tbuckley/cabot-search huggingface dataset:
VEGF Upregulates Mcl-1 Expression and Protects Multiple Myeloma Cells Against Starvation Induced-Apoptosis.
Authors: Steven Le Gouill, Klaus Podar, Martine Amiot, Teru Hideshima, Dharminder Chauhan, Kenji Ishitsuka, Shaji Kumar, Noopur Raje, Paul Richardson, Jean-Luc Harousseau, Kenneth Anderson
Journal: Blood (2004)
Abstract 1565: Magnetic bead-based serum peptidome profiling for identifying potential biomarkers in esophageal squamous cell carcinoma
Authors: Kun Jia, Wei Li, Feng Wang, Fang Liu, Xiaofei Liu, Yuanyuan Qiao, Yang Xu, Lanping Zhou, Yulin Sun, Qingwei Ma, Xiaohang Zhao
Journal: Cancer Research (2015)

Abstract Esophageal squamous cell carcinoma (ESCC) is one of the most common malignant neoplasms worldwide, especially in China. Patients are often diagnosed at advanced stages with poor prognosis due to the absence of obvious early symptoms. Therefore, there is an urgent need to develop novel serological biomarkers for ESCC. Here, we performed a two-stage serum peptide profiling in 477 unique samples using weak cationic exchange magnetic beads coupled with matrix-assisted laser desorption/ionization time-of-flight mass spectrometry. The three significantly differentially expressed peaks were used to establish a genetic algorithm model for ESCC. The sensitivity and specificity were 97% and 95.92% in the training set, and 97.03% and 100% in the validation set, respectively. It was significantly better than the other well studied serum proteins such as squamous cell carcinoma antigen (SCC-Ag) and cytokeratin 19 fragment 21-1 (Cyfra 21-1). Notably, the diagnostic capability of this model was superior for early stage ESCC with a sensitivity of 96.94% and a specificity of 100%. Furthermore, the three diagnostic peptides were identified as fragments of alpha-2-HS-glycoprotein, thrombospondin-1, and fibrinogen alpha, respectively. The immunohistochemical staining assay showed that TSP1 was significantly overexpressed in tumor tissues and associated with lymph node metastasis and poor prognosis. Overall, we constructed a novel diagnostic model which will benefit the screening, early detection and diagnosis of ESCC. And the identified proteins and their derivative peptides will deepen our understanding of tumorigenesis and serve as potential serological biomarkers for ESCC. Note: This abstract was not presented at the meeting. Citation Format: Kun Jia, Wei Li, Feng Wang, Fang Liu, Xiaofei Liu, Yuanyuan Qiao, Yang Xu, Lanping Zhou, Yulin Sun, Qingwei Ma, Xiaohang Zhao. Magnetic bead-based serum peptidome profiling for identifying potential biomarkers in esophageal squamous cell carcinoma. [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 1565. doi:10.1158/1538-7445.AM2015-1565
IL7Rα Signaling Prevents Premature Expression of AID In Human Pre-B Cells: Implications for Clonal Evolution of Childhood Leukemia
Authors: Srividya Swaminathan, Lars Klemm, Soo-mi Kweon, Anthony Ford, Klaus Schwarz, Rafael Casellas, Lothar Hennighausen, David G. Schatz, Michael R. Lieber, Mel F. Greaves, Markus Muschen
Journal: Blood (2010)
High-Dose Melphalan and Autologous Stem Cell Transplantation in Unusual Non-Amyloid Light Chain Deposition Disorders.
Authors: Karin I. Weichman, David C. Seldin, Karen Quillen, Michael Rosenzweig, Laura M. Dember, Martha Skinner, Daniel G. Wright, Vaishali Sanchorawala
Journal: Blood (2005)
The Democratization of Medical Research and Education Through Social Media
Authors: C. Michael Gibson
Journal: JAMA Cardiology (2016)

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 Cardiology 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 Cardiology journal
Abstract 2909: LC3 protein expression associates with UV exposure in melanoma histopathology
Authors: Kirsten A. M. White, Salina Torres, Todd A. Thompson, Chien-An A. Hu, Orrin Myers, Marianne Berwick
Journal: Cancer Research (2015)

Abstract The 5-year survival rate for stage IV melanoma is estimated to remain unchanged at only 15%, even with new therapies. One emerging hallmark of cancer is the reprogramming of energy metabolism including the role of autophagy. In cancer, autophagy appears to be an important energy source for nutrient-depleted tumors. Ultraviolet-radiation (UVR) exposure is an established risk factor for melanoma and increases autophagic flux. We hypothesize that UV exposure is independently associated with both levels of autophagy and melanoma survival. To address this hypothesis, we are investigating the association between UVR exposure, autophagy, and development of melanoma. Basal levels of autophagy appear to vary by tumor stage, and higher levels of autophagy are associated with poor clinical prognosis. Melanoma cells contain high levels of autophagosomes, a cellular structure associated with autophagy, as measured by the proxy marker LC3. Also, the expression of the autophagy marker Beclin 1 has been associated with increased risk of early death from melanoma. These findings suggest that autophagy provides metabolic support for tumors as it localizes to hypoxic tumor areas, supports tumor cell survival, and is activated in response to stress. Autophagy can act as a cytoprotective mechanism against UV-induced apoptosis. We have shown that rates of autophagy vary by oncogene status. Autophagy was evaluated in formalin-fixed, paraffin embedded melanoma and normal tissue sections, by staining for LC3 and Beclin 1 using IHC. These markers of autophagy, along with clinical tumor characteristics, were correlated with extensive questionnaire data on UV exposure from the same patients to evaluate the impact of estimated lifetime sun exposure and sunburns on survival. A trend in the expression of Beclin1 was not observed; however, LC3 expression was increased in melanoma sections compared to normal. Our results provide enticing support that lifetime UVR exposure is associated with autophagy protein expression in melanoma. Citation Format: Kirsten A. M. White, Salina Torres, Todd A. Thompson, Chien-An A. Hu, Orrin Myers, Marianne Berwick. LC3 protein expression associates with UV exposure in melanoma histopathology. [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 2909. doi:10.1158/1538-7445.AM2015-2909
Abstract 718: The effects of trastuzumab, paclitaxel, and carboplatin on HER2-positive cancer stem cells that are isolated from primary breast cancer cultures: a preliminary report
Authors: Mehmet Artac, Gozde Kayadibi, Ayca Ceylan, Meltem Demirel Kars, Hasibe Artac, Murat Cakır, Cem Boruban, Ahmet Tekin, Lema Tavlı, Adil Kartal
Journal: Cancer Research (2015)

Abstract Introduction: It is generally accepted that trastuzumab has only effective in HER2+ breast cancer patients who have HER2 gene amplification or HER2 over expression. On the other hand, trastuzumab resistance is a problem in HER2+ patients. Our aim is to investigate the effects of trastuzumab, paclitaxel and carboplatin on cancer stem cells which is isolated from primary breast cancer cultures. Methods: Tumor tissue was obtained in the routine surgery of a breast cancer patient who was HER2+ by immunohistochemistry. Primary breast cancer culture were established. CD44+CD24- and ALDH+ breast cancer stem cells were sorted by flowcytometry from these culture. HER2 receptor status of the sorted cells was also determined by flowcytometry. HER2+ and HER2- breast cancer stem cells were treated with trastuzumab, paclitaxel and carboplatin, and combination of these drugs by checker board microplate method for 96 h. For all of these breast cancer stem cell subgroups, the responses to the drugs were determined. Results: Breast cancer stem cells were isolated from a HER2+ breast cancer patient. The cell sorting analysis results demonstrates that 43% of the population is CD44+CD24- and 22% of the population is ALDH+. CD44+CD24- breast cancer stem cell subpopulation contains 84% HER2+ and 16% HER2- cells. Carboplatin has the highest antiproliferative effect on cancer stem cells among the three drugs which means carboplatin application resulted in the lowest IC50 values in all subgroups (IC50: 0.26 μM- 0.41 μM). HER2- cancer stem cells are more resistant to the drugs (1.5- 2 fold resistance) than HER2+ subcultures. Although combination of drugs exerted synergistic effect on the subcultures, ‘breast cancer stem cells’ were found to be more resistant to the combination therapy by exhibiting higher proliferation in drug combinations. Conclusions: HER2- cancer stem cells may be one of reason for trastuzumab resistance in HER2+ breast cancer patients. The result of this experimental study may be used to suggest new treatment strategies in HER2+ breast cancer patients. Citation Format: Mehmet Artac, Gozde Kayadibi, Ayca Ceylan, Meltem Demirel Kars, Hasibe Artac, Murat Cakır, Cem Boruban, Ahmet Tekin, Lema Tavlı, Adil Kartal. The effects of trastuzumab, paclitaxel, and carboplatin on HER2-positive cancer stem cells that are isolated from primary breast cancer cultures: a preliminary report. [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 718. doi:10.1158/1538-7445.AM2015-718
Abstract 3265: Thrombopoietin and megakaryocytes in breast cancer metastasis to bone
Authors: Walter Jackson, Andrea M. Mastro, Donna M. Sosnoski
Journal: Cancer Research (2015)

Abstract Bone is one of the preferred sites for breast cancer cells to metastases. Once patients are diagnosed with skeletal metastases, the relative five-year survival rate falls from 90% to less than16%. Thrombocytosis is a sign of poor prognosis for survival, and thromboembolisms are one of the leading causes of death in all cancers patients. These conditions are due to high numbers and/or high platelet activity. Megakaryocytes (MKs) are responsible for platelet production, but also play a role in bone metabolism and skeletal homeostasis. We had determined in two mouse models of experimental metastasis (MDA-MB-231 in athymic mice, and 4T1.2 in Balb/c mice), that bone metastasis was associated with increased numbers of MKs. Under normal conditions MKs represent less than 1% of the total bone marrow cell population, but after analysis of the femurs of the mice with metastasis, we found at least a two-fold increase in the numbers of MKs present in the bone marrow in the MDA-MB-231mice. The Balb/c mice injected in the mammary glands with mouse 4T1.2 cells showed a four-fold increase in MKs in the spleen (extrameduallary hematopoiesis). Therefore we hypothesized that increased megakaryocytosis was linked to metastasis, and that decreasing the number of MKs would decrease metastasis. We transferred a thrombopoietin (TPO) expression deletion mutation to a Balb/c background and inoculated the mice with 4T1.2 cells. These TPO -/- mice showed approximately a 90% decrease in bone marrow MKs compared to the wild type mice. The numbers of blood platelets was also decreased by 90%. We tested our hypothesis by inoculation of 4T1.2LUC cells into the mammary gland, and then followed the course of the cancer and metastasis by luciferase imaging. Contrary to our hypothesis the TPO -/- mice developed metastasis to the bone more rapidly than the heterozygotes or wild type mice. Literature suggests that platelets interact with tumor cells to contribute to hematogenous metastasis and angiogenesis. In the TPO-/- mice with very few platelets, metastasis was more aggressive and developed more rapidly than in the wild type or the heterozygote mice. The next step will be to separate the role of the megakaryocytes from the platelets. This work was sponsored by the U.S. Army Medical Research and Materiel W81XWH-10-1-0253 Citation Format: Walter Jackson, Andrea M. Mastro, Donna M. Sosnoski. Thrombopoietin and megakaryocytes in breast cancer metastasis to bone. [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 3265. doi:10.1158/1538-7445.AM2015-3265
571. Precise Control of CRISPR-Cas9 Mediated Gene Editing for Correcting Mutation of Duchenne Muscular Dystrophy in iPS Cells
Authors: Hongmei L. Li, Norko Sasakawa, Kentaro Ishida, Peter Gee, Akitsu Hotta
Journal: Molecular Therapy (2015)

Duchenne Muscular Dystrophy (DMD) is one of the most common and severe inherited neuromuscular disease caused by the loss-of-function mutations in Dystrophin gene on X chromosome. Currently, no effective treatment available for DMD, including gene augmentation therapy, since large size of the Dystrophin gene hamper the delivery by viral vectors. Exon skipping to modulate mRNA splicing patterns using antisense oligonucleotide is a promising approach currently investigated in clinical trials, however, the effect of antisense oligos is transient. Recent progress on targeted gene editing by engineered nucleases, such as TALENs or CRISPR/Cas9, have evolutionally broaden our ability to precisely modify the genomic sequence at desired locus, including genetic correction of Dystrophin gene. At the same time, however, undesired mutagenesis at the off-target loci with a few base-pair mismatches is a big concern. To this end, we previously developed a method to identify "unique sequence" in the human genome by using a database of short and unique k-mer sequences [Li HL et al., Stem Cell Reports, 4(1):143-54, 2015]. Our "uniqueness" data is useful to design a target site for engineered nucleases with high sequence specificity and minimum number of putative off-target sites, and the data is publically available at https://apps.cira.kyoto-u.ac.jp/igeats/. Moreover, to precisely control the genomic cleavage activity of CRISPR-Cas9, we constructed doxycycline inducible expression vector and Cas9 protein fused a nuclear receptor to mediate nuclear shuttling upon addition of receptor substrate. We show that both transcriptional and posttranscriptional regulations of CRISPR-Cas9 protein are effective to modulate DNA cleavage activity. To test the effectiveness of CRISPR system to correct disease mutation, we took advantages of patient-derived induced pluripotent stem cells (iPSCs) as a platform for testing various gene correction approaches. As a disease modeling for DMD gene thrapy, we derived integration-free iPS cell lines from a DMD patient who lacks the exon 44 in the Dystrophin gene, which is one of the most comon deletions of single exon. We will evaluate the dual-controlable Cas9 approache in patient-derived iPSCs, since gene-corrected iPSCs hold a promise to serve as a cell source for future DMD therapy.
A Phase II Trial of Induction Plus Maintenance Rituximab and Bortezomib in Patients with Relapsed/Refractory Mantle Cell (MCL) and Follicular (FL) Non-Hodgkin’s Lymphoma
Authors: Kristie A. Blum, Robert A. Baiocchi, Lapo Alinari, Thomas S. Lin, Pierluigi Porcu, Jeffrey Jones, Joseph Flynn, William Hicks, Margaret S. Lucas, Lai Wei, Jeffrey S. Johnston, John C. Byrd
Journal: Blood (2008)
Abstract 5052: The association between estrogen receptor alpha and platinum sensitivity in ovarian cancer cells
Authors: Sohei Matsumura, Tsuyoshi Ohta, Toshifumi Takahashi, Kazuhiro Takahashi, Satoru Nagase
Journal: Cancer Research (2015)

Abstract [Objective] The objective of this study was to examine whether estrogen receptor alpha (ERα) is associated with the sensitivity to cisplatin in ovarian cancer cells. [Methods] Using two human ovarian cancer cell lines (Caov-3, Ovcar-3) which express ERα, we investigated the effect of cisplatin on ERα activation. We evaluated the association between ERα activation and Erk cascade in the cells treated with cisplatin. We next examined the antitumor effects of estradiol (E2) with cisplatin by using MTS [3-(4, 5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium, inner salt], and Western blot assay. Then, ERα expression was down-regulated in Caov-3 and Ovcar-3 by using lentiviral shRNA against ERα, and we generated batch clonal lines. The nontarget shRNA (NTS) served as control. Finally, we determined the effect of ERα down-regulation on the sensitivity to cisplatin. [Results] Cisplatin induced the phosphorylation of ERα at serine 118 via Erk cascade. Pretreatment with E2 antagonized cisplatin-induced cytotoxicity, and decreased the expression of cleaved PARP induced by cisplatin. Pretreatment of E2 followed by cisplatin increased the expression of Bcl-2, which is anti-apoptotic protein. The shRNA- mediated down-regulation of ERα increased the sensitivity to cisplatin compared with NTS. [Conclusions] These results indicate that E2 promotes resistance to cisplatin via ERα, and down-regulation of ERα may increase efficacy of cisplatin in ovarian cancer. Citation Format: Sohei Matsumura, Tsuyoshi Ohta, Toshifumi Takahashi, Kazuhiro Takahashi, Satoru Nagase. The association between estrogen receptor alpha and platinum sensitivity in ovarian 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 5052. doi:10.1158/1538-7445.AM2015-5052
Antihistone Properties of C1 Esterase Inhibitor Protect against Lung Injury
Authors: Malgorzata Wygrecka, Djuro Kosanovic, Lukasz Wujak, Katrin Reppe, Ingrid Henneke, Helena Frey, Miroslava Didiasova, Grazyna Kwapiszewska, Leigh M. Marsh, Nelli Baal, Holger Hackstein, Dariusz Zakrzewicz, Holger C. Müller-Redetzky, Steven de Maat, Coen Maas, Marc W. Nolte, Con Panousis, Ralph T. Schermuly, Werner Seeger, Martin Witzenrath, Liliana Schaefer, Philipp Markart
Journal: American Journal of Respiratory and Critical Care Medicine (2017)

Acute respiratory distress syndrome is characterized by alveolar epithelial cell injury, edema formation, and intraalveolar contact phase activation.To explore whether C1 esterase inhibitor (C1INH), an endogenous inhibitor of the contact phase, may protect from lung injury in vivo and to decipher the possible underlying mechanisms mediating protection.The ability of C1INH to control the inflammatory processes was studied in vitro and in vivo.Here, we demonstrate that application of C1INH alleviates bleomycin-induced lung injury via direct interaction with extracellular histones. In vitro, C1INH was found to bind all histone types. Interaction with histones was independent of its protease inhibitory activity, as demonstrated by the use of reactive-center-cleaved C1INH, but dependent on its glycosylation status. C1INH sialylated-N- and -O-glycans were not only essential for its interaction with histones but also to protect against histone-induced cell death. In vivo, histone-C1INH complexes were detected in bronchoalveolar lavage fluid from patients with acute respiratory distress syndrome and multiple models of lung injury. Furthermore, reactive-center-cleaved C1INH attenuated pulmonary damage evoked by intravenous histone instillation.Collectively, C1INH administration provides a new therapeutic option for disorders associated with histone release.
Synthetic vs Natural: Diatoms Bioderived Porous Materials for the Next Generation of Healthcare Nanodevices
Authors: Ilaria Rea, Monica Terracciano, Luca De Stefano
Journal: Advanced Healthcare Materials (2016)

Nanostructured porous materials promise a next generation of innovative devices for healthcare and biomedical applications. The fabrication of such materials generally requires complex synthesis procedures, not always available in laboratories or sustainable in industries, and has adverse environmental impact. Nanosized porous materials can also be obtained from natural resources, which are an attractive alternative approach to man‐made fabrication. Biogenic nanoporous silica from diatoms, and diatomaceous earths, constitutes largely available, low‐cost reservoir of mesoporous nanodevices that can be engineered for theranostic applications, ranging from subcellular imaging to drug delivery. In this progress report, main experiences on nature‐derived nanoparticles with healthcare and biomedical functionalities are reviewed and critically analyzed in search of a new collection of biocompatible porous nanomaterials.