tbuckley/cabot-search huggingface dataset:
Abstract 1994: Honokiol reduces drug resistance by down-regulation of survivin expression in multidrug resistant squamous cell carcinoma of the head and neck
Authors: Xu Wang, Jonathan J. Beitler, Hong Wang Hong, Michael J. Lee, Zhengjia Chen, Lydia Koenig, A. R. Ruhul Amin, Zhuo (Georgia) Chen, Jack L. Arbiser, Dong M. Shin
Journal: Cancer Research (2012)

Abstract Background: Resistance to chemotherapy is a major obstacle in cancer therapy. The purpose of this study is to evaluate honokiol in combination with paclitaxel in controlling proliferation of multi-drug resistant (MDR) cancer cells. Honokiol is a small molecule purified from Magnolia officinalis. Honokiol has been shown to suppress tumor growth through apoptosis and inhibition of angiogenesis. In this study, we investigated the effects and mechanisms of those effects of honokiol on MDR squamous cell cancers of the head and neck (SCCHN) Methods: Serial MDR SCCHN lines including KB-8-5, KB-C1, and KB-V1 derived from the drug sensitive parental KB-3-1 cells were used in this study. Cytotoxic effects of honokiol alone and in combination with paclitaxel on apoptosis in drug-sensitive and -resistant cells were evaluated in vitro and in a subcutaneous KB-8-5 xenograft model, Results: The cell growth inhibition analysis revealed a wide range of IC50 values of paclitaxel from 1.66±0.09 to 6560.9 ±439.52 ng/ml in the KB serial cell lines, indicating that those cell lines have different levels of resistance to the paclitaxel treatment. In contrast, honokiol effectively inhibited proliferation and induced apoptosis in all four cell lines with IC50 values from 3.35±0.13 to 2.77±0.22 μg/ml. Mechanistic studies revealed that honokiol induced similar mitochondria-dependent apoptosis in drug resistant cell lines regardless of the differential resistance levels to paclitaxel treatment. Moreover these effects were associated with inhibition of STAT3 phosphorylation and down-regulation of STAT3 target gene expression, including survivin and Mcl-1. Combined treatment with honokiol and paclitaxel synergistically increased cytotoxicity as compared to the single drug treatment. This combination also significantly inhibited growth of xenografted tumors in nude mice. Conclusion: These results suggest that honokiol may be a promising drug in overcoming paclitaxel resistence of SCCHN. Targeting MDR SCCHN using honokiol in combination with paclitaxel, may benefit patients with SCCHN. (Supported by grants P50CA128613, GCC Distinguished Cancer Scholar to Dong M. Shin and Jonathan J Beitler) Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 1994. doi:1538-7445.AM2012-1994
Abstract 2433: Comparisons between an IRDye 800CW-labeled PSMA-targeted small molecule and antibody for preclinical small animal imaging
Authors: Joy L. Kovar, Lael L. Cheung, Melanie A. Simpson, D Michael Olive
Journal: Cancer Research (2012)

Abstract Prostate cancer continues to be the second leading cause of cancer death in men in 2011. Deciphering the progression and mechanisms contributing to the metastatic spread of this disease is critical to our overall understanding of how to approach treatment and/or therapy. Prostate-specific membrane antigen (PSMA) is a possible therapeutic target for the disease and is the focus of several cancer therapies currently in clinical trials. Near infrared (NIR) fluorescence imaging for cancer diagnosis and treatment is gaining attention for preclinical as well as clinical applications. IRDye 800CW is a NIR fluorophore exhibiting superior target-to-background ratios when conjugated to targeting moieties such as antibodies, peptides, and small molecules. Here we assess two different PSMA-targeted compounds conjugated to IRDye 800CW: the small molecule YC-27 and a PSMA-specific antibody. In vitro binding kinetics for both compounds exhibit expected dose dependent increases with increasing concentrations. Both compounds were successfully blocked with their unlabeled counterpart; however, neither blocked the other suggesting different PSMA epitopes. Although direct comparisons are inappropriate due to differences in molecular structures and labeling density, assessment of their respective pharmacokinetics is possible. Microscopy of prostate tumor cells incubated with each probe revealed a slower internalization of the small molecule when compared to the internalization of the antibody. Specificity of the labeled compounds in vivo was determined in male athymic nu/nu mice implanted with 22Rv1 (PSMA positive) or PC3M-LN4 (PSMA negative) prostate cancer cells (106). Mice received either IRDye 800CW YC27 (1 nmole) or IRDye 800CW PSMA (50 µg) followed by non-invasive fluorescent optical imaging of 800nm signals on the Pearl Impulse Small Animal Imager. At the study endpoint, organs and tumors were excised and imaged to assess residual probe localization. In vivo clearance patterns for these labeled molecules differed with the YC27 clearing via the kidneys and the antibody clearing through the liver. These subtle differences between the two imaging agents provide valuable options to investigators with specific requirements in their animal research. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 2433. doi:1538-7445.AM2012-2433
Abstract LB-36: Antibody mediated neutralization of sema4D reduces tumor angiogenesis and growth <i>In Vivo.</i>
Authors: Alan Jonason, Terrance Fisher, Sebold Torno, Holm Bussler, Ji Li, Laurie Winter, Renee Kirk, Alan Howell, Jeff Caplan, Patrick Kenney, Christine Reilly, Maria Scrivens, Elizabeth Evans, Mark Paris, Raymond Watkins, Maurice Zauderer, John E. Leonard, Ernest S. Smith
Journal: Cancer Research (2010)

Abstract It has been demonstrated that semaphorin 4D (SEMA4D; CD100) is a potent pro-angiogenic molecule. SEMA4D binding to its receptor plexin-B1 (PLXNB1) on endothelial cells transactivates c-MET and promotes formation of new blood vessels and tumor growth in vivo. SEMA4D is over-expressed in a wide array of tumor types, and is also produced by inflammatory cells present in the tumor microenvironment. It has recently been demonstrated that in an environment lacking SEMA4D, the ability of mouse breast cancer cells to originate tumor masses and metastases is severely impaired, and that SEMA4D produced by tumor associated macrophages is required for tumor angiogenesis and growth. In addition to its effects on endothelial cells, SEMA4D binding to PLXNB1 on tumor cells results in MET transactivation and migration of tumor cells. It has been further reported that overexpression of PLXNB1 and MET in breast and ovarian cancers is a negative prognostic factor. Tumors co-expressing PLXNB1 and MET were characterized as having a higher grade and an increased frequency of metastases. Collectively, these results suggest that expression of SEMA4D, either by tumor cells or by tumor associated macrophages, may represent a mechanism of tumor neovascularization, and that expression of the SEMA4D receptor in tumors may further induce tumor invasion, thereby enhancing their growth, survival, and metastatic potential. Antibody neutralization of SEMA4D thus may represent a new therapeutic strategy for cancer treatment. We selected a high affinity human IgG4 antibody that is specific for both mouse and human SEMA4D, and utilized several in vitro functional assays to demonstrate that this antibody blocks SEMA4D - PLXNB 1 interactions. Using both transplanted and orthotopic tumor models we demonstrated that antibody mediated SEMA4D neutralization in vivo inhibits tumor growth and tumor angiogenesis. This human antibody is currently in IND-enabling toxicology testing and we anticipate the initiation of human clinical trials in 2H 2010. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr LB-36.
CB-19 * PID1, A NEW GROWTH-INHIBITORY GENE, SENSITIZES MEDULLOBLASTOMA AND GLIOMA CELL LINES TO CHEMOTHERAPY
Authors: J. Xu, X. Ren, A. Tran, A. Erdreich-Epstein
Journal: Neuro-Oncology (2014)

BACKGROUND: Phosphotyrosine Interaction Domain containing protein-1 (PID1) was discovered in 2006. We recently showed that PID1 inhibits growth of brain tumor cell lines and its mRNA level is directly correlated with survival in glioma and medulloblastoma patients (Erdreich-Epstein et al, Clin Cancer Res). The growth-inhibitory effect of PID1 was due to decreased proliferation and increased cell death. METHODS/RESULTS: We hypothesized that PID1 sensitizes brain tumors to therapy, thus accounting for the longer survival in patients with higher PID1 mRNA. Indeed, while cisplatin (10 µg/ml) or transient PID1 overexpression each increased apoptosis of glioma and medulloblastoma cell lines, combining cisplatin with PID1 resulted in markedly higher apoptosis. Moreover, knockdown of PID1 by siRNA inhibited the cisplatin-induced mitochondrial membrane depolarization and apoptosis, suggesting that PID1 is partially required for cisplatin-induced apoptosis. Taken together, this suggests that PID1 sensitizes both glioma and medulloblastoma cell lines to cisplatin. Intriguingly, PID1 mRNA increased in response to chemotherapy in a time- and dose-dependent manner in brain tumor cell lines. The chemotherapy-induced increase in PID1 mRNA was blocked by inhibitors of NFkB, suggesting that regulation of PID1 mRNA increase may be an NF-kB-dependent process. Consistent with this, cisplatin increased activity of an NF-kB promoter reporter. Surprisingly, despite the chemotherapy-induced increase in PID1 mRNA, PID1 protein decreased in response to cisplatin, suggesting post-translational modification(s) of PID1 induced by cisplatin. Ongoing work is focusing on the mechanism and role of PID1 in response to chemotherapy, and examining the effect of PID1 on the response of tumors to chemotherapy in vivo. CONCLUSIONS: Our data show that PID1 sensitizes glioma and medulloblastoma cell lines to chemotherapy, possibly explaining the correlation between higher PID1 mRNA and longer patient survival. This suggests also that PID1 mimetics may act as chemotherapy sensitizers in brain tumor treatment.
TCTAP A-118 12 Months Results from a CE Mark Trial of a 2nd Generation, Self-Expanding, Transfemoral Aortic Bioprosthesis for the Treatment of Patients with Severe Aortic Stenosis
Authors: Helge Moellmann, Won-Keun Kim, Hendrick Treede, Patrick Diemert, Eberhard Grube, Georg Nickenig, Stefan Baldus, Kuratani Toru, Thomas Walther, Alexandre Abizaid
Journal: Journal of the American College of Cardiology (2015)
The Use of ACTH in Acute Viral Hepatitis
Authors: James W. Colbert, James F. Holland, Ivan Heissler, Marjorie Knowlton
Journal: New England Journal of Medicine (1951)

THE reports of the effectiveness of ACTH against many diseases resistant to all previous therapeutic measures1 , 2 suggested a trial of ACTH in the management of acute viral hepatitis. The following is a report of the investigation of the use of ACTH in treatment of viral hepatitis at the Hepatitis Center, Ninety-Eighth General Hospital, U. S. Zone of Occupation, Germany.At this center over 4000 cases of viral hepatitis have been treated during the past three years, 1947–1950.3 Materials and MethodsThe patients studied in this investigation were 5 male enlisted personnel of the United States Army of Occupation in Germany . . .
A pilot study to assess mediastinal emphysema after esophageal endoscopic submucosal dissection with carbon dioxide insufflation
Authors: Y. Maeda, D. Hirasawa, N. Fujita, T. Obana, T. Sugawara, T. Ohira, Y. Harada, T. Yamagata, K. Suzuki, Y. Koike, Y. Yamamoto, Z. Kusaka, Y. Noda
Journal: Endoscopy (2012)

<b>Background and aims</b>: Mediastinal emphysema sometimes develops following esophageal endoscopic submucosal dissection (ESD) without perforation because the esophagus has no serosa. Carbon dioxide (CO<sub>2</sub>) insufflation during esophageal ESD may reduce the incidence of mediastinal emphysema. The aim of the present study was to compare the incidence and severity of post-ESD mediastinal emphysema in patients receiving CO<sub>2</sub> insufflation vs. standard air insufflation during esophageal ESD. <b>Patients and methods</b>: A total of 27 patients who had undergone esophageal ESD with insufflation of CO<sub>2</sub> between July 2009 and March 2010 were enrolled in this study (CO<sub>2</sub> group). Another 105 patients who had undergone esophageal ESD with air insufflation between March 2004 and May 2009 were included as historical controls (air group). Multi-detector row computed tomography (MDCT) was carried out immediately after ESD. A conventional chest radiograph was taken the next day. Mediastinal emphysema findings on MDCT and radiography were compared between the groups. <b>Results</b>: Mediastinal emphysema detected by chest radiography was 0 % in the CO<sub>2</sub> group vs. 6.6 % in the air group (n.s.). Mediastinal emphysema on MDCT was significantly less frequent in the CO<sub>2</sub> group compared with the air group (30 % vs. 63 %; <i>P</i> = 0.002). The severity of mediastinal emphysema also tended to be lower in the CO<sub>2</sub> group. <b>Conclusions</b>: Whereas mediastinal emphysema detected by radiography is not so common, MDCT immediately after ESD revealed a certain prevalence of post-ESD mediastinal emphysema. Insufflation of CO<sub>2</sub> rather than air during esophageal ESD significantly reduced postprocedural mediastinal emphysema. CO<sub>2</sub> can be considered as insufflating gas for esophageal ESD.
UK spread the myth that doctors' language skills may not be tested, says EU commissioner
Authors: C. Dyer
Journal: BMJ (2012)

Michel Barnier, the European Union commissioner responsible for the internal market, has criticised the United Kingdom for perpetuating the “myth” that EU rules are endangering British citizens by banning language tests for doctors from other European countries who come to practise in the UK.

The 2005 EU directive on the mutual recognition of professional qualifications provides for doctors and other professionals from the European Economic Area to have their qualifications automatically recognised in any other member state. Regulators such as the UK General Medical …
Smoking and Mortality among Older Men and Women in Three Communities
Authors: Andrea Z. LaCroix, Janet Lang, Paul Scherr, Robert B. Wallace, Joan Cornoni-Huntley, Lisa Berkman, J. David Curb, Denis Evans, Charles H. Hennekens
Journal: New England Journal of Medicine (1991)

Although cigarette smoking is the leading avoidable cause of premature death In middle age, some have claimed that no association is present among older persons.
Eosinophilic enteritis presenting as a perforated duodenal ulcer
Authors: H. Issa, B. Bseiso, A. Al-Salem
Journal: Endoscopy (2011)

Eosinophilic gastroenteritis (EGE) is a rare condition of unknown etiology that is characterized by eosinophilic infiltration in the layers of the gastrointestinal tract [1]. It can affect any part of the gastrointestinal tract but most commonly affects the stomach [1] [2]. This report describes a rare case of EGE presenting as a perforated duodenal ulcer with subsequent duodenal stenosis.
P607 RNA BINDING PROTEIN-HuR REGULATES SPHINGOSINE 1-PHOSPHATE (S1P) RECEPTOR 3 EXPRESSION AND MEDIATES S1P-INDUCED HUMAN BONE MARROW-DERIVED MESENCHYMAL STEM CELLS MIGRATION IN LIVER FIBROGENESIS
Authors: N. Chang, L. Yang, J. Ge, L. Xiu, L. Li
Journal: Journal of Hepatology (2014)
Abstract 3958: A miRNA inhibitor screen for synthetic lethal interactions in KRAS-driven NSCLC
Authors: Robert Borkowski, Liqin Du, John D. Minna, Adi F. Gazdar, Alexander Pertsemlidis
Journal: Cancer Research (2011)

Abstract Lung cancer, especially non-small cell lung cancer (NSCLC), is currently the leading cause of cancer fatalities in the United States, accounting for 30% of the fatalities in males, and 26% in females. Additionally, the five-year survival rate for individuals affected by lung cancer has only improved by 3% in the past 35 years. As suggested by the survival data, very few effective treatment options are available for NSCLC, and many vary dramatically in efficacy depending on the genetic status of the tumor. In particular, the presence of mutant KRAS in NSCLC serves as a negative predictor for drug efficacy. KRAS mutations are found in ∼22% of NSCLC tumors, and tumors harboring these mutations are especially refractory to treatment. We have identified synthetic lethal miRNAs in the background of KRAS-dependence through a four-armed miRNA inhibitor screen. A miRNA inhibitor screen can serve to not only identify miRNAs involved in context-dependent survival, but also genes and pathways that would be obscured by genomic redundancy in a conventional RNAi screen. Using a comprehensive library of miRNA inhibitors coupled with an endpoint assay for cell viability, we can identify miRNAs that modulate viability or paclitaxel sensitivity in KRAS-dependent NSCLC cell line NCI-H358 with minimal effect in the wild-type KRAS cell line NCI-H1993. Candidate miRNAs are validated in an expanded panel of ten cell lines including four KRAS mutant, four KRAS wild-type, and two immortalized human bronchial epithelial cell lines. The miRNAs identified here will allow us to elucidate vulnerable pathways in KRAS-dependent tumors that can be exploited for a therapeutic or predictive benefit in a typically difficult to manage class of tumor. This research was supported by NIH R01 CA129632 from the National Cancer Institute and by P50 CA70907 from the UT Southwestern/MD Anderson Cancer Center Lung Specialized Program of Research Excellence. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 3958. doi:10.1158/1538-7445.AM2011-3958
Basic Problems of Behavior
Journal: JAMA (1941)

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 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) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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
Administrative claims: a novel approach in monitoring long term adherence to anti-hormonal therapy in breast cancer.
Authors: AN Meguerditchian, N Watroba, J Roistacher, A Stewart, M Cropp, SB Edge
Journal: Cancer Research (2009)

Abstract Abstract #1135 Background:&amp;#x2028; Anti-hormonal therapy (AHT) is a key component of therapy that improves survival in breast cancer. However, many women do not complete the prescribed treatment course. There is currently limited reliable information regarding long-term adherence to AHT. We hypothesize that health payer administrative claims for prescription benefits may allow more reliable monitoring of AHT use.&amp;#x2028; Methods:&amp;#x2028; Claims for women diagnosed with breast cancer between 2001 and 2003 from a single insurance carrier covering about 1/3 of the regional population were matched to disease stage and treatment information from the National Cancer Data Base (NCDB) for women treated at NCDB hospitals in Western New York. Claims were searched for AHT drugs identified by National Drug Codes (NDC). Start date, end date, type of agent, switch in drugs, patterns of discontinuation, and dates of insurance coverage eligibility were recorded. A compliance index was attributed to each patient, reflecting the ratio of AHT claims identified, over the ideal number of claims that should have been recorded based on treatment start date.&amp;#x2028; Results: &amp;#x2028; AHT was initiated in 230 women at a median of 165 days from breast cancer diagnosis. Stage was 0: 3.5%; I: 54.3%; II: 33.4%; III: 7%; unknown: &amp;lt;2%. Tamoxifen was the first AHT agent in 66.5% of cases. A switch in agents occurred in 36.1% women. There was a gap in prescription renewal in 57% of patients. The average gap length was 5.9 months. The maximum gap duration was 1 month in 27% of cases; however 16% of patients had a treatment gap of 6 months or more. The annual compliance rate for the study population was 79.6%, 60.9%, 52.7%, 24.1% and 6.9% for each of the 5 consecutive years of treatment. After adjusting for time from start of AHT, the compliance index was ≤0.66 in 50% of women. Less than 20% of patients had an index of 1.0 .&amp;#x2028; Discussion: &amp;#x2028; Administrative claims data combined with cancer stage data proved to be effective at defining gaps in use of AHT among breast cancer patients. By applying this strategy, we found that over 50% of women treated with AHT had gaps in treatment averaging 6 months. The annual compliance rate to AHT decreased steadily over each of the 5 years of treatment. Real time monitoring of administrative claims for patients who start AHT can identify those who discontinue treatment and may allow counseling on side effects and benefits and improve treatment compliance and outcome. Citation Information: Cancer Res 2009;69(2 Suppl):Abstract nr 1135.