tbuckley/cabot-search huggingface dataset:
Abstract 14173: Stable Incidence of Acute Aortic Syndrome From 1995-2015
Authors: Randall DeMartino, Sen Indrani, Ying Huang, William S Harmsen, Thanila Macedo, Jay Mandrekar, Alanna M Chamberlain, Philip P Goodney, Veronique Roger
Journal: Circulation (2017)

Introduction: Acute aortic syndromes (AAS), including aortic dissection (AD), intramural hematoma (IMH) and penetrating aortic ulcer (PAU), carry significant acute and long-term morbidity and morta...
Progress toward measles elimination--Western Pacific Region, 2009-2012.
Authors: W. William Schluter, Wang Xiaojun, Jorge Mendoza-Aldana, Youngmee Jee, Sergey Diorditsa, Alya Dabbagh, Mick Mulders, Christopher Gregory, James L. Goodson
Journal: MMWR Morbidity and Mortality Weekly Report (2013)
FRI-198-A Phase, double-blind, randomized, placebo-controlled, first-in-human study of the safety, tolerability, pharmacokinetics and pharmacodynamics of oral JNJ-64794964, a toll-like receptor-7 agonist, in healthy adults
Authors: Ed Gane, Mina Pastagia, An De Creus, Christian Schwabe, Joris Vandenbossche, Leen Slaets, Bart Fevery, Liviawati S Wu, Rui Li, Samia Siddiqui, Abbie Oey, Clark Musto, Bruce Bryan, Pieter Van Remoortere
Journal: Journal of Hepatology (2019)
FRI-432-Current long-term outcome of 302 patients with noncirrhotic nontumoral extrahepatic portal vein thrombosis
Authors: Hui Chen, Chuangye He, Yong Lv, jiahao fan, Qiuhe Wang, Shihao Tang, Jing Niu, Jie Yuan, Zhanxin Yin, Guohong Han
Journal: Journal of Hepatology (2019)
Abstract 17816: KChIP2 Regulates Cardiac Excitability and Ion Channel Dysregulation by Novel Transcriptional Regulation of miR-34s
Authors: Drew Nassal, Haiyan Liu, Xiaoping Wan, Eckhard Ficker, Isabelle Deschenes
Journal: Circulation (2014)

Cardiac ion channel dysregulation is a hallmark of heart failure. Consistently, the disease yields dramatic decline in Ito through loss in Kv4 and its auxiliary partner K+ channel interacting prote...
The Chinese Society of Clinical Oncology (CSCO): clinical guidelines for the diagnosis and treatment of gastric cancer
Authors: Feng‐Hua Wang, Lin Shen, Jin Li, Zhi‐Wei Zhou, Han Liang, Xiao‐Tian Zhang, Lei Tang, Yan Xin, Jing Jin, Yu‐Jing Zhang, Xiang‐Lin Yuan, Tian‐Shu Liu, Guo‐Xin Li, Qi Wu, Hui‐Mian Xu, Jia‐Fu Ji, Yuan‐Fang Li, Xin Wang, Shan Yu, Hao Liu, Wen‐Long Guan, Rui‐Hua Xu
Journal: Cancer Communications (2019)

Abstract China is one of the countries with the highest incidence of gastric cancer. There are differences in epidemiological characteristics, clinicopathological features, tumor biological characteristics, treatment patterns, and drug selection between gastric cancer patients from the Eastern and Western countries. Non‐Chinese guidelines cannot specifically reflect the diagnosis and treatment characteristics for the Chinese gastric cancer patients. The Chinese Society of Clinical Oncology (CSCO) arranged for a panel of senior experts specializing in all sub‐specialties of gastric cancer to compile, discuss, and revise the guidelines on the diagnosis and treatment of gastric cancer based on the findings of evidence‐based medicine in China and abroad. By referring to the opinions of industry experts, taking into account of regional differences, giving full consideration to the accessibility of diagnosis and treatment resources, these experts have conducted experts’ consensus judgement on relevant evidence and made various grades of recommendations for the clinical diagnosis and treatment of gastric cancer to reflect the value of cancer treatment and meeting health economic indexes. This guideline uses tables and is complemented by explanatory and descriptive notes covering the diagnosis, comprehensive treatment, and follow‐up visits for gastric cancer.
Inhibition of protein disulfide isomerase in glioblastoma causes marked downregulation of DNA repair and DNA damage response genes
Authors: Shili Xu, Yajing Liu, Kai Yang, Hanxiao Wang, Andrea Shergalis, Anahita Kyani, Armand Bankhead, Shuzo Tamura, Suhui Yang, Xi Wang, Chih-Chen Wang, Alnawaz Rehemtulla, Mats Ljungman, Nouri Neamati
Journal: Theranostics (2019)

Aberrant overexpression of endoplasmic reticulum (ER)-resident oxidoreductase protein disulfide isomerase (PDI) plays an important role in cancer progression. In this study, we demonstrate that PDI promotes glioblastoma (GBM) cell growth and describe a class of allosteric PDI inhibitors that are selective for PDI over other PDI family members.
Prognostic significance of β2 adrenergic receptor expression in the patients with non-small cell lung cancer.
Authors: Tomohiro Yazawa, Kyoichi Kaira, Akira Shimizu, Toshiteru Nagashima, Yoichi Ohtaki, Kai Obayashi, Takayuki Asao, Tetsunari Oyama, Izumi Takeyoshi, Kimihiro Shimizu
Journal: Journal of Clinical Oncology (2015)

11081 Background: β2 adrenergic receptor (β2-AR) is highlty expressed in cancer cells and has a relationship with tumor cell progression and metastases. However, it remains unclear about the prognostic role of β2-AR expression in non-small cell lung cancer (NSCLC). The aim of this study is to clarify the clinicopathological importance of β2-AR expression in patients with NSCLC. Methods: Three hundreds and twenty eight patients with surgically resected NSCLC were investigated retrospectively. Tumor sections were stained by immunohistochemistry for β2-AR, Ki-67, and microvessel density (MVD) determined by CD34. Results: β2-AR was positively expressed in 27% of all patients, 29% of adenocarcinoma (AC) patients, and 24% of non-AC patients, respectively. The β2-AR expression was significantly correlated with lymphatic permeation (r = 0.240, p < 0.001) and vascular invasion (r = 0.239, p < 0.001), and Ki-67 (r = 0.175, p = 0.009) in AC patients, but not non-AC. A positive β2-AR expression indicated poor prognosis of AC patients (overall survival, OS: p = 0.045; progression-free survival, PFS: p = 0.001), especially stage I (OS, p = 0.017; PFS, p = 0.003). Multivaritate analysis confirmed that β2-AR expression was an independent factor for predicting poor progression-free survival in stage I AC patients (hazard ratio: 2.220; 95% confidence interval: 1.077-4.573; p = 0.031). Conclusions: β2-AR expression was identified as an independent prognostic factor for early stage AC patients. β2-AR could be a promising marker for predicting outcome after surgery in lung cancer.
Retrospective analysis between PD-L1 expression and prognosis for stage III non-small cell lung cancer patients who received concurrent chemoradiotherapy.
Authors: Takaaki Tokito, Koichi Azuma, Hidenobu Ishii, Kazuhiko Yamada, Tomoaki Hoshino
Journal: Journal of Clinical Oncology (2015)

7542 Background: Programmed cell death 1 (PD-1) receptor-ligand interaction is a major pathway often hijacked by tumors in order to suppress immune control. We investigated whether the expression of programmed death–ligand 1 (PD-L1) is related to clinicopathologic or prognostic factors in patients with locally advanced NSCLC who received concurrent chemoradiotherapy (CRT). Methods: We retrospectively reviewed consecutive stage III NSCLC patients who received CRT at Kurume University. The expression of PD-L1 was evaluated by immunohistochemical analysis in specimens of NSCLC. Survival analysis was obtained by Kaplan-Meier methods. Results: A total of 52 patients with a median age of 67 years were eligible for this study. Forty-three patients were men, and 46 patients were current or ever smokers. The most predominant histological type was adenocarcinoma (28 patients), followed by squamous cell carcinoma (21 patients). All of the patients received platinum-based doublets. Expression of PD-L1 in tumor cells was observed in 73%. NSCLC patients with PD-L1-negative tumors showed longer progression-free and overall survival than those with PD-L1-positive (median PFS, 17 versus 11 months; p = 0.31, median OS, 52 vs 25 months; P = 0.38; respectively), and higher progression-free rate at 2 years and overall survival rate (38% and 26%, 83% and 52%, respectively). Conclusions: There was a trend toward a poor survival in expression of PD-L1 in stage III NSCLC patients who received CRT.
Cellular Plasticity in Cancer
Authors: Salina Yuan, Robert J. Norgard, Ben Z. Stanger
Journal: Cancer Discovery (2019)

Abstract During cancer progression, tumor cells undergo molecular and phenotypic changes collectively referred to as cellular plasticity. Such changes result from microenvironmental cues, stochastic genetic and epigenetic alterations, and/or treatment-imposed selective pressures, thereby contributing to tumor heterogeneity and therapy resistance. Epithelial–mesenchymal plasticity is the best-known case of tumor cell plasticity, but recent work has uncovered other examples, often with functional consequences. In this review, we explore the nature and role(s) of these diverse cellular plasticity programs in premalignant progression, tumor evolution, and adaptation to therapy and consider ways in which targeting plasticity could lead to novel anticancer treatments. Significance: Changes in cell identity, or cellular plasticity, are common at different stages of tumor progression, and it has become clear that cellular plasticity can be a potent mediator of tumor progression and chemoresistance. Understanding the mechanisms underlying the various forms of cell plasticity may deliver new strategies for targeting the most lethal aspects of cancer: metastasis and resistance to therapy.
Learning About Dupilumab-Associated Conjunctivitis
Authors: Aleksi J. Hendricks, Vivian Y. Shi
Journal: JAMA Dermatology (2019)

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 Dermatology 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 Dermatology journal
SAT-397-HIC-5 and GARP expression is upregulated by hydrogen peroxide and TGF beta in primary human hepatic stellate cells cultured on decellularized human liver 3D ECM scaffolds
Authors: Simona Onali, Elisabetta Caon, Kessarin Thanapirom, Martina Marrali, Maria Giovanna Vilia, Luca Frenguelli, Walid Al-Akkad, Giuseppe Mazza, Massimo Pinzani, Krista Rombouts
Journal: Journal of Hepatology (2019)
Abstract 12302: Transition Readiness in Teens and Young Adults With Congenital Heart Disease: Can We Make a Difference?
Authors: Karen Uzark, Sunkyung Yu, Ray Lowery, Katherine Afton, Angela Yetman, Jonathan Cramer, Nancy Rudd, Scott Cohen, Russell Gongwer, Michelle Gurvitz
Journal: Circulation (2018)

Introduction: Transition is “the process by which adolescents and young adults with chronic childhood illnesses are prepared to take charge of their lives and their health in adulthood”. We previou...
Multivariate survival analysis of adult malignant melanoma in Florida: An analysis from a population-based cancer registry (1981-2009).
Authors: Kevin Joseph Moore, Erin Dunn, Feng Miao, Tulay Koru-Sengul
Journal: Journal of Clinical Oncology (2015)

e20100 Background: Malignant melanoma (MM) is one of the most aggressive neoplasms of melanocytes. In the US, melanoma of the skin accounts for 4.6% of all new cancers and 1.7% of all cancer deaths. Statewide population based cancer registries provide prevalence, trend, and determinant data to identify disparities in the burden and survival of MM. We report the sociodemographics and survival of MM in the Florida adult population ( ≥ 18 yrs) to identify the disparities between gender, racial, ethnic, socioeconomic (SES) groups, and mortality. Methods: Data from the Florida Cancer Data System (1981-2009) was linked with US census to explore median survival and 1-, 3-, 5-year survival rates by demographic characteristics for MM. Survival was compared by gender, race, ethnicity, SES. Multivariate Cox regression was used to obtain hazard ratio (HR) and 95% confidence interval (95%CI). Results: There were 54,296 patients with MM where majority was male (59%), White (99%), never smoked (39%), middle-high/highest SES (75%) and living in urban setting (95%). Overall median survival was 4.8 yrs (95%CI: 4.7-4.9) where Whites had the longest (4.8; 4.7-4.9) compared to Blacks (2.5;2.0-3.2) and Others (4.1;2.8-5.9). Overall 5-year survival rate was 49%, but the rates were higher for Whites (49%) than Blacks (31%) and Others (39%). Compared to Whites, Blacks had significantly worse survival (HR = [1.43]; 95%CI: 1.16-1.76). Females had significantly better survival compared to males ([0.78]; 0.71-0.81). There was a monotonic significant improvement in survival for each higher SES category. Older age was also negatively associated with survival ([1.03];1.03-1.03). Current smokers had worse survival than those who had never smoked ([1.25]; 1.18-1.33). Conclusions: Our results show clear gender, racial, ethnic, SES and smoking status disparities in survival for those diagnosed with MM. With the incidence of MM on the rise, it is important to address these sociodemographic disparities and recognize the increased need for specific interventions to promote skin cancer awareness, detection, and access to treatment.
Noncanonical TGFβ Pathway Relieves the Blockade of IL1β/TGFβ-Mediated Crosstalk between Tumor and Stroma: TGFBR1 and TAK1 Inhibition in Colorectal Cancer
Authors: Natalia Guillén Díaz-Maroto, Rebeca Sanz-Pamplona, Mireia Berdiel-Acer, Francisco J. Cimas, Elena García, Samuel Gonçalves-Ribeiro, Nerea Albert, Gemma Garcia-Vicién, Gabriel Capella, Victor Moreno, Ramon Salazar, Alberto Villanueva, David G. Molleví
Journal: Clinical Cancer Research (2019)

Abstract Purpose: The aim of the study is blocking the recruitment of a protective stroma by altering the crosstalk between normal stromal cells and tumor cells for stripping tumors of the protection conferred by the microenvironment. Experimental Design: A transcriptomic analysis of cocultured normal colonic fibroblasts and colorectal tumor cells was performed. We focused on the study of molecules that mediate the communication between both compartments and that entail fibroblasts’ activation and the alteration of the sensitivity to chemotherapy. We identified targets for the blocking of the tumor–stroma interaction. Finally, we tested, in vivo, the blockade of the tumor–stroma interaction in orthotopic models derived from patients and in models of acquired resistance to oxaliplatin. Results: IL1β/TGFβ1 are the triggers for fibroblasts’ recruitment and conversion into carcinoma-associated fibroblasts (CAF) in colorectal cancer. CAFs then secrete proinflammatory factors that alter sensitivity in tumor cells, activating JAK/STAT and PI3KCA/AKT pathways. Blocking such crosstalk with a neutralizing IL1β antibody and a TGFBR1 inhibitor is relieved by the TAK1-mediated activation of the noncanonical TGFβ pathway, which induces a change in the cytokine/chemokine repertoire that maintains a sustained activation of AKT in tumor cells. TAK1 plus TGFBR1 inhibition blocks IL1β/TGFβ1-mediated fibroblast activation, decreasing the secretion of proinflammatory cytokines. In turn, tumor cells became more sensitive to chemotherapy. In vivo, the combination of a TAK1 inhibitor plus TGFBR1 inhibitor reduced the metastatic capacity of tumor cells and the recruitment of fibroblasts. Conclusions: Our findings provide a translational rationale for the inhibition of TAK1 and TGFBR1 to remove the chemoprotection conferred by CAFs.
The rational of treating the primary cancer in patients with metastatic disease.
Authors: Petr Frantisek Hausner
Journal: Journal of Clinical Oncology (2015)

e22218 Background: The value of treating the primary cancer in patients with metastatic disease is unknown. The differential response of the primary and metastases cannot be studied in clinical trials which use RECIST for evaluation of response, since the response of the primary is not distinguished from responses of metastases. Methods: The rational for addressing the primary separately, e.g. by surgery or radiation, while treating with systemic therapy is deduced from novel information about the development of tumor heterogeneity over time and from reinterpretation of data from trials of adjuvant chemotherapy. Results: Since the extent of tumor heterogeneity increases with time, one can assume that the primary tumor, which developed over a long period of time, during which novel clones appeared, expanded and competed with the older ones, is more heterogeneous than a metastasis, which expanded from one or a small group of cells over a shorter period of time. This is now well documented by dendrograms of sequenced primaries and respective metastases. It is obvious, that the less heterogenous the composition of a tumorous lesion, the better the chance to identify systemic therapy, which would destroy the lesion. Thus, predictive models show that it is easier to destroy metastases, than the primary tumor. This is clearly shown by a great wealth of data geathered in clinical trials of adjuvant chemotherapy, in which the primary was removed surgically, and micrometastatic disease treated with chemotherapy. Consistently 10% of patients with micrometastatic disease are cured of their disease. A fair question is how often macrometastatic disease can be cured in the absence of a primary. Conclusions: Clinical trials should collect data allowing answering the question about the benefit of treating the primary. Response criteria should not treat all disease sites the same, but distinguish sites by presumed or documented tumor heterogeneity. Also simple stratification by whether the primary is present or absent should be entertained in analyzing clinical trials. Clinical trials in diseases with a pronounced difference in heterogeneity between the primary and metastases should address the question of treating the primary tumor in light of metastases.
PS-072-Is homelessness the biggest hurdle to treatment success in the management of HCV in the era of direct acting antivirals? Results from the TraP HepC nationwide treatment initiative in Iceland
Authors: Magnús Gottfredsson, Thorvardur Love, Ragnheidur H. Fridriksdottir, Thorarinn Tyrfingsson, Valgerdur Runarsdottir, Ingunn Hansdottir, Ottar M. Bergmann, Einar S. Bjornsson, Birgir Johannsson, Bryndis Sigurdardottir, Arthur Löve, Gudrun Sigmundsdottir, Kamilla Josefsdottir, Ubaldo B. Hernandez, Maria Heimisdottir, Sigurdur Olafsson
Journal: Journal of Hepatology (2019)
Bone Morphogenetic Protein 9 Is a Paracrine Factor Controlling Liver Sinusoidal Endothelial Cell Fenestration and Protecting Against Hepatic Fibrosis
Authors: Agnès Desroches‐Castan, Emmanuelle Tillet, Nicolas Ricard, Marie Ouarné, Christine Mallet, Lucid Belmudes, Yohann Couté, Olivier Boillot, Jean‐Yves Scoazec, Sabine Bailly, Jean‐Jacques Feige
Journal: Hepatology (2019)

Bone morphogenetic protein 9 (BMP9) is a circulating factor produced by hepatic stellate cells that plays a critical role in vascular quiescence through its endothelial receptor activin receptor‐like kinase 1 (ALK1). Mutations in the gene encoding ALK1 cause hereditary hemorrhagic telangiectasia type 2, a rare genetic disease presenting hepatic vessel malformations. Variations of both the circulating levels and the hepatic mRNA levels of BMP9 have been recently associated with various forms of hepatic fibrosis. However, the molecular mechanism that links BMP9 with liver diseases is still unknown. Here, we report that Bmp9 gene deletion in 129/Ola mice triggers hepatic perisinusoidal fibrosis that was detectable from 15 weeks of age. An inflammatory response appeared within the same time frame as fibrosis, whereas sinusoidal vessel dilation developed later on. Proteomic and mRNA analyses of primary liver sinusoidal endothelial cells (LSECs) both revealed that the expression of the LSEC‐specifying transcription factor GATA‐binding protein 4 was strongly reduced in Bmp9 gene knockout ( Bmp9 ‐KO) mice as compared with wild‐type mice. LSECs from Bmp9 ‐KO mice also lost the expression of several terminal differentiation markers ( Lyve1 , S tab1 , Stab2 , Ehd3 , Cd209b , eNos, Maf , Plvap ). They gained CD34 expression and deposited a basal lamina, indicating that they were capillarized. Another main characteristic of differentiated LSECs is the presence of permeable fenestrae. LSECs from Bmp9 ‐KO mice had a significantly reduced number of fenestrae. This was already observable in 2‐week‐old pups. Moreover, we could show that addition of BMP9 to primary cultures of LSECs prevented the loss of their fenestrae and maintained the expression levels of Gata4 and Plvap . Conclusion: Taken together, our observations show that BMP9 is a key paracrine regulator of liver homeostasis, controlling LSEC fenestration and protecting against perivascular hepatic fibrosis.
Metastatic breast cancer patients: Attitudes toward tissue donation for rapid autopsy.
Authors: Tala Achkar, John W Wilson, Jacqueline Simon, Margaret Quinn Rosenzweig, Shannon Leigh Huggins-Puhalla
Journal: Journal of Clinical Oncology (2015)

e20502 Background: Rapid autopsy (RA) offers a unique opportunity to obtain a large amount of metastatic tissue and deepen understanding of cancer evolution and heterogeneity. Studies suggest that patients and families may look favorably on RA. We aimed to elucidate the attitudes of patients with metastatic breast cancer (MBC) toward RA and to identify associated demographic or disease characteristics that may influence patient interest. Methods: Surveys were completed by 93 MBC patients at the UPMC Womens Cancer Center outpatient clinic. Data collected included demographics, disease characteristics, time with metastatic disease, willingness to donate tissue at death, and preferred time to be asked about tissue donation. Fischer’s exact test was employed for categorical variables, and t-test and rank sum tests for continuous variables. p-values ≤ 0.05 were considered statistically significant. Results: Of the 93 MBC patients, 87% were willing to donate tissue at death. Marital status was associated with willingness to donate, with divorced, separated, or widowed patients less likely to donate (p = 0.000). Race, employment status, religion, and cancer subtype were not associated with likelihood of donating. Younger people were more willing to donate to RA (p = 0.025; mean age 56.2 vs 64.4 for patients with positive and negative attitudes, respectively). The number of lines of chemotherapy was not significantly associated with attitude toward RA. The median time from cancer diagnosis to metastasis was 36.2 months in those willing to donate and 67.4 in those who were not, but this difference was not statistically significant (p = 0.32). 45% of patients felt that doctors should ask about RA at diagnosis of early stage breast cancer. Conclusions: Patient attitudes toward RA are positive, particularly among younger patients. There is an association between more aggressive disease and a positive attitude toward donation, possibly due to altruistic motivations to contribute to the field. Nearly half of the patients felt that the most appropriate time to discuss RA was early in their disease course. These data provide evidence that an RA program would be welcomed by patients and requires initiative by providers.