tbuckley/cabot-search huggingface dataset:
Composition, Spatial Characteristics, and Prognostic Significance of Myeloid Cell Infiltration in Pancreatic Cancer
Authors: Sara A. Väyrynen, Jinming Zhang, Chen Yuan, Juha P. Väyrynen, Andressa Dias Costa, Hannah Williams, Vicente Morales-Oyarvide, Mai Chan Lau, Douglas A. Rubinson, Richard F. Dunne, Margaret M. Kozak, Wenjia Wang, Diana Agostini-Vulaj, Michael G. Drage, Lauren Brais, Emma Reilly, Osama Rahma, Thomas Clancy, Jiping Wang, David C. Linehan, Andrew J. Aguirre, Charles S. Fuchs, Lisa M. Coussens, Daniel T. Chang, Albert C. Koong, Aram F. Hezel, Shuji Ogino, Jonathan A. Nowak, Brian M. Wolpin
Journal: Clinical Cancer Research (2020)

Although abundant myeloid cell populations in the pancreatic ductal adenocarcinoma (PDAC) microenvironment have been postulated to suppress antitumor immunity, the composition of these populations, their spatial locations, and how they relate to patient outcomes are poorly understood.
Re: Carlo A. Bravi, Nicoal Fossati, Giorgio Gandaglia, et al. Long-term Outcomes of Salvage Lymph Node Dissection for Nodal Recurrence of Prostate Cancer After Radical Prostatectomy: Not as Good as Previously Thought. Eur Urol 2020;78:661–9
Authors: Vérane Achard, Alan Dal Pra, Thomas Zilli
Journal: European Urology (2020)
Abstract 772: Calcitonin-gene Related Peptide Receptor Regulation In Human Heart Failure
Authors: Jamin Morrison, Christine S Moravec, W.H. Wilson Tang, Jeff Southard, Lee Southard, Randall C Starling, Sathyamangla V Naga Prasad
Journal: Circulation (2007)

Human alpha-Calcitonin gene-related peptide (CGRP) is a 37 amino-acid neuropeptide that is a potent vasodilator found widely in the nervous and cardiovascular systems. Plasma CGRP levels are signif...
286P Improved diagnostic accuracy on MR imaging in post-surgical recurrent head and neck SCC lesions using decision tree classification system
Authors: A. Jajodia, B. Amrith, A. Madhukar, A. Chaturvedi, A. Mehta, R. Kapur, A. Dewan, M. Agarwal, V. Mahwar, V. Yadav, S. Pasricha, V.P.B. Koyyala
Journal: Annals of Oncology (2020)
75P The evaluation of selective sensitivity of EZH2 inhibitors based on synthetic lethality in ARID1A-deficient gastric cancer
Authors: L. Yamada, M. Saito, K. Kase, S. Nakajima, E. Endo, D. Ujiie, A.K.T. Min, M. Ashizawa, T. Matsumoto, Y. Kanke, H. Nakano, M. Ito, H. Onozawa, H. Okayama, S. Fujita, W. Sakamoto, Z. Saze, T. Momma, K. Mimura, K. Kono
Journal: Annals of Oncology (2020)
Abstract PO-54: Mechanistic consequences of histone-deacetylase inhibition towards sensitizing PD1 blockade-resistant B-cell lymphomas
Authors: Xiaoguang Wang, Brittany C. Waschke, Rachel A. Woolaver, Zhangguo Chen, Gan Zhang, Anthony D. Piscopio, Xuedong Liu, Jing H. Wang
Journal: Blood Cancer Discovery (2020)

Abstract PD1 blockade is effective in a subset of B-cell lymphoma patients (e.g., classical Hodgkin lymphomas); however, most patients do not respond to anti-PD1 therapy. To overcome PD1 resistance, we employ a newly developed isoform-selective histone-deacetylase-inhibitor (HDACi) (OKI-179) and a novel mouse mature B-cell lymphoma, G1XP lymphoma, that resembles immunosuppressive features of human B-cell lymphomas including downregulation of major histocompatibility complex (MHC) class I and II, exhaustion of CD8 and CD4 tumor-infiltrating lymphocytes (TILs), and PD1-blockade resistance. Using multiple lymphoma models, we show that combined treatment of OKI-179/anti-PD1 significantly inhibited growth of B-cell lymphomas refractory to PD1 blockade; furthermore, sensitivity to single or combined treatment required tumor-derived MHC class I, and positively correlated to MHC class II level. We conclude that OKI-179 sensitizes lymphomas to PD1 blockade by enhancing tumor immunogenicity. Additionally, we found that different HDACi exhibited distinct effects on tumors and T cells, yet the same HDACi could differentially affect HLA expression on different human B-cell lymphomas. Thus, our study highlights the importance of immunologic effects of HDACi on antitumor responses and suggests that optimal treatment efficacy requires personalized design and rational combination based on prognostic biomarkers (e.g., MHCs) and unique profiles of HDACi. Citation Format: Xiaoguang Wang, Brittany C. Waschke, Rachel A. Woolaver, Zhangguo Chen, Gan Zhang, Anthony D. Piscopio, Xuedong Liu, Jing H. Wang. Mechanistic consequences of histone-deacetylase inhibition towards sensitizing PD1 blockade-resistant B-cell lymphomas [abstract]. In: Proceedings of the AACR Virtual Meeting: Advances in Malignant Lymphoma; 2020 Aug 17-19. Philadelphia (PA): AACR; Blood Cancer Discov 2020;1(3_Suppl):Abstract nr PO-54.
233TiP Pembrolizumab (pembro) or placebo added to docetaxel and prednisone/prednisolone for metastatic castration-resistant prostate cancer (mCRPC) previously treated with next-generation hormonal agents (NHAs): KEYNOTE-921 phase III study
Authors: D.P. Petrylak, N.D. Shore, M. Bennamoun, R. Ratta, J.M. Piulats, B. Li, C. Schloss, K. Fizazi
Journal: Annals of Oncology (2020)
17409 A new method for in vitro production of Fonsecaea pedrosoi fumagoid cells in a synthetic medium
Authors: Thelma Laura Orizaga y Quiroga, José E. Gonzalez, Carmen Molina-Torres, Debanhi K. Luna Garza, Sonia S. Ocampo-Garza
Journal: Journal of the American Academy of Dermatology (2020)
Balancing and Differentiating p53 Activities toward Longevity and No Cancer?
Authors: Izumi Horikawa
Journal: Cancer Research (2020)

Abstract Aging and death of cells (cellular senescence and apoptosis, respectively), triggered by or associated with cellular stress and DNA damage, impair organ function and homeostasis, leading to organismal aging and death. On the other hand, defects in physiologic regulations of cellular aging and death (escape from cellular senescence and failed apoptosis of severely damaged cells) contribute to uncontrolled cell division and genetic instability in cancer. In an oversimplified scenario, p53, an inducer of cellular senescence and apoptosis, may thus unfavorably contribute to aging and favorably suppress tumorigenesis. However, physiologic mechanisms should exist and therapeutic approaches may be developed to balance between aging and tumor suppression, for example, by differentially regulating cellular senescence, apoptosis, and other p53-mediated biological processes, such as DNA repair, autophagy, and energy metabolism. Possible mechanisms for such differential regulation of different subsets of p53 target genes may involve posttranslational modifications (e.g., phosphorylation and acetylation) and DNA binding cooperativity of p53. In this issue of Cancer Research, Timofeev and colleagues show that a previously uncharacterized phosphorylation in the p53 core DNA-binding domain regulates the DNA binding cooperativity and transcriptional activity of p53. Their mice deficient for this p53 phosphorylation were resistant to spontaneous and induced tumorigenesis, while they had shortened lifespan, but did not show progeria-like phenotypes. Prompted by this study, research on p53, aging, and cancer will explore balancing and differentiating different p53 activities toward a challenging goal of achieving longevity with no cancer. See related article by Timofeev et al., p. 5231
Interleukin-6 and Mycobacterium tuberculosis dormancy antigens improve diagnosis of tuberculosis
Authors: Ernest Adankwah, Norman Nausch, Difery Minadzi, Mohammed K. Abass, Kees L.M.C. Franken, Tom H.M. Ottenhoff, Ertan Mayatepek, Richard O. Phillips, Marc Jacobsen
Journal: Journal of Infection (2020)
Assessing the role of amino acids in systemic inflammation and organ failure in patients with ACLF
Authors: Giacomo Zaccherini, Ferran Aguilar, Paolo Caraceni, Joan Clària, Juan José Lozano, François Fenaille, Florence Castelli, Christophe Junot, Anna Curto, Chiara Formentin, Emmanuel Weiss, Mauro Bernardi, Rajiv Jalan, Paolo Angeli, Richard Moreau, Vicente Arroyo
Journal: Journal of Hepatology (2020)
Decreased IDO1-dependent tryptophan metabolism in aged lung during influenza
Authors: Soo Jung Cho, Kyung Sook Hong, Edward Schenck, Stefi Lee, Rebecca Harris, Jianjun Yang, Augustine M.K. Choi, Heather Stout-Delgado
Journal: European Respiratory Journal (2020)

Influenza epidemics remain a leading cause of morbidity and mortality worldwide. In the current study, we investigated the impact of chronological ageing on tryptophan metabolism in response to influenza infection. Examination of metabolites present in plasma collected from critically ill patients identified tryptophan metabolism as an important metabolic pathway utilised specifically in response to influenza. Using a murine model of influenza infection to further these findings illustrated that there was decreased production of kynurenine in aged lung in an indoleamine-pyrrole 2,3-dioxygenase-dependent manner that was associated with increased inflammatory and diminished regulatory responses. Specifically, within the first 7 days of influenza, there was a decrease in kynurenine pathway mediated metabolism of tryptophan, which resulted in a subsequent increase in ketone body catabolism in aged alveolar macrophages. Treatment of aged mice with mitoquinol, a mitochondrial targeted antioxidant, improved mitochondrial function and restored tryptophan metabolism. Taken together, our data provide additional evidence as to why older persons are more susceptible to influenza and suggest a possible therapeutic to improve immunometabolic responses in this population.
Robotic Surgery in Gastrointestinal Surgery
Authors: Kenoki Ohuchida
Journal: Cyborg and Bionic Systems (2020)

Robotic surgery is expanding in the minimally invasive treatment of gastrointestinal cancer. In the field of gastrointestinal cancer, robotic surgery is performed using a robot-assisted surgery system. In this system, the robot does not operate automatically but is controlled by the surgeon. The surgery assistant robot currently used in clinical practice worldwide is the leader-follower type, including the da Vinci® Surgical System (Intuitive Surgical). This review describes the current state of robotic surgery in the treatment of gastrointestinal cancer and discusses the future development of robotic systems in gastrointestinal surgery.
Changes in Racial Disparities in Mortality After Cancer Surgery in the US, 2007-2016
Authors: Miranda B. Lam, Katherine Raphael, Winta T. Mehtsun, Jessica Phelan, E. John Orav, Ashish K. Jha, Jose F. Figueroa
Journal: JAMA Network Open (2020)

<h3>Importance</h3> Racial disparities are well documented in cancer care. Overall, in the US, Black patients historically have higher rates of mortality after surgery than White patients. However, it is unknown whether racial disparities in mortality after cancer surgery have changed over time. <h3>Objective</h3> To examine whether and how disparities in mortality after cancer surgery have changed over 10 years for Black and White patients overall and for 9 specific cancers. <h3>Design, Setting, and Participants</h3> In this cross-sectional study, national Medicare data were used to examine the 10-year (January 1, 2007, to November 30, 2016) changes in postoperative mortality rates in Black and White patients. Data analysis was performed from August 6 to December 31, 2019. Participants included fee-for-service beneficiaries enrolled in Medicare Part A who had a major surgical resection for 9 common types of cancer surgery: colorectal, bladder, esophageal, kidney, liver, ovarian, pancreatic, lung, or prostate cancer. <h3>Exposures</h3> Cancer surgery among Black and White patients. <h3>Main Outcomes and Measures</h3> Risk-adjusted 30-day, all-cause, postoperative mortality overall and for 9 specific types of cancer surgery. <h3>Results</h3> A total of 870 929 cancer operations were performed during the 10-year study period. In the baseline year, a total of 103 446 patients had cancer operations (96 210 White patients and 7236 Black patients). Black patients were slightly younger (mean [SD] age, 73.0 [6.4] vs 74.5 [6.8] years), and there were fewer Black vs White men (3986 [55.1%] vs 55 527 [57.7%]). Overall national mortality rates following cancer surgery were lower for both Black (−0.12%; 95% CI, −0.17% to −0.06% per year) and White (−0.14%; 95% CI, −0.16% to −0.13% per year) patients. These reductions were predominantly attributable to within-hospital mortality improvements (Black patients: 0.10% annually; 95% CI, −0.15% to −0.05%;<i>P</i> &lt; .001; White patients: 0.13%; 95% CI, −0.14% to −0.11%;<i>P</i> &lt; .001) vs between-hospital mortality improvements. Across the 9 different cancer surgery procedures, there was no significant difference in mortality changes between Black and White patients during the period under study (eg, prostate cancer: 0.35; 95% CI, 0.02-0.68; lung cancer: 0.61; 95% CI, −0.21 to 1.44). <h3>Conclusions and Relevance</h3> These findings offer mixed news for policy makers regarding possible reductions in racial disparities following cancer surgery. Although postoperative cancer surgery mortality rates improved for both Black and White patients, there did not appear to be any narrowing of the mortality gap between Black and White patients overall or across individual cancer surgery procedures.
Blood Urea Nitrogen: A Marker for Adverse Effects of Loop Diuretics?⁎⁎Editorials published in the Journal of the American College of Cardiology reflect the views of the authors and do not necessarily represent the views of JACC or the American College of Cardiology
Authors: JoAnn Lindenfeld, Robert W. Schrier
Journal: Journal of the American College of Cardiology (2011)
Colchicine After Pulmonary Vein Isolation to Prevent the Early Recurrence of Atrial Fibrillation: Mollifying an Inflammatory Response?⁎⁎Editorials published in the Journal of the American College of Cardiology reflect the views of the authors and do not necessarily represent the views of JACC or the American College of Cardiology.
Authors: Gregory M. Marcus, Jonathan C. Hsu
Journal: Journal of the American College of Cardiology (2012)
鎌状赤血球貧血の腎症に対するロサルタン:フェーズ-2,多施設試験【Powered by NICT】
Authors: T Quinn Charles, L Saraf Santosh, R Gordeuk Victor, D Fitzhugh Courtney, E Creary Susan, Bodas Prasad, George Alex, B Raj Ashok, C Nero Alecia, E Terrell Catherine, McCord Lisa, Lane Adam, C Ackerman Hans, Yang Yu, Niss Omar, D Taylor Michael, Devarajan Prasad, Malik Punam
Journal: American Journal of Hematology (2017)
Efficacy of the bivalent HPV vaccine against HPV 16/18-associated precancer: long-term follow-up results from the Costa Rica Vaccine Trial
Authors: Carolina Porras, Sabrina H Tsang, Rolando Herrero, Diego Guillén, Teresa M Darragh, Mark H Stoler, Allan Hildesheim, Sarah Wagner, Joseph Boland, Douglas R Lowy, John T Schiller, Mark Schiffman, John Schussler, Mitchell H Gail, Wim Quint, Rebeca Ocampo, Jorge Morales, Ana C Rodríguez, Shangying Hu, Joshua N Sampson, Aimée R Kreimer, Bernal Cortés, Paula González, Rolando Herrero, Silvia E Jiménez, Carolina Porras, Ana Cecilia Rodríguez, Allan Hildesheim, Aimée R Kreimer, Douglas R Lowy, Mark Schiffman, John T Schiller, Mark Sherman, Ligia A Pinto, Troy J Kemp, Mary K Sidawy, Wim Quint, Leen-Jan Van Doorn, Linda Struijk, Joel M Palefsky, Teresa M Darragh, Mark H Stoler
Journal: The Lancet Oncology (2020)
Myocardial Perfusion Imaging and Multidetector Computed Tomographic Coronary Angiography: Appropriate for All Patients With Suspected Coronary Artery Disease?⁎⁎Editorials published in the Journal of the American College of Cardiologyreflect the views of the authors and do not necessarily represent the views of JACCor the American College of Cardiology.
Authors: Sharmila Dorbala, Rory Hachamovitch, Marcelo F. Di Carli
Journal: Journal of the American College of Cardiology (2006)
Sphingosine-1-Phosphate Receptor 3 Potentiates Inflammatory Programs in Normal and Leukemia Stem Cells to Promote Differentiation
Authors: Stephanie Z. Xie, Kerstin B. Kaufmann, Weijia Wang, Michelle Chan-Seng-Yue, Olga I. Gan, Elisa Laurenti, Laura Garcia-Prat, Shin-ichiro Takayanagi, Stanley W.K. Ng, ChangJiang Xu, Andy G.X. Zeng, Liqing Jin, Jessica McLeod, Elvin Wagenblast, Amanda Mitchell, James A. Kennedy, Qiang Liu, Héléna Boutzen, Melissa Kleinau, Joseph Jargstorf, Gareth Holmes, Yang Zhang, Veronique Voisin, Gary D. Bader, Jean C.Y. Wang, Yusuf A. Hannun, Chiara Luberto, Timm Schroeder, Mark D. Minden, John E. Dick
Journal: Blood Cancer Discovery (2020)

Abstract Acute myeloid leukemia (AML) is a caricature of normal hematopoiesis driven from leukemia stem cells (LSC) that share some hematopoietic stem cell (HSC) programs including responsiveness to inflammatory signaling. Although inflammation dysregulates mature myeloid cells and influences stemness programs and lineage determination in HSCs by activating stress myelopoiesis, such roles in LSCs are poorly understood. Here, we show that S1PR3, a receptor for the bioactive lipid sphingosine-1-phosphate, is a central regulator that drives myeloid differentiation and activates inflammatory programs in both HSCs and LSCs. S1PR3-mediated inflammatory signatures varied in a continuum from primitive to mature myeloid states across cohorts of patients with AML, each with distinct phenotypic and clinical properties. S1PR3 was high in LSCs and blasts of mature myeloid samples with linkages to chemosensitivity, whereas S1PR3 activation in primitive samples promoted LSC differentiation leading to eradication. Our studies open new avenues for therapeutic target identification specific for each AML subset. Significance: S1PR3 is a novel regulator of myeloid fate in normal hematopoiesis that is heterogeneously expressed in AML. S1PR3 marks a subset of less primitive AML cases with a distinct inflammatory signature and therefore has clinical implications as both a therapeutic target and a biomarker to distinguish primitive from mature AML. See related commentary by Yang et al., p. 3. This article is highlighted in the In This Issue feature, p. 1
Genetic Architecture of Bipolar Disorder in Individuals of Han Chinese and European Ancestries
Authors: Niamh Mullins, Hailiang Huang
Journal: JAMA Psychiatry (2020)

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Author Correction: Ensemble learning predicts multiple sclerosis disease course in the SUMMIT study
Authors: Yijun Zhao, Summit Investigators, Tong Wang, Riley Bove, Bruce Cree, Roland Henry, Hrishikesh Lokhande, Mariann Polgar-Turcsanyi, Mark Anderson, Rohit Bakshi, Howard L. Weiner, Tanuja Chitnis
Journal: npj Digital Medicine (2020)

A correction to this paper has been published: https://doi.org/10.1038/s41746-020-00361-9.
Blocking of Transient Receptor Potential Vanilloid 1 (TRPV1) promotes terminal mitophagy in multiple myeloma, disturbing calcium homeostasis and targeting ubiquitin pathway and bortezomib-induced unfolded protein response
Authors: Katia Beider, Evgenia Rosenberg, Valeria Dimenshtein-Voevoda, Yaarit Sirovsky, Julia Vladimirsky, Hila Magen, Olga Ostrovsky, Avichai Shimoni, Zohar Bromberg, Lola Weiss, Amnon Peled, Arnon Nagler
Journal: Journal of Hematology & Oncology (2020)

Abstract Background Chemoresistance remains a major treatment obstacle in multiple myeloma (MM). Novel new therapies are thus in need. Transient Receptor Potential Vanilloid type 1 (TRPV1) is a calcium-permeable ion channel that has been demonstrated to be expressed in solid tumors. Calcium channels have been shown to be involved in the regulation of cell proliferation, chemoresistance, migration and invasion. The aim of the current study was to evaluate its possible role in MM. Methods Pharmacological inhibitor was used to evaluate the role of TRPV1 in MM cell lines and primary MM cells. Flow cytometry, molecular analysis, fluorescent microscopy, proteomic analysis and xenograft in vivo model of MM with BM involvement were employed to assess the effect of TRPV1 inhibition and decipher its unique mechanism of action in MM. Results TRPV1 was found to be expressed by MM cell lines and primary MM cells. TRPV1 inhibition using the antagonist AMG9810-induced MM cell apoptosis and synergized with bortezomib, overcoming both CXCR4-dependent stroma-mediated and acquired resistance. In accordance, AMG9810 suppressed the expression and activation of CXCR4 in MM cells. TRPV1 inhibition increased mitochondrial calcium levels with subsequent mitochondrial ROS accumulation and depolarization. These effects were reversed by calcium chelation, suggesting the role of calcium perturbations in oxidative stress and mitochondrial destabilization. Furthermore, AMG9810 abolished bortezomib-induced accumulation of mitochondrial HSP70 and suppressed protective mitochondrial unfolded protein response. Proteomics revealed unique molecular signature related to the modification of ubiquitin signaling pathway. Consequently, 38 proteins related to the ubiquitylation machinery were downregulated upon combined bortezomib/AMG9810 treatment. Concomitantly, AMG9810 abolished bortezomib-induced ubiquitination of cytosolic and mitochondrial proteins. Furthermore, bortezomib/AMG9810 treatment induced mitochondrial accumulation of PINK1, significantly reduced the mitochondrial mass and promoted mitochondrial-lysosomal fusion, indicating massive mitophagy. Finally, in a recently developed xenograft model of systemic MM with BM involvement, bortezomib/AMG9810 treatment effectively reduced tumor burden in the BM of MM-bearing mice. Conclusions Altogether, our results unravel the mechanism mediating the strong synergistic anti-MM activity of bortezomib in combination with TRPV1 inhibition which may be translated into the clinic.