tbuckley/cabot-search huggingface dataset:
Abstract 4010: Tonggyu-tang, a traditional Korean medicine, suppresses inflammation, potential implications in tumor microenvironment
Authors: Hyoin Kim, Seong-Gyu Ko, Yong Cheol Shin, Ji Hye Kim, Hye-Sook Seo, Tai Young Kim, Se Hyang Hong, Kangwook Lee, Jin Mo Ku, Myeong-Sun Kim, Yu-Jeong Choi, Soo-yeon Kang, Chunhoo Cheon, Youme Ko, Huang Ching Wen, Yui Sasaki, Sohyeon Kang
Journal: Cancer Research (2017)

Abstract The critical roles of inflammation in the development of cancer have long been appreciated. A growing body of evidence supports the notion that infiltrates of inflammatory cells into tumor microenvironment influence the tumor progression by providing bioactive molecules including pro-inflammatory cytokines. Importantly, the increased number of mast cells within tumor microenvironment has been associated with a poor survival in cancer patients. Moreover, keratinocyte inflammation is known to be crucial for skin tumor development. The use of natural products to reduce inflammation in tumor microenvironment is gaining an interest, because of their reduced toxicity toward normal cells. In this study, we tested the effects of Tonggyu-tang (TGT) which is composed of 14 different herbal extracts on the activity of mast cells. We found that TGT significantly reduced the expression and production of inflammatory cytokines such as IL-4, IL-6, IL-8, and TNF-α in PMA and ionomycin- stimulated HMC-1 (human mast cell line-1). In an attempt to determine molecular mechanism underlying the inhibitory effects of TGT on cytokine expression, we revealed that TGT suppressed MAPK signaling pathway including ERK, p38, and JNK as well as NF-κB pathway, which are known to regulate inflammatory cytokine expression. Similar results were obtained from the LPS-stimulated HaCaT cells, immortalized human keratinocytes. Taken together, our results demonstrate that TGT suppresses inflammation by inhibiting the expression of pro-inflammatory cytokine in both mast cells and keratinocytes, thereby potentially leading to inhibition of tumor progression. Citation Format: Hyoin Kim, Seong-Gyu Ko, Yong Cheol Shin, Ji Hye Kim, Hye-Sook Seo, Tai Young Kim, Se Hyang Hong, Kangwook Lee, Jin Mo Ku, Myeong-Sun Kim, Yu-Jeong Choi, Soo-yeon Kang, Chunhoo Cheon, Youme Ko, Huang Ching Wen, Yui Sasaki, Sohyeon Kang. Tonggyu-tang, a traditional Korean medicine, suppresses inflammation, potential implications in tumor microenvironment [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 4010. doi:10.1158/1538-7445.AM2017-4010
Abstract 5891: DCIS to invasive progression in breast cancer is delayed by restoring CCN5
Authors: Sandipto Sarkar, Arnab Ghosh, Gargi Maity, Snigdha Banerjee, Sushanta Banerjee
Journal: Cancer Research (2017)

Abstract Malignant progression of breast cancer from pre-invasive to invasive lesions remains a mechanistically unknown event and a major challenge in medical research. By revealing the mechanism of action, our new and substantially different approach aims to demonstrate that CCN5/WISP2 might play a role in negative regulation of progression of pre-invasive lesion ductal carcinoma in-situ (DCIS) to invasive carcinoma (IC). DCIS to IC transition results primarily from the loss of the myoepithelial cell (MEC) layer surrounding the breast ducts &amp; lobules and basement membrane (BM) degradation followed by invasion of cancer cells into the surrounding stromal tissue and vasculature. It has been recently discovered that CCN5, a matricellular protein, is highly expressed in DCIS patient specimens and facilitates regression of aggressive phenotypes. Our in-vitro studies with myoepithelial cell lines (MECs) indicate that CCN5 may prevent the DCIS to IC transition through the protection of the MEC layer. CCN5 performs it’s protective role by regulating sonic hedgehog (SHh) expression in MECs. It has been previously shown in separate studies that Neuropilin1 (Nrp1) positively regulates expression of SHh and Nrp1 is exclusively expressed in MEC layer in breast tissues. An extension of our studies indicate that CCN5 might regulate the integrity of the mammary ductal architecture by protecting the MEC layer through a novel Nrp1-SHh signaling axis. Collectively, our studies indicate that regulating CCN5 expression level in breast cancer tissues might help us controlling the rate of progression of the disease from DCIS to an invasive stage. Citation Format: Sandipto Sarkar, Arnab Ghosh, Gargi Maity, Snigdha Banerjee, Sushanta Banerjee. DCIS to invasive progression in breast cancer is delayed by restoring CCN5 [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 5891. doi:10.1158/1538-7445.AM2017-5891
Abstract 2788: High ALDH1, S phase fraction, p16INK4A in esophageal squamous cell carcinoma could predict response to neoadjuvant chemotherapy
Authors: Rajeev Kumar, R. Ravi Kannan, Akalesh Kumar Verma, Anuradha Talukdar, Monoj Kumar Deka, Ritesh Tapkire, Litika Vermani, Sankar Kumar Ghosh
Journal: Cancer Research (2017)

Abstract Background: The prevalence of locally advanced esophageal squamous cell carcinoma (ESCC) remains high despite technological advancements in its diagnosis. This leads to prolonged multimodality treatment often resulting in poor response eventually leading to poor prognosis. Currently, there are no biomarkers available to predict response to neoadjuvant chemotherpy. Aldehyde dehydrogenase 1 (ALDH1), human epidermal growth factor receptor-2 (HER2), p16INK4A, ploidy and S phase fraction are considered significant biomarkers in various solid malignancies. However, there is paucity of data on their clinical significance in ESCC. In the present study, we investigated their significance in predicting the response to neoadjuvant chemotherapy (NACT) in ESCC patients. Methods: Immunohistochemisty of ALDH1, HER2, p16INK4A and propidium iodide based cell cycle analysis through flow cytometer was performed in pre treatment biopsy sample collected from 108 ESCC patients who were presented at a comprehensive cancer centre in northeast India and all of them subsequently received neo adjuvant chemotherapy. Results: ALDH 1, HER2 and p16INK4A were found positive in 65.7%, 7.4% and 22% of pre treatment ESCC specimens respectively. ALDH1 expression correlates with poor response to neo adjuvant chemotherapy (P&amp;lt;0.001). A significant proportion of poor responders were found to be smokers (P=0.004). Poor responders also tends to correlate with increased mortality (P=0.009). HER2 couldn’t predict response to NACT. However, all HER2 positive cases were associated with high ALDH1 expression (P=0.034). 50% of those with pathologically complete response were p16 positive on the contrary only 15% non responders were positive for p16 (P&amp;lt;0.001). 84% of the ESCC patients reported aneuploid tumor status and responder's were found having high S phase fraction (P=0.041). Conclusion: High ALDH1 expression can predict poor response whereas high p16 and S phase fraction can indicate good response to neoadjuvant chemotherapy in ESCC patients. HER2 seems having no clinical significance in the response assessment of neo adjuvant chemotherapy in ESCC. Citation Format: Rajeev Kumar, R. Ravi Kannan, Akalesh Kumar Verma, Anuradha Talukdar, Monoj Kumar Deka, Ritesh Tapkire, Litika Vermani, Sankar Kumar Ghosh. High ALDH1, S phase fraction, p16INK4A in esophageal squamous cell carcinoma could predict response to neoadjuvant chemotherapy [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 2788. doi:10.1158/1538-7445.AM2017-2788
Abstract 17437: Hyperinsulinemia and Cardiovascular Disease in Japan and the United States
Authors: Hiroaki Ikezaki, Masumi Ai, Ernst J Schaefer, Seiko Otokozawa, Bela F Asztalos, Katsuyuki Nakajima, Yanhua Zhou, Ching-Ti Liu, Paul F Jacques, L Adrienne Cupples, Norihiro Furusyo
Journal: Circulation (2016)

Introduction: Age adjusted cardiovascular disease (CVD) prevalence rates are significantly lower in Japan than in the United States although the levels of lipids have become similar. Hypothesis: Le...
Abstract 2129: Assessing the efficacy of targeting mitochondrial respiration in delaying lung tumor growth by using subcutaneous xenografts in mouse models
Authors: Sarada Preeta Kalainayakan, Poorva Ghosh, Sanchareeka Dey, Li Zhang
Journal: Cancer Research (2017)

Abstract Previously, studies have focused mainly on the precept that tumors depend on glycolysis for energy and growth (the Warburg effect) and that the mitochondria are dysfunctional in cancer cells. However, there is mounting evidence that some cancer cells exhibit elevated mitochondrial respiration. Recent studies in our lab have demonstrated that Non-Small Cell Lung Cancer (NSCLC) cells exhibit intensified mitochondrial respiration and oxygen consumption. We further demonstrated that targeting increased mitochondrial respiration by a therapeutic agent effectively hampers proliferation of Non-Small cell lung cancer (NSCLC) cells in vitro. The purpose of the study is to determine to what extent mitochondrial respiration is affected by the therapeutic agent in vivo. In order to achieve this goal, NSCLC cells were transduced with lentiviral particles carrying luciferase sequence. NSCLC cells expressing luciferase cells were implanted on the right flank of 4-6 weeks old female NOD/SCID mice to generate subcutaneous xenografts. The therapeutic agent was administered intravenously. Tumor implantation and growth were monitored by bioluminescence imaging (BLI) using Perkin Elmer’s IVIS Lumina III Imager. On sacrificing the mice, the tumors were harvested, formalin fixed and paraffin embedded for Immunohistochemistry (IHC). Our BLI data suggest that there is a considerable reduction in radiance (total flux in photons per second) in the group of mice that were treated with therapeutic agent in comparison to control. Further, there is a significant reduction in tumor volume in mice that received treatment. Our IHC data suggest that there is a reduction in expression of a vital enzyme involved in heme synthesis and hemoproteins involved in mitochondrial respiration. Our BLI and IHC data suggest that the therapeutic agent affects mitochondrial respiration by affecting mitochondrial complexes in vivo. Additional experiments to corroborate the results are underway. Citation Format: Sarada Preeta Kalainayakan, Poorva Ghosh, Sanchareeka Dey, Li Zhang. Assessing the efficacy of targeting mitochondrial respiration in delaying lung tumor growth by using subcutaneous xenografts in mouse models [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 2129. doi:10.1158/1538-7445.AM2017-2129
Experimental Roentgen Injury. II. Changes Produced with Intermediate-Range Doses and a Comparison of the Relative Susceptibility of Different Kinds of Animals
Authors: Paul S. Henshaw
Journal: JNCI Journal of the National Cancer Institute (1944)

Journal Article Experimental Roentgen Injury. II. Changes Produced with Intermediate-Range Doses and a Comparison of the Relative Susceptibility of Different Kinds of Animals Get access Paul S. Henshaw Paul S. Henshaw senior radiobiologist National Cancer Institute, National Institute of Health, United States Public Health Service Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 4, Issue 5, April 1944, Pages 485–501, https://doi.org/10.1093/jnci/4.5.485 Published: 01 April 1944
Abstract 5471: LSD1 stimulates cell survival and epigenetic homeostasis via snail in hepatocellular carcinoma
Authors: Yong Hwa Jo, Minh Nam Nguyen, Tae Gyu Choi, Sung Soo Kim
Journal: Cancer Research (2017)

Abstract HCC is the fifth most common malignancy in the world. HCC generally arises in the context of chronic liver diseases, or other metabolic, dietary or toxic factors. Hypoxia is a critical microenvironment in hepatcarcinogenesis. It occurs in series of distinct steps that include tumor cell invasion and proliferation. The process of EMT required for liver cancer cell invasion is regulated by a family of E-box-binding transcription repressors, which include Snail and Slug. Protein N, the first discovered histone methylase, is an epigenetic enzyme playing important role in regulation of gene expression and function by removing mono- or dimethyl moieties from H3K4 and H3K9. However, the molecular mechanisms underlying these biological behaviors have not been completely elucidated. Here, we present the first evidence that expression of Protein N was transcriptionally induced by Hif1 under hypoxia condition. We also showed that the up-regulated Protein N enhanced HCC cell survival and sustained epigenetic homeostasis via activating Snail under hypoxic conditions in vitro/in vivo. Furthermore, we revealed that Protein N/Snail stimulated Hif1 expression by a positive feedback loop. Conclusively, we elicited that Protein N is an essential mediator in epigenetic aberrances of HCC (This work was supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (MEST) (NRF-2016R1D1A1B03933763)). Note: This abstract was not presented at the meeting. Citation Format: Yong Hwa Jo, Minh Nam Nguyen, Tae Gyu Choi, Sung Soo Kim. LSD1 stimulates cell survival and epigenetic homeostasis via snail in hepatocellular carcinoma [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 5471. doi:10.1158/1538-7445.AM2017-5471
Abstract 15086: Caveolin-1 Dependent APPL1 Nuclear Translocation as a Novel Mechanism Mediating Adiponectin Endothelial Protection in Diabetes
Authors: Yunhui Du, Yajing Wang, Wayne Lau, Theodore A Christopher, Bernard Lopez, Xinliang Ma
Journal: Circulation (2016)

Introduction: Adiponectin (APN) regulates multiple genes and exerts pleiotropic vascular protective effects. However, intracellular signaling mediating APN gene regulatory effect and vasculoprotect...
Abstract 5480: Peroxiredoxin 2 mediates the survival of ECM-detached ovarian cancer cells
Authors: Calli A. Davison-Versagli
Journal: Cancer Research (2017)

Abstract Non-tumorigenic epithelial cells require anchorage to the extracellular matrix (ECM) in order to survive; however, it has been recognized that metastatic cancer cells must have the ability to survive in anchorage independence. Approximately 70% of epithelial ovarian cancer (EOC) cases are diagnosed after EOC cells have already metastasized, making EOC more difficult to treat. EOC cells shed from the primary tumor and accumulate in ascites in the peritoneal cavity before attaching and forming secondary tumors throughout the peritoneal cavity. A better understanding of the molecular mechanisms involved in the survival of this non-adhesive subset of cells that survive in anchorage independence in the ascites could lead to the development of improved chemotherapeutics and thus resulting in better survival rates of EOC patients. Striking increases of reactive oxygen species (ROS) mediated by ECM-detachment has been shown to inhibit survival in non-tumorigenic mammary epithelial cells. Furthermore, previous publications from our laboratory suggest that the antioxidant enzymes catalase, superoxide dismutase 1 (SOD1), and superoxide dismutase 2 (SOD2) are critical for metabolic maintenance and survival of ECM-detached breast cancer cells; however, many other antioxidant enzymes and their role in the survival of ECM-detached ovarian cancer cells have yet to be unveiled. Here, we have found that the antioxidant enzyme, Peroxiredoxin 2, is important in the survival of ECM-detached ovarian cancer cells, and elimination of this enzyme in SKOV3 cells results in decreased ability to survive in anchorage independence. Thus, our data reveal that Peroxiredoxin 2 may be an attractive target for the design of chemotherapeutics aimed at eliminating metastatic ovarian cancer cells. Given these data, we are working to understand the role of other members of the Peroxiredoxin family, namely Peroxiredoxin 1, in the survival of ovarian cancer cells in anchorage independence. Citation Format: Calli A. Davison-Versagli. Peroxiredoxin 2 mediates the survival of ECM-detached ovarian cancer cells [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 5480. doi:10.1158/1538-7445.AM2017-5480
Survival of Head and Neck Cancer Cells Relies upon LZK Kinase-Mediated Stabilization of Mutant p53
Authors: Zoe C. Edwards, Eleanor W. Trotter, Pedro Torres-Ayuso, Phil Chapman, Henry M. Wood, Katherine Nyswaner, John Brognard
Journal: Cancer Research (2017)

Abstract Head and neck squamous cell carcinoma (HNSCC) includes epithelial cancers of the oral and nasal cavity, larynx, and pharynx and accounts for ∼350,000 deaths per year worldwide. Smoking-related HNSCC is associated with few targetable mutations but is defined by frequent copy-number alteration, the most common of which is gain at 3q. Critical 3q target genes have not been conclusively determined for HNSCC. Here, we present data indicating that MAP3K13 (encoding LZK) is an amplified driver gene in HNSCC. Copy-number gain at 3q resulted in increased MAP3K13 mRNA in HNSCC tumor samples and cell lines. Silencing LZK reduced cell viability and proliferation of HNSCC cells with 3q gain but not control cell lines. Inducible silencing of LZK caused near-complete loss of colony-forming ability in cells harboring 3q gain. These results were validated in vivo by evidence that LZK silencing was sufficient to reduce tumor growth in a xenograft model of HNSCC. Our results establish LZK as critical for maintaining expression of mutant stabilized p53. Cancer Res; 77(18); 4961–72. ©2017 AACR.
2017 National Standards for Diabetes Self-Management Education and Support
Authors: Joni Beck, Deborah A. Greenwood, Lori Blanton, Sandra T. Bollinger, Marcene K. Butcher, Jo Ellen Condon, Marjorie Cypress, Priscilla Faulkner, Amy Hess Fischl, Theresa Francis, Leslie E. Kolb, Jodi M. Lavin-Tompkins, Janice MacLeod, Melinda Maryniuk, Carolé Mensing, Eric A. Orzeck, David D. Pope, Jodi L. Pulizzi, Ardis A. Reed, Andrew S. Rhinehart, Linda Siminerio, Jing Wang
Journal: Diabetes Care (2017)

By the most recent estimates, 30.3 million people in the U.S. have diabetes. An estimated 23.1 million have been diagnosed with diabetes and 7.2 million are believed to be living with undiagnosed diabetes. At the same time, 84.1 million people are at increased risk for type 2 diabetes. Thus, more than 114 million Americans are at risk for developing the devastating complications of diabetes (1).

Diabetes self-management education and support (DSMES) is a critical element of care for all people with diabetes. DSMES is the ongoing process of facilitating the knowledge, skills, and ability necessary for diabetes self-care, as well as activities that assist a person in implementing and sustaining the behaviors needed to manage his or her condition on an ongoing basis, beyond or outside of formal self-management training. In previous National Standards for Diabetes Self-Management Education and Support (Standards), DSMS and DSME were defined separately, but these Standards aim to reflect the value of ongoing support and multiple services.

The Standards define timely, evidence-based, quality DSMES services that meet or exceed the Medicare diabetes self-management training (DSMT) regulations, however, these Standards do not guarantee reimbursement. These Standards provide evidence for all diabetes self-management education providers including those that do not plan to seek reimbursement for DSMES. The current Standards’ evidence clearly identifies the need to provide person-centered services that embrace the ever-increasing technological engagement platforms and systems. The hope is that payers will view these Standards as a tool for reviewing DSMES reimbursement requirements and consider change to align with the way their beneficiaries’ engagement preferences have evolved. Research confirms that less than 5% of Medicare beneficiaries utilize their DSMES benefits (2,3). Changes in reimbursement policies stand to increase DSMES access and utilization, which will result in positive impact to beneficiaries’ clinical outcomes, quality of …
Abstract 2846: Identify urinary biomarkers for colorectal carcinoma liver metastasis
Authors: Meng Cai, Yulin Sun, Jiajia Gao, Lina Zhao, Fang Liu, Wei Sun, Zhixiang Zhou, Xiaohang Zhao
Journal: Cancer Research (2017)

Abstract Colorectal cancer (CRC) is the third leading prevalent cause of death from cancer in adults, and more than one third of CRC patients are accompanied by liver metastasis. The disease begins as a benign adenomatous polyp, and it subsequently develops into an advanced adenoma and gradually progresses to an invasive cancer. The driving factors behind CRC comprise a series of successive accumulated gene mutations that follow the order “APC-KRAS-TP53-DCC”. Moreover, urine is an important display window for tumor-derived exosomes. Here, to explore the roles of TP53 in CRC and identify novel urinary biomarkers for colorectal cancer metastatic to the liver, a comprehensive proteomic analysis of exosomal proteins from HCT116 TP53-wild type (WT), TP53-knockout (KO) and constructed TP53 (R273H)-mutant (MT) cells, as well as urine samples from CRC patients with and without liver metastasis was performed using the isobaric tag for relative and absolute quantitation (iTRAQ)-2D-LC-MS/MS strategy. The exosomes from the MT and KO cells exhibited significantly reduced sizes compared with the WT cells. A total of 3437 protein groups with ≥2 matched peptides were identified. Specifically, hepatocyte growth factor-regulated tyrosine kinase substrate (HGS) was consistently down-regulated in the exosomes from the MT and KO cells. Functional studies demonstrated that low HGS levels were responsible for the decreased exosome size. TP53 regulated HGS expression and thus HGS-dependent exosome formation. Furthermore, the HGS expression was gradually increased concomitant with CRC carcinogenesis and was an independent poor prognostic factor. In addition, HGS was one of the differentially expressed urine proteins between CRC liver metastasis and healthy individuals. In conclusion, HGS mediates TP53-regulated exosome formation. HGS may serve as a novel histological and urinary prognostic biomarker and a candidate target for therapeutic interventions in CRC. Citation Format: Meng Cai, Yulin Sun, Jiajia Gao, Lina Zhao, Fang Liu, Wei Sun, Zhixiang Zhou, Xiaohang Zhao. Identify urinary biomarkers for colorectal carcinoma liver metastasis [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 2846. doi:10.1158/1538-7445.AM2017-2846