tbuckley/cabot-search huggingface dataset:
Blockade of PD-1 in Combination with Dendritic Cell/Myeloma Fusion Cell Vaccination Following Autologous Stem Cell Transplantation Is Well Tolerated, Induces Anti-Tumor Immunity and May Lead to Eradication of Measureable Disease
Authors: Jacalyn Rosenblatt, Irit Avivi, Noam Binyamini, Lynne Uhl, Poorvi Somaiya, Dina Stroopinsky, Kristen Anna Palmer, Maxwell Douglas Coll, Tami Katz, Lina Bisharat, Robin Joyce, James D. Levine, Jon E. Arnason, Katarina Luptakova, Malgorzata McMasters, Salvia Jain, Merav Leiba, Aya Sato-Dilorenzo, Emma Logan, Mary Paty Bryant, Viki Held, Paul G. Richardson, Jacob P. Laubach, Arnon Nagler, Kenneth C. Anderson, Nikhil C. Munshi, Jacob M. Rowe, Donald Kufe, David Avigan
Journal: Blood (2015)
Abstract 3234: Genetic deletion of macrophage migration inhibitory factor reduces oral carcinogenesis
Authors: Steve Oghumu, Thomas Knobloch, Cesar Terrazas, Sanjay Varikuti, Claire Bollinger, Hans Iwenofu, Christopher Weghorst, Abhay Satoskar
Journal: Cancer Research (2016)

Abstract Oral cancer kills about 1 person every hour, each day in the United States and is the 6th most prevalent cancer worldwide. The pro-inflammatory cytokine ‘macrophage migration inhibitory factor’ (MIF) has been shown to be expressed in oral cancer patients, yet its precise role in oral carcinogenesis is not clear. In this study, we examined the impact of global Mif deletion on the cellular and molecular process occurring during oral carcinogenesis using a well-established mouse model of oral cancer with the carcinogen 4-nitroquinoline-1-oxide (4NQO). C57BL/6 Wild-type (WT) and Mif knock-out mice were administered with 4NQO in drinking water for 16 weeks, then regular drinking water for 8 weeks. Mif knock-out mice displayed fewer oral tumor incidence and multiplicity, accompanied by a significant reduction in the expression of pro-inflammatory cytokines Il-1β, Tnf-α, chemokines Cxcl1, Cxcl6, Cxcl8 and Ccl3 and other molecular biomarkers of oral carcinogenesis Mmp1 and Ptgs2. Further, recruitment of myeloid-derived tumor promoting immune cells was inhibited in Mif knock-out mice. Our results demonstrate that genetic Mif deletion reduces the incidence and severity of oral carcinogenesis, by inhibiting the expression inflammatory cytokines and infiltration of tumor promoting immune cells. Thus, targeting MIF is a promising strategy for the prevention or therapy of oral cancer. Citation Format: Steve Oghumu, Thomas Knobloch, Cesar Terrazas, Sanjay Varikuti, Claire Bollinger, Hans Iwenofu, Christopher Weghorst, Abhay Satoskar. Genetic deletion of macrophage migration inhibitory factor reduces oral carcinogenesis. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 3234.
Abstract 4052: The role of the phosphorylated RXRα on diethylnitrosamine-induced liver tumorigenesis in mice
Authors: Hiroyasu Sakai, Yohei Shirakami, Masahito Shimizu
Journal: Cancer Research (2016)

Abstract We have previously reported that a malfunction of RXRα due to aberrant phosphorylation at serine 260 by MAPK is associated with the development of hepatocellular carcinoma (HCC). The phosphorylated RXRα impairs normal receptor functions of either RXR or RAR, which are respective homodimeric or heterodimeric partner of RXRα, in a dominant-negative manner. Besides, these impaired receptor functions result in the downregulation of their target gene expression and inducing hepatocarcinogenesis by stimulating cell proliferation and inhibiting apoptosis, suggesting that phosphorylated RXRα plays a crucial role in the development of HCC. However, these findings were revealed primarily using HCC cell lines that express the phosphorylated-RXRα (p-RXRα) proteins and it still remains unclear whether p-RXRα may impact in the process of hepatocarcinogenesis in vivo. Therefore, in order to investigate the biological functions of p-RXRα on hepatocarcinogenesis in vivo, we generated doxycycline-inducible ES cell line and transgenic mouse, both of which overexpress phosphomimic mutant of RXRα (T82D/S260D). Interestingly, the transcriptional activities of Retinoid X Receptor Response Element (RXRE) were significantly reduced in the Mouse Embryonic Fibroblasts (MEFs) derived from the transgenic mice, suggesting that the retinoid signaling via RXRα were impaired in the mice. Moreover, the development of liver tumors induced by liver carcinogen diethylnitrosamine (DEN) was enhanced in the transgenic mice that overexpress T82D/S260D protein in the liver. Notably, the increased liver tumors in the transgenic mice resulted from the promotion of cell cycle progression, not the inhibition of apoptosis. Interestingly, expression of β-catenin and its target genes, cyclin D1 and c-myc, were increased in transgenic liver tumors, although the expression of retinoid-related genes, such as RARβ, p21 and p27, were not altered compared with control mice. These results suggest that the phospho-modification of RXRα may promote the development of DEN-induced liver tumors through the activation of β-catenin signaling pathways in mice. Citation Format: Hiroyasu Sakai, Yohei Shirakami, Masahito Shimizu. The role of the phosphorylated RXRα on diethylnitrosamine-induced liver tumorigenesis in mice. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 4052.
Abstract 85: Macrophage inflammatory protein-1β and interleukin 15 modulate gene expression patterns associated with prostate cancer progression
Authors: Krizia Rohena-Rivera, Diana A. Aponte-Colón, María M. Sánchez-Vázquez, Carmen L. Cadilla, Magaly Martínez-Ferrer
Journal: Cancer Research (2016)

Abstract Prostate Cancer (PCa) is the second-leading cause of cancer-related deaths in the United States. Inflammation is associated with PCa development and progression. Cytokines such as macrophage inflammatory protein-1β (MIP1β or CCL4) and Interleukin 15 (IL-15) are differentially expressed in prostate cancer patients with recurrent disease (MIP1β) or recurrence-free survival (IL-15). However, the specific pathway by which these cytokines affect PCa progression is unknown. We evaluated the changes in gene expression patterns using in vivo models of prostate cancer and microarray analysis. To generate prostate tumors in vivo we used a mouse orthotopic xenograft model. Androgen-receptor-positive (AR+) cells, 22RV1, were orthotopically injected in the anterior prostate lobes. MIP1β and IL-15 were administered bi-weekly with intraperitoneal injections during 4 weeks. Tumor tissue was collected and snap frozen for RNA extraction, and microarray analysis with the Affymetrix Human Gene 2.0 Gene Array. Differences in gene expression were analyzed with Ingenuity Pathway Analysis (IPA) software and confirmation was done via real-time PCR. Microarray analysis showed 179 genes differentially expressed between MIP1β and control. In addition, 952 genes were differentially expressed between IL-15 and control. Ingenuity Pathway Analysis revealed that MIP1β affected networks associated with cell development, proliferation and movement while IL-15 affected networks involved in lymphocyte development and movement, cell death, and the inhibition of cancer cell invasion. Knowledge of the role of MIP1β and IL-15 in the alteration of gene expression patterns is pertinent to elucidate the significance of these cytokines in prostate cancer progression. Citation Format: Krizia Rohena-Rivera, Diana A. Aponte-Colón, María M. Sánchez-Vázquez, Carmen L. Cadilla, Magaly Martínez-Ferrer. Macrophage inflammatory protein-1β and interleukin 15 modulate gene expression patterns associated with prostate cancer progression. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 85.
Metabolic consequences of obesity as an “outside in” mechanism of disease severity in asthma
Authors: Michael C. Peters, John V. Fahy
Journal: European Respiratory Journal (2016)

The clinical features of asthma are highly varied. Most patients have relatively mild disease that is easily controlled with inhaled β-adrenergic agonists with or without low or medium doses of inhaled corticosteroids. However, a subset of patients has more severe disease, and many of these patients suffer persistent symptoms in spite of treatments that include high doses of inhaled corticosteroids. Furthermore, some asthma patients are exacerbation prone, and these patients require frequent treatment with systemic corticosteroids to control these exacerbations. Studies that have systematically examined the heterogeneity of disease severity in asthma have noted that older age and higher body weight are clinical features of patients with more severe disease [1, 2]. In addition, it has been noted that age has a greater effect than asthma duration on risk of severe asthma [3]. These clinical features provide clues about disease mechanisms of asthma, and work is now being done to understand how ageing and obesity lead to severe asthma. For example, it has recently been shown that systemic interleukin (IL)-6 inflammation occurs in a subset of patients with asthma who are characterised by older age, obesity and severe disease (low lung function and frequent exacerbations) [4]. Notably, increases in plasma IL-6 occur in some but not all obese patients, and obese patients with high IL-6 levels have more severe asthma than obese patients with low IL-6 levels. In addition, increases in plasma IL-6 remain strongly associated with asthma severity, even when controlling for body mass index and age in regression models. This means that systemic IL-6 inflammation is an independent predictor of disease severity in asthma and that the heterogeneity of asthma severity that occurs in obese patients with asthma can be explained at least in part by the presence or absence of low-grade systemic inflammation in these patients (figure 1). Low-grade systemic inflammation in obesity is characterised by increases in systemic levels of inflammatory cytokines such as IL-6, IL-1 and tumour necrosis factor-α, and adipokines such as leptin. These mediators originate in adipocytes and activated macrophages in adipose tissue, and contribute to mechanisms of metabolic dysfunction and metabolic syndrome in obese patients [5, 6]. These inflammatory cytokines could alter lung function in a variety of ways, including through activation of vascular endothelial cells, airway fibroblasts, airway smooth muscle cells or airway epithelial cells [7]. In addition, IL-6 influences the differentiation of naïve T-cells into Th17-cells and could indirectly affect lung function through the effects of IL-17 [8]. "Outside in" asthma: inflammatory events that drive asthma severity arise in tissue compartments outside the lung <http://ow.ly/aEcZ301mcLc>
Pulmonary metastasectomy—A single institution experience
Authors: S. Noonan, J. McCaffrey, J. Comiskey, A. Treacy
Journal: Journal of Clinical Oncology (2008)

18505 Background: Resection of pulmonary metastases is a common procedure as part of the multidisciplinary management of a patient with metastatic disease confined to the lung. It is being utilized in a range of cancers including soft tissue sarcoma, renal cell carcinoma and colorectal cancer. Methods: We present twenty-one cases of metastatic cancer treated with pulmonary metastasectomy, identified on retrospective analysis of case files, over a period from 1994 to 2007. Results: Twenty-one cases were identified in total. The primary lesion was colorectal adenocarcinoma in 5 cases, head and neck squamous cell carcinoma in 5 cases, osteogenic sarcoma in 3 cases, melanoma in 2 cases, uterine myosarcoma in 2 cases, synovial sarcoma in 2 cases, adenocarcinoma of the ampulla and in 1 case and non-seminomatous germ cell tumor in 1 case. 57% of patients were female. The median disease free interval, from initial diagnosis to development of pulmonary metastases, was 34 months (range 7 mths to 11yrs). The median age at surgery was 53 yrs (range 20-75 yrs). 6 patients underwent repeat pulmonary metastasectomy for recurrent pulmonary disease. Two patients had both liver and pulmonary metastases resected. The median follow-up from date of pulmonary resection was 36 months (range 1 month-104 months). Three years post metastasectomy, 55% of patients were alive. Conclusions: This series illustrates the evolving role of pulmonary metastasectomy in the management of patients with metastatic cancer. Advances in imaging have led to the identification of small, potentially resectable lesions. New systemic therapies have led to down-staging of lesions, thus, pulmonary metastasectomy is increasingly an option in a broadening range of cancers. A survival advantage for pulmonary metastasectomy has been shown in several published series. However, there are no randomized prospective trials examining the role of metastasectomy and this remains a procedure in highly selected patients in a multi disciplinary setting. No significant financial relationships to disclose.
GPR91 senses extracellular succinate released from inflammatory macrophages and exacerbates rheumatoid arthritis
Authors: Amanda Littlewood-Evans, Sophie Sarret, Verena Apfel, Perrine Loesle, Janet Dawson, Juan Zhang, Alban Muller, Bruno Tigani, Rainer Kneuer, Saijel Patel, Stephanie Valeaux, Nina Gommermann, Tina Rubic-Schneider, Tobias Junt, José M. Carballido
Journal: The Journal of Experimental Medicine (2016)

When SUCNR1/GPR91-expressing macrophages are activated by inflammatory signals, they change their metabolism and accumulate succinate. In this study, we show that during this activation, macrophages release succinate into the extracellular milieu. They simultaneously up-regulate GPR91, which functions as an autocrine and paracrine sensor for extracellular succinate to enhance IL-1β production. GPR91-deficient mice lack this metabolic sensor and show reduced macrophage activation and production of IL-1β during antigen-induced arthritis. Succinate is abundant in synovial fluids from rheumatoid arthritis (RA) patients, and these fluids elicit IL-1β release from macrophages in a GPR91-dependent manner. Together, we reveal a GPR91/succinate-dependent feed-forward loop of macrophage activation and propose GPR91 antagonists as novel therapeutic principles to treat RA.
Same Sex Marriage and the Perceived Assault on Opposite Sex Marriage
Authors: Alexis Dinno, Chelsea Whitney
Journal: PLoS Medicine (2013)

Background Marriage benefits both individuals and societies, and is a fundamental determinant of health. Until recently same sex couples have been excluded from legally recognized marriage in the United States. Recent debate around legalization of same sex marriage has highlighted for anti-same sex marriage advocates and policy makers a concern that allowing same sex couples to marry will lead to a decrease in opposite sex marriages. Our objective is to model state trends in opposite sex marriage rates by implementation of same sex marriages and other same sex unions.  Methods and Findings Marriage data were obtained for all fifty states plus the District of Columbia from 1989 through 2009. As these marriage rates are non-stationary, a generalized error correction model was used to estimate long run and short run effects of same sex marriages and strong and weak same sex unions on rates of opposite sex marriage. We found that there were no significant long-run or short run effects of same sex marriages or of strong or weak same sex unions on rates of opposite sex marriage.  Conclusion A deleterious effect on rates of opposite sex marriage has been argued to be a motivating factor for both the withholding and the elimination of existing rights of same sex couples to marry by policy makers–including presiding justices of current litigation over the rights of same sex couples to legally marry. Such claims do not appear credible in the face of the existing evidence, and we conclude that rates of opposite sex marriages are not affected by legalization of same sex civil unions or same sex marriages.
Neuroendocrine Tumors
Authors: Matthew H. Kulke, Al B. Benson, Emily Bergsland, Jordan D. Berlin, Lawrence S. Blaszkowsky, Michael A. Choti, Orlo H. Clark, Gerard M. Doherty, James Eason, Lyska Emerson, Paul F. Engstrom, Whitney S. Goldner, Martin J. Heslin, Fouad Kandeel, Pamela L. Kunz, Boris W. Kuvshinoff, Jeffrey F. Moley, Venu G. Pillarisetty, Leonard Saltz, David E. Schteingart, Manisha H. Shah, Stephen Shibata, Jonathan R. Strosberg, Jean-Nicolas Vauthey, Rebekah White, James C. Yao, Deborah A. Freedman-Cass, Mary A. Dwyer
Journal: Journal of the National Comprehensive Cancer Network (2012)

Neuroendocrine tumors comprise a broad family of tumors, the most common of which are carcinoid and pancreatic neuroendocrine tumors. The NCCN Neuroendocrine Tumors Guidelines discuss the diagnosis and management of both sporadic and hereditary neuroendocrine tumors. Most of the recommendations pertain to well-differentiated, low- to intermediate-grade tumors. This updated version of the NCCN Guidelines includes a new section on pathology for diagnosis and reporting and revised recommendations for the surgical management of neuroendocrine tumors of the pancreas.
89P Surgical resection for lung oligometastases of breast cancer: A review of 31 cases
Authors: T. Kin, M. Kochi, M. Fujihara, Y. Yoshimura, Y. Kajiwara, M. Ito, T. Fujiwara, M. Matsuura, S. Takada, S. Ohtani
Journal: Annals of Oncology (2015)
Enzalutamide in Men with Chemotherapy-naïve Metastatic Castration-resistant Prostate Cancer: Extended Analysis of the Phase 3 PREVAIL Study
Authors: Tomasz M. Beer, Andrew J. Armstrong, Dana Rathkopf, Yohann Loriot, Cora N. Sternberg, Celestia S. Higano, Peter Iversen, Christopher P. Evans, Choung-Soo Kim, Go Kimura, Kurt Miller, Fred Saad, Anders S. Bjartell, Michael Borre, Peter Mulders, Teuvo L. Tammela, Teresa Parli, Suha Sari, Steve van Os, Ad Theeuwes, Bertrand Tombal
Journal: European Urology (2016)
Molecular Characterization Of Myelofibrosis Patients With Cytopenia Treated With Pomalidomide: Results From The Mpnsg 01-09 Study
Authors: Frank Stegelmann, Maximilian Laaths, Andreas Reiter, Edgar Jost, Martin Griesshammer, Norbert Gattermann, Holger Hebart, Cornelius F. Waller, Philippe Schafhausen, Uwe Platzbecker, Andreas Hochhaus, Walter Verbeek, Igor W. Blau, Carmen Blersch, Susanne Kuhn, Hartmut Döhner, Richard F. Schlenk, Konstanze Döhner
Journal: Blood (2013)
Congenital Zika syndrome with arthrogryposis: retrospective case series study
Authors: Vanessa van der Linden, Epitacio Leite Rolim Filho, Otavio Gomes Lins, Ana van der Linden, Maria de Fátima Viana Vasco Aragão, Alessandra Mertens Brainer-Lima, Danielle Di Cavalcanti Sousa Cruz, Maria Angela Wanderley Rocha, Paula Fabiana Sobral da Silva, Maria Durce Costa Gomes Carvalho, Fernando José do Amaral, Joelma Arruda Gomes, Igor Colaço Ribeiro de Medeiros, Camila V Ventura, Regina Coeli Ramos
Journal: BMJ (2016)

To describe the clinical, radiological, and electromyographic features in a series of children with joint contractures (arthrogryposis) associated with congenital infection presumably caused by Zika virus.Retrospective case series study.Association for Assistance of Disabled Children, Pernambuco state, Brazil.Seven children with arthrogryposis and a diagnosis of congenital infection presumably caused by Zika virus during the Brazilian microcephaly epidemic.Main clinical, radiological, and electromyographic findings, and likely correlation between clinical and primary neurological abnormalities.The brain images of all seven children were characteristic of congenital infection and arthrogryposis. Two children tested positive for IgM to Zika virus in the cerebrospinal fluid. Arthrogryposis was present in the arms and legs of six children (86%) and the legs of one child (14%). Hip radiographs showed bilateral dislocation in seven children, subluxation of the knee associated with genu valgus in three children (43%), which was bilateral in two (29%). All the children underwent high definition ultrasonography of the joints, and there was no evidence of abnormalities. Moderate signs of remodeling of the motor units and a reduced recruitment pattern were found on needle electromyography (monopolar). Five of the children underwent brain computed tomography (CT) and magnetic resonance imaging (MRI) and the remaining two CT only. All presented malformations of cortical development, calcifications predominantly in the cortex and subcortical white matter (especially in the junction between the cortex and white matter), reduction in brain volume, ventriculomegaly, and hypoplasia of the brainstem and cerebellum. MRI of the spine in four children showed apparent thinning of the cord and reduced ventral roots.Congenital Zika syndrome should be added to the differential diagnosis of congenital infections and arthrogryposis. The arthrogryposis was unrelated to the abnormalities of the joints themselves, but was possibly of neurogenic origin, with chronic involvement of central and peripheral motor neurones leading to deformities as a result of fixed postures in utero. Based on the neurophysiological observations, we suggest two possible mechanisms: tropism of neurones, with involvement of peripheral and central motor neurones, or a relation with vascular disorders.
From Emotional Tsunami to Empathy
Authors: Stephanie K. Doupnik
Journal: JAMA Pediatrics (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 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
New Pakistani visa controls leave patients from Afghanistan without treatment
Authors: Ashfaq Yusufzai
Journal: BMJ (2016)

People from Afghanistan travelling to neighbouring Pakistan for medical treatment are reporting increasing difficulties accessing hospitals after the Pakistan government introduced new visa controls last month.

Last year the Pakistan government imposed restrictions on Afghans’ access to local hospitals, forcing them to pay for treatment in private hospitals. And last month the authorities in Pakistan ended the free border crossing that patients from Afghanistan had used, after the killing of a Pakistan Army officer in Afghanistan on 14 June.

Khawaja Asif, Pakistan’s defence …