kim, Yuna Pyee, Hyen Joo Park, Ji-Young Hong, Sang Kook Lee. Antitumor activity of spicatoside A, a steroidal saponin, via induction of switch from autophagy to apoptotic cell death [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 2322. doi:10.1158/1538-7445.AM2017-2322
Resection plane-dependent error in computed tomography volumetry of the right hepatic lobe in living liver donors
Authors: Heon-Ju Kwon, Kyoung Won Kim, Bohyun Kim, So Yeon Kim, Chul Seung Lee, Jeongjin Lee, Gi Won Song, Sung Gyu Lee
Journal: Clinical and Molecular Hepatology (2017)

See the commentary-article "Clinical implication of hepatic volumetry for living donor liver transplantation" on page 51.
Time to Diagnostic Testing After a Positive Colorectal Cancer Screening Test—Reply
Authors: Carolyn M. Rutter, John M. Inadomi
Journal: JAMA (2017)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Abstract 4783: Regulation of GBM stemness and mesenchymal transition
Authors: Kin-Hoe Chow, Hee Jung Park, Joshy George, Yuanxin Chen, Andrew Gallup, Wen Jiang, Betty Y. Kim, Kyuson Yun
Journal: Cancer Research (2017)

Abstract While growing evidence suggests that tumor microenvironment can modulate stemness and the mesenchymal phenotype, little is known about how these cell states are coordinately regulated. We report that S100A4 controls both stemness and mesenchymal transition in GBM cells. In a spontaneous mouse glioma model and in primary human GBM tumorspheres, S100A4 expression is enriched in tumor-initiating cells and is required for self-renewal and tumor growth in vivo. In addition, greater than 80 percent of S100A4+ cells are associated with the tumor vasculature, a known niche for glioma stem cells, and S100A4 promotes pro-angiogenic factor expression. Interestingly, acidosis induces expression of S100A4 and the EMT regulators SNAIL1/2 and acidosis-induced EMT regulator expression requires S100A4 function. Importantly, S100A4 functions as a molecular switch between the proneural and mesenchymal states in GBM as S100A4 knockdown results in down-regulation of the mesenchymal signature genes, including the “master transcriptional regulators of mesenchymal transition”, and concurrent up-regulation of proneural signature genes. Together, these results indicate that S100A4 sits in a critical node in the molecular network that controls both glioma stem cells and the mesenchymal phenotype. Citation Format: Kin-Hoe Chow, Hee Jung Park, Joshy George, Yuanxin Chen, Andrew Gallup, Wen Jiang, Betty Y. Kim, Kyuson Yun. Regulation of GBM stemness and mesenchymal transition [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 4783. doi:10.1158/1538-7445.AM2017-4783
The Benefit of Early Preventive Dental Care for Children—Reply
Authors: Justin Blackburn, Michael A. Morrisey, Bisakha Sen
Journal: JAMA Pediatrics (2017)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Pediatrics HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Pediatrics journal
Abstract 2286: Atopic allergic conditions and risk of pancreatic cancer: the Multiethnic Cohort
Authors: Brian Z. Huang, Loic Le Marchand, Christopher A. Haiman, Kristine Monroe, Lynne Wilkens, Zuo-Feng Zhang, Veronica Wendy Setiawan
Journal: Cancer Research (2017)

Abstract Background: Previous studies, mostly case-control studies, have suggested that atopic allergic conditions (AACs) are associated with a decreased risk of pancreatic cancer. Scarce data, however, are available from prospective, US multiethnic populations. In this largest prospective study to date, we investigated the association between AACs (asthma, hay fever, or allergy) and risk of developing pancreatic cancer in the US Multiethnic Cohort Study (MEC). Methods: AACs were assessed via a baseline questionnaire when participants joined the MEC in 1993-1996. Hazard ratios (HRs) and 95% confidence intervals (CIs) for pancreatic cancer incidence by AACs status were calculated using Cox regression, adjusting for age, sex, race/ethnicity, education, smoking status, family history of pancreatic cancer, body mass index, diabetes, and alcohol intake. Results: During an average of 16.2-year follow-up, 1,455 incident cases of pancreatic cancer were identified among 187,226 white, African-American, Native Hawaiian, Japanese-American, and Latino men and women. AACs were not associated with pancreatic cancer incidence (HR=1.00; 95% CI: 0.88, 1.12). The null association was observed in men and women and across racial/ethnic groups, smoking status, BMI groups, diabetes status, and family history of pancreatic cancer. Conclusions: Based on these results, AACs is unlikely to be associated with risk of pancreatic cancer. Citation Format: Brian Z. Huang, Loic Le Marchand, Christopher A. Haiman, Kristine Monroe, Lynne Wilkens, Zuo-Feng Zhang, Veronica Wendy Setiawan. Atopic allergic conditions and risk of pancreatic cancer: the Multiethnic Cohort [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 2286. doi:10.1158/1538-7445.AM2017-2286
Abstract 2665: Green tea catechin, EGCG, enhances antitumor immunity by down-regulation of PD-L1 expression in non-small human lung cancer cell lines
Authors: Anchalee Rawangkan, Keisuke Iida, Ryo Sakai, Hirota Fujiki, Masami Suganuma
Journal: Cancer Research (2017)

Abstract (-)-Epigallocatechin gallate (EGCG) is now widely accepted as a non-toxic, effective cancer preventive compound. EGCG also acts as a synergist with anti-cancer drugs for cancer treatment. Considering the wide beneficial effects of EGCG, we think EGCG might have antitumor immunity. Programmed death-ligand 1 (PD-L1) expression on tumor cells is involved in PD-L1/PD-1 pathway. PD-L1 protein levels varied among 6 non-small human lung cancer cell lines (NSCLCs): LC-AI and Lu99 cell lines showed the highest PD-L1 expression, A549 and H322 cell lines were medium, and H1703 and H1299 were very low, independent on cancer cell lines. Since PD-L1 expression is induced by various cytokines and growth factors, we studied the effects of IFN-γ and EGF on cell-surface PD-L1 level using flow cytometry, and its gene expression using RT-PCR. Treatment with IFN-γ dose-dependently stimulated PD-L1 expression in both A549 and H1299 cells, and not effective on Lu99 cells, whereas treatment with EGF stimulated PD-L1 in Lu99 cells only. Pretreatment with EGCG for 3 h, dose-dependently inhibited INF-γ-induced PD-L1 gene expression and protein level on cell-surface in both A549 and H1299. It is important to note that EGCG also inhibited phosphorylation of STAT1. In addition, EGCG inhibited EGF-induced PD-L1 gene expression and protein level in Lu99 cells via inhibition of phosphorylation of Akt. In order to study the effects of EGCG in between rodent carcinogenesis experiment and antitumor immunity, green tea extract (GTE) was given to NNK-induced lung tumors in A/J mice, which showed significant reduction of PD-L1 protein level, determined by immunohistochemical analysis using anti-PD-L1 antibody. Furthermore, the group treated with NNK + GTE significantly showed reduced number of tumors per mouse from 3.2 to 2.2, and decreased tumor size. Treatment with Wortmannin, a PI3K inhibitor, as a control, did not inhibit PD-L1 expression in A549 and H1299 cells. The results strongly suggest that EGCG enhances antitumor immunity via inhibition of PD-L1 expression in cancer cells, resulting in significant cancer preventive activity. Citation Format: Anchalee Rawangkan, Keisuke Iida, Ryo Sakai, Hirota Fujiki, Masami Suganuma. Green tea catechin, EGCG, enhances antitumor immunity by down-regulation of PD-L1 expression in non-small human lung cancer cell lines [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 2665. doi:10.1158/1538-7445.AM2017-2665
Abstract 5281: Komen Tissue Bank donors: Genetically determined ethnicity and race
Authors: Julia R. McCarty, Guanlong Jiang, Mariah L. Johnson, Teresa Mahin, Nicholas Scherer, Jonathon Dunn, Anna Maria Storniolo, Natascia Marino
Journal: Cancer Research (2017)

Abstract Background: Several evidences indicate that different racial and ethnic backgrounds affect the incidence and severity of diseases such as breast cancer and diabetes, and the response to therapy. For example White and African American women are more likely to develop breast cancer than Hispanic and Asian women. Moreover, African American women are more likely to develop more aggressive (Triple Negative Breast Cancer), more advanced-stage breast cancer at a young age. Therefore, given the health disparity and with the advance of personalized medicine, it is becoming critical to address population stratification. The Komen Tissue Bank at IU Simon Cancer Center (KTB), the only biobank of normal breast tissue from healthy women, is employing a more accurate approach to detect population stratification through the use of Ancestry Informative Markers (AIMs). Methodology: A total of 2,973 DNA samples were obtained from the KTB. Genotyping was performed using the KASP technology (LGC Genomics) and a 41-SNP panel (labeled 41-AIM panel) selected from Nievergelt et al, 2013. Genotype analysis using the 41-AIM panel along with a Bayesian clustering method (STRUCTURE) was able to discern continental origins including European/ Middle East (Caucasian), East Asia, Central/South Asia, Africa, Americas, and Oceania. A reference set was obtained from the HeatMap. The results were compared with the self-reported data. Results/Conclusion: Our genetic ancestry analysis indicates that out of 2,973 KTB tissue donors, 2,132 are primarily Caucasian, 532 African, 234 of Asian, 72 Latino, 3 Oceanic origins. High mixture of racial markers was observed in several samples. Moreover, when we compare these findings with the self-reported data we find a 10.9% of discrepancies indicating the imprecision of the self-reported information. The implementation of the genetic ancestry data into the KTB creates the potential for a more accurate study of health disparities. Citation Format: Julia R. McCarty, Guanlong Jiang, Mariah L. Johnson, Teresa Mahin, Nicholas Scherer, Jonathon Dunn, Anna Maria Storniolo, Natascia Marino. Komen Tissue Bank donors: Genetically determined ethnicity and race [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 5281. doi:10.1158/1538-7445.AM2017-5281
Abstract 2229: Prevention by tolfenamic acid and characterization of the molecular targets in Pirc and FAP colorectal adenomas
Authors: Furkan U. Ertem, Wenqian Zhang, Kyle Chang, Wan-Mohaiza Dashwood, Praveen Rajendran, Deqiang Sun, Ala Abudayyeh, Maen Abdulrahim, Eduardo Vilar, Roderick H. Dashwood
Journal: Cancer Research (2017)

Abstract A critical need exists in sporadic and high-risk colorectal cancer patients for endoscopic screening combined with safe and effective preventive agents. To prioritize molecular targets for prevention studies in vivo, RNA-seq analyses were conducted on colorectal adenomas from familial adenomatous polyposis (FAP) patients, and from the Apc-mutant polyposis in rat colon (Pirc) model. Using a new murine endoscopic polypectomy methodology (F.U. Ertem et al., Gastrointest Endosc 2016;83:1272-6), we evaluated agents that might substitute for the current standard of care, Sulindac, and identified tolfenamic acid (TA) as a promising candidate for further investigation. At clinically-relevant doses in the Pirc model, TA suppressed tumorigenesis significantly both in the small intestine and in the colon. Inhibition by TA of colonic crypt cell proliferation, and the concomitant activation of apoptosis, coincided with reduced expression in target tissues of β-catenin, cyclin D1, Survivin and matrix metalloproteinase 7. Based on the oncogene candidates defined by RNA-seq analysis, endoscopic tracking revealed the time-course of tumor suppression by TA, and the temporal changes in S100a9, Nppb, Aldh1a3 and Mmp7, highlighting their value as potential early biomarkers for prevention in the clinical setting. As an “old drug” repurposed from migraine, TA appears to offer an exciting new therapeutic avenue in FAP and other high-risk colorectal cancer patient populations. This work was supported in part by NIH grants CA090890, CA122959, ES00210, ES023512, the John S. Dunn Foundation, and a Chancellor’s Research Initiative. 1 Citation Format: Furkan U. Ertem, Wenqian Zhang, Kyle Chang, Wan-Mohaiza Dashwood, Praveen Rajendran, Deqiang Sun, Ala Abudayyeh, Maen Abdulrahim, Eduardo Vilar, Roderick H. Dashwood. Prevention by tolfenamic acid and characterization of the molecular targets in Pirc and FAP colorectal adenomas [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 2229. doi:10.1158/1538-7445.AM2017-2229
Abstract 5343: The HIV shell protein Gp120 stimulates U87 glioma cell proliferation through the activation of glycolysis
Authors: Gabriel Valentin-Guillama, Sheila Lopez, Jose Perez, Luis Cubano, Natalia Chorna, Jeffrey Harrison, Nawal Boukli, Lilia Kucheryavykh
Journal: Cancer Research (2017)

Abstract Patients infected with human immunodeficiency virus (HIV) are more prone to develop cancers, including glioblastomas (GBM). The median survival of GBM patients with HIV is significantly shorter compared to HIV-negative GBM patients, despite the fact that they receive the same treatments. This indicates that HIV infection is associated with more aggressive tumor behavior and with treatment resistance. Taking into account that HIV itself is not found in GBM specimens, the nature of the GBM-HIV association remains poorly understood and the underlying molecular mechanism is still unknown. Here we study the effect of Gp120, a glycoprotein found in the HIV shell, on GBM cell growth and chemotherapeutic resistance. U87 glioma cells were used in this study. Flow cytometry analyses based on 7-aminoactinomycin D staining and viability assays were used for identification of cell cycle, proliferation rates, and resistance to temozolomide (TMZ). Combined proteomics, metabolomics, and western blot approaches together with colorimetric pyruvate kinase activity assays were used for evaluation of metabolic pathways. U87 cells treated with Gp120 (200ng/ml) for 10 days showed higher proliferation rates and increased cell survival in response to treatment with TMZ (100µM) compared to un-treated cells. Quantitative proteomics studies using isobaric tags and western blot analysis identified expression up-regulation of several glycolytic enzymes, including enolase 2, pyruvate kinase, hexokinase, and glyceraldehyde 3-phosphate dehydrogenase in Gp120 treated U87 cells. Additionally, metabolite analysis revealed an increase of pyruvate, amino acid and lipid synthesis, together with reduction of protein degradation, in response to treatment with Gp120. In summary, we demonstrated that Gp120 promoted proliferation and resistance to TMZ in U87 cells through the activation of glycolysis, resulting in increased protein and lipid synthesis This research was made possible by NIH grant numbers: 1SC2GM102040, R25GM110513, INBRE-PR NIH Grant 8P20GM103475, the UCC RCMI Biomedical Proteomics Facility grant G12MD007583 and US Department of Education Grant number P031S130068. Citation Format: Gabriel Valentin-Guillama, Sheila Lopez, Jose Perez, Luis Cubano, Natalia Chorna, Jeffrey Harrison, Nawal Boukli, Lilia Kucheryavykh. The HIV shell protein Gp120 stimulates U87 glioma cell proliferation through the activation of glycolysis [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 5343. doi:10.1158/1538-7445.AM2017-5343