tbuckley/cabot-search huggingface dataset:
Abstract 15992: Post Operative Outcomes After Cardiac Surgery in Patients With Interstitial Lung Disease
Authors: Julius I Ejiofor, Gary M Hunninghake, Anthony V Norman, Fernando Ramirez-Del Val, Siobhan McGurk, Marc P Pelletier, Sary F Aranki, James Rawn, Prem S Shekar, Tsuyoshi Kaneko
Journal: Circulation (2016)

Introduction: Interstitial lung disease(ILD) is a risk factor for pulmonary complications after lung resection. Acute exacerbations are associated with high mortality. Surgical outcomes after cardi...
Transitions in <i>JAMA Psychiatry</i>
Authors: Dost Öngür
Journal: JAMA Psychiatry (2018)

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 Psychiatry 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 Psychiatry journal
Abstract 5733: IL-11 as a therapeutic target to treat colorectal cancer
Authors: Jennifer Huynh, Ashwini Chand, Matthias Ernst
Journal: Cancer Research (2018)

Abstract Introduction Colorectal cancer is a pressing health concern and there is a demand to develop novel therapeutics and improve current therapies to treat this disease. Immune checkpoint inhibitors (i.e. anti-PD-1 treatment) have been highly successful for the treatment of solid malignancies however, the majority of colorectal cancers do not typically respond to immunotherapy. Accumulating evidence alludes to a role for IL-11 signaling in tumor development although the mechanisms underlying IL-11 biology in colorectal cancer remain largely unknown. We postulate that IL-11 could be a mode of immunosuppression which can be targeted to overcome the poor responses of colorectal cancer to immunotherapy. Here we aim to investigate IL-11 signaling as a therapeutic strategy which can also be targeted in combination with anti-PD-1 treatment. Moreover, we present data that indicates an immunological function for IL-11 in modulating T cell anti-tumor activity. Method To assess the therapeutic potential for targeting IL-11 signaling in colon cancer in vivo, wild type and Il11r-/- C57BL/6 mice were injected subcutaneously in the flank on Day 0 with 1 x 106 MC38 colon cancer cells. The mice were then treated with an anti-PD-1 antibody i.p. dose once every 3 days. Mice were euthanised at Day 18. Harvested tumors were analysed by FACs and immunohistochemistry. To ascertain a role for IL-11 signaling in T cell activity, CD8+ and CD4+ T cells were FACs-sorted from wild type and il11r-/- mice, and activated with PMA/ionomycin for 24h. T cell activation was assessed by measuring mRNA levels of granzyme B and perforin by qPCR, and IFNγ production by ELISA. Results MC38 growth was attenuated in il11r-/- mice compared to wild type hosts. Lower tumor burden corresponded with a modest increase in tumor-infiltrating CD8+ T cells however we observed no differences in other immune cell subtypes (i.e. CD4+ T cells, MDSCs and macrophages). In addition, lower tumor burden corresponded with a marked reduction in Ki67 as assessed by immunohistochemistry. In addition, T cells harvested from il11r-/- hosts expressed lower levels of granzyme B, perforin and IFNγ under both basal conditions and following PMA/ionomycin stimulation. Conclusion Here we report that IL-11 signaling supports tumorigenesis using the MC38 colon cancer mouse model. For the first time, we have characterized a functional role for IL-11 in modulating T cell function. Overall, the findings from this study indicate IL-11R as a potential therapeutic target to improve the efficacy of immune checkpoint inhibitors for the treatment of colorectal cancer. Citation Format: Jennifer Huynh, Ashwini Chand, Matthias Ernst. IL-11 as a therapeutic target to treat colorectal cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 5733.
Human Salivary Amylase Gene Copy Number Impacts Oral and Gut Microbiomes
Authors: Angela C. Poole, Julia K. Goodrich, Nicholas D. Youngblut, Guillermo G. Luque, Albane Ruaud, Jessica L. Sutter, Jillian L. Waters, Qiaojuan Shi, Mohamed El-Hadidi, Lynn M. Johnson, Haim Y. Bar, Daniel H. Huson, James G. Booth, Ruth E. Ley
Journal: Cell Host & Microbe (2019)
Abstract 537: CK1 delta as a therapeutic target in bladder cancer
Authors: Chun-Han Chen
Journal: Cancer Research (2018)

Abstract Bladder cancer is a common malignancy worldwide, but targeted therapy is currently unavailable. Therefore, there is an unmet medical need for bladder cancer patients. Oncomine database revealed that gene expression of CK1 delta is higher in bladder cancer compared to normal tissue. The purpose of this study is to investigate the role of CK1 delta in the progression of bladder cancer, and the feasibility of CK1 delta as a therapeutic target. Lentiviral delivery of shRNA and CK1 delta inhibitors was used to modulate gene expression or kinase activity of CK1 delta in bladder cancer cell lines. Cell viability, cell cycle progression, apoptosis, migration and downstream signaling pathway were analyzed. The results showed that knocking down CK1 delta or treatment of CK1 delta inhibitors decreased cell viability and inhibited wnt/β-catenin pathway in bladder cancer cell lines. CK1 delta inhibitors increased the accumulation of sub-G1 phase by flow cytometry analysis, as well as the activation of caspase-3, 8, 9 and PARP cleavage by Western blot, indicating the promotion of cell apoptosis. Knocking down of CK1 delta and the treatment of CK1 delta inhibitors impaired cell migration activity, and altered protein expression of EMT markers, such as E-cadherin, vimentin, snail and slug. In conclusion, this study demonstrates that CK1 delta is a potential target for bladder cancer therapy. Citation Format: Chun-Han Chen. CK1 delta as a therapeutic target in bladder cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 537.
Abstract 17106: Impact of Communication Format and Risk Horizon on Patient Perceptions of CVD Risk: Findings From the PALM Registry
Authors: Ann M Navar, Tracy Y Wang, Pearl Zakroysky, Shuang Li, Anne C Goldberg, Jennifer G Robinson, Veronique L Roger, Salim S Virani, Peter W Wilson, L. Veronica Lee, Joseph Elassal, Eric D Peterson
Journal: Circulation (2016)

Background: Engaging patients in decision making regarding cardiovascular disease (CVD) prevention requires patients to understand their CVD risk, but optimal formats for communicating CVD risk are...
Combined CDK4/6 and Pan-mTOR Inhibition Is Synergistic Against Intrahepatic Cholangiocarcinoma
Authors: Xinhua Song, Xianqiong Liu, Haichuan Wang, Jingxiao Wang, Yu Qiao, Antonio Cigliano, Kirsten Utpatel, Silvia Ribback, Maria G. Pilo, Marina Serra, John D. Gordan, Li Che, Shanshan Zhang, Antonio Cossu, Alberto Porcu, Rosa M. Pascale, Frank Dombrowski, Hongbo Hu, Diego F. Calvisi, Matthias Evert, Xin Chen
Journal: Clinical Cancer Research (2018)

Intrahepatic cholangiocarcinoma (ICC) is an aggressive cancer type, lacking effective therapies and associated with a dismal prognosis. Palbociclib is a selective CDK4/6 inhibitor, which has been shown to suppress cell proliferation in many experimental cancer models. Recently, we demonstrated that pan-mTOR inhibitors, such as MLN0128, effectively induce apoptosis, although have limited efficacy in restraining proliferation of ICC cells. Here, we tested the hypothesis that palbociclib, due to its antproliferative properties in many cancer types, might synergize with MLN0128 to impair ICC growth.Human ICC cell lines and the AKT/YapS127A ICC mouse model were used to test the therapeutic efficacy of palbociclib and MLN0128, either alone or in combination.Administration of palbociclib suppressed in vitro ICC cell growth by inhibiting cell-cycle progression. Concomitant administration of palbociclib and MLN0128 led to a pronounced, synergistic growth constraint of ICC cell lines. Furthermore, while treatment with palbociclib or MLN0128 alone resulted in tumor growth reduction in AKT/YapS127A mice, a remarkable tumor regression was achieved when the two drugs were administered simultaneously. Mechanistically, palbociclib was found to potentiate MLN0128 mTOR inhibition activity, whereas MLN0128 prevented the upregulation of cyclin D1 induced by palbociclib treatment.Our study indicates the synergistic activity of palbociclib and MLN0128 in inhibiting ICC cell proliferation. Thus, combination of CDK4/6 and mTOR inhibitors might represent a novel, promising, and effective therapeutic approach against human ICC.See related commentary by Malumbres, p. 6.
Abstract LB-178: Oxidation markers in relation to prostate cancer and BPH and progression of prostate cancer
Authors: Tianying Wu, Bruce Bracken, Susan Kasper
Journal: Cancer Research (2018)

Abstract Prostate cancer (PCa) is the leading cancer affecting men of all races in the U.S. Benign prostatic hyperplasia (BPH) is prostate enlargement and is not malignant. BPH and PCa have similar symptoms and both have elevated PSA levels. A biomarker which can distinguish PCa from BPH will help the diagnosis of PCa and avoid unnecessary biopsies. Further, many PCa patients after prostatectomy can have recurrence. Currently, PSA is the only monitoring marker for recurrence; however, the underlying mechanism for recurrence is unknown. A mechanistic marker that can predict the progression and recurrence this will allow us to design prevention strategies. Many animal studies have linked oxidative stress with PCa progression and recurrence. The aim of this study is to compare the levels of several oxidation markers between PCa and BPH, and compare the levels of oxidation marker in different stages of PCa and determine their associations with PSA velocities after prostatectomy. We have measured multiple oxidation markers including lipid, protein, DNA, carbohydrate and global oxidation markers. We have collected blood samples among 15 BPH and 22 prostate cancer patients who have prostatectomy. We have found that levels of advanced glycation end products (AGEs), a marker of glucose oxidation, formed under nonenzymatic glycation of lipids and proteins, are higher in PCa patients than BPH. However, among PCa patients, AGEs levels are lower among those with Gleason score higher than 7 than those with Gleason score less than 7. Finally, we have found F2-isoprostanes, a well-established lipid oxidation marker, are associated with PSA velocities among PCa patients who had prostatectomy. Our results suggest that AGEs can help distinguish BPH and PCa but are associated with lower grade PCa. Measurement of F2-isoprostanes, a marker of lipid oxidation can predict PCa progression among men with prostatectomy. Citation Format: Tianying Wu, Bruce Bracken, Susan Kasper. Oxidation markers in relation to prostate cancer and BPH and progression of prostate cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr LB-178.
Edward “Eamonn” Michael Fottrell
Authors: Edward Fottrell
Journal: BMJ (2018)

Edward Michael Fottrell (“Eamonn”) was born in Youghal, County Cork, Ireland, in November 1935. Brother to Pat and Muriel, Eamonn enjoyed relaying tales of mischief and joy from his days growing up in the small coastal town. Encouraged by his mother and aunt to continue his education beyond school, he enrolled in teacher training, where he most likely would have continued, had he not become ill with tuberculosis in the mid-1950s. During an extended stay in hospital, he developed a fascination with medicine and, on discharge, changed to a medical degree.

After periods of general practice and psychiatry north and south of the Irish border, Eamonn moved to England, where he worked as a registrar in psychiatry at West Park Hospital in Epsom from 1966 to 1968. He left this post to travel—by bus—from London to Calcutta, India. He continued his adventures through Nepal and the Malay peninsula, …
Rise in Fall-Related Deaths
Authors: Bridget M. Kuehn
Journal: JAMA (2018)

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
HPV “Coverage”
Authors: Anne Schuchat
Journal: New England Journal of Medicine (2015)

This issue of the Journal presents a milestone in expanding the coverage of cancers associated with the human papillomavirus (HPV). Joura and colleagues1 report the results of a randomized, controlled trial of a new 9-valent HPV vaccine versus a quadrivalent HPV vaccine in more than 14,000 young women. The authors found that the new vaccine had an efficacy of nearly 97% against high-grade cervical, vulvar, and vaginal disease related to HPV types 31, 33, 45, 52, and 58. In the intention-to-treat analysis, the 9-valent vaccine was not found to be more beneficial than the quadrivalent vaccine, presumably because so many . . .
Horizontal transfer of BovB and L1 retrotransposons in eukaryotes
Authors: Atma M. Ivancevic, R. Daniel Kortschak, Terry Bertozzi, David L. Adelson
Journal: Genome biology (2018)

Transposable elements (TEs) are mobile DNA sequences, colloquially known as jumping genes because of their ability to replicate to new genomic locations. TEs can jump between organisms or species when given a vector of transfer, such as a tick or virus, in a process known as horizontal transfer. Here, we propose that LINE-1 (L1) and Bovine-B (BovB), the two most abundant TE families in mammals, were initially introduced as foreign DNA via ancient horizontal transfer events.Using analyses of 759 plant, fungal and animal genomes, we identify multiple possible L1 horizontal transfer events in eukaryotic species, primarily involving Tx-like L1s in marine eukaryotes. We also extend the BovB paradigm by increasing the number of estimated transfer events compared to previous studies, finding new parasite vectors of transfer such as bed bug, leech and locust, and BovB occurrences in new lineages such as bat and frog. Given that these transposable elements have colonised more than half of the genome sequence in today's mammals, our results support a role for horizontal transfer in causing long-term genomic change in new host organisms.We describe extensive horizontal transfer of BovB retrotransposons and provide the first evidence that L1 elements can also undergo horizontal transfer. With the advancement of genome sequencing technologies and bioinformatics tools, we anticipate our study to be a valuable resource for inferring horizontal transfer from large-scale genomic data.
Man with advanced MND vows to keep fighting for assisted death after losing case in Court of Appeal
Authors: Clare Dyer
Journal: BMJ (2018)

A man with advanced motor neurone disease who wants a doctor to help him end his life hopes to take his case to the UK Supreme Court after losing in the Court of Appeal.1

Noel Conway, 68, needs artificial ventilation for up to 23 hours a day and says that he feels “entombed” in his own body. He sought a court ruling that the blanket ban on assisting suicide in England and Wales breached his right to respect for his private life under the European Convention on Human Rights.

Conway proposed that assisted suicide should be allowed if an adult with mental capacity …
A multicentre randomized pilot trial on the effectiveness of different levels of cooling in comatose survivors of out-of-hospital cardiac arrest: the FROST-I trial
Authors: Esteban Lopez-de-Sa, Miriam Juarez, Eduardo Armada, José C. Sanchez-Salado, Pedro L. Sanchez, Pablo Loma-Osorio, Alessandro Sionis, Maria C. Monedero, Manuel Martinez-Sellés, Juán C. Martín-Benitez, Albert Ariza, Aitor Uribarri, José M. Garcia-Acuña, Patricia Villa, Pablo J. Perez, Christian Storm, Anne Dee, Jose L. Lopez-Sendon
Journal: Intensive Care Medicine (2018)
“Illogical” cannabis regulation blocks research into therapeutic uses, say doctors
Authors: Richard Hurley
Journal: BMJ (2018)

Doctors should be able to prescribe cannabis legally and research its therapeutic use more easily, 20 prominent UK clinicians and academics have said.

In a letter to The Times on 20 June,1 they “strongly urge the government” to recategorise cannabis from schedule 1 to schedule 2 under the UK Misuse of Drugs Regulations 2001.

Schedule 1 is for illicit substances deemed to have no clinical application and which doctors cannot prescribe; schedule 2 drugs, including, for example, diamorphine (heroin), are subject to requirements relating to prescriptions.

Last week, Savid Javid, the home secretary, said that a panel would be set up to review the evidence for medical cannabis that could see the drug rescheduled.2

Valerie Curran, professor of psychopharmacology at University College London and one of the letter’s …
Abstract 5145: PAH-metabolizing microorganism in the oral cavity of smokers
Authors: Guy R. Adami, Lin Tao, Sylvia Pavlova, Stefan J. Green, Ankur Naqib, Benjamin Salameh, Jessica L. Tang, Joel L. Schwartz
Journal: Cancer Research (2018)

Abstract Certain soil microorganisms have been identified as being not only resistant to polycyclic aromatic hydrocarbons (PAHs) but also capable of metabolizing these compounds. We hypothesized that a subset of oral bacteria may be enriched by the altered oral environment of the tobacco smoker with relatively high levels of PAHs. We identified microorganisms that survived long term in minimal media with PAH as the sole carbon source and showed they were much more likely to be isolated from smokers. To start to determine their contribution to oral health, we measured their level in vivo on two mucosal surfaces. On both gingival and lateral border of the tongue mucosa, a group of bacteria were seen to be at lower relative numbers in those exposed to cigarette smoke, while a minority increased. Three taxons were shown to be enriched on gingiva on the family, Streptococcaceae, or genus level, Staphylococcus and Granulicatella. On tongue, genera Mogibacterium and Dialister were enriched. Of bacteria genera that survived harsh PAH exposure in vitro, one was found at substantial levels in the oral mucosal microbiome. Staphylococcus was enriched approximately 6x in smokers, suggesting that the reason for its increase in smokers is due to its resistance to PAH. We will report on this and other oral microbes that can metabolize PAHs. This study highlights the possibility that the oral microbiome can metabolize PAHs like those in cigarette smoke, resulting in carcinogenic products that may contribute to the cancer process in vivo. Citation Format: Guy R. Adami, Lin Tao, Sylvia Pavlova, Stefan J. Green, Ankur Naqib, Benjamin Salameh, Jessica L. Tang, Joel L. Schwartz. PAH-metabolizing microorganism in the oral cavity of smokers [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 5145.
Abstract 1749: CXCR4 inhibition modulates tumor microenvironment and robustly inhibits growth of B16-OVA melanoma
Authors: Ruchi Saxena, Yan Wang, James W. Mier
Journal: Cancer Research (2018)

Abstract Background: The chemokine receptor CXCR4 is expressed on a range of immune cells. Additionally, CXCR4 has been found to be overexpressed in a variety of cancers and promotes cancer cell proliferation and metastasis, possibly by activating prosurvival signals that render cancer cells resistant to immune attack. Blockade of immune inhibitory pathways is emerging as an important therapeutic approach for the treatment of cancer. In our previous studies, X4-136, a CXCR4 antagonist, alone and in combination with various immune checkpoint inhibitor,s exhibited potent antitumor activity in the B16-OVA murine melanoma model. We report here results from additional in vivo studies as well as in vitro mechanistic experiments to determine the impact of CXCR4 inhibition on tumor cell gene expression and on immune phenotypes within the tumor microenvironment. Methods: B16-OVA cells were implanted into C57BL/6 mice. Seven days post implantation, mice were treated with X4-136, anti-PD-L1, or the combination for 16 days. At sacrifice, tumors were excised and flash frozen in liquid nitrogen for Western blot analysis or treated with collagenase for the analysis of subpopulations of T-cells by FACS. Gene expression was determined by PCR and protein expression was analyzed by Western blot. Results: X4-136 alone demonstrated more robust activity than anti-PD-L1. The antitumor activity of the anti-PD-L1 was further enhanced in combination with X4-136. Analysis of infiltrating immune cells by flow cytometry showed that X4-136 alone or in combination led to an increase of CD8+ T cells as well as CD8 and perforin double-positive T cells. A trend of decrease in both immunosuppressive populations, Treg and MDSC, was observed. This combination also led to a decrease in the expression of HIF-2α and cyclin D1 in comparison to tumors from vehicle-treated mice by Western blot analysis, suggesting an antiproliferative effect. Additional analysis of impacted genes and pathways will also be presented. Conclusion: X4-136 alone increased tumor-infiltrating CD8+ T-cells and exhibited potent antitumor activity in the B16-OVA murine melanoma model. The enhanced antitumor activity was observed when X4-136 was added to anti-PD-L1 treatment. The activities observed were associated with the improved CD8+ T cells to Treg cells ratio and with improved tumor microenvironment. Citation Format: Ruchi Saxena, Yan Wang, James W. Mier. CXCR4 inhibition modulates tumor microenvironment and robustly inhibits growth of B16-OVA melanoma [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 1749.