tbuckley/cabot-search huggingface dataset:
The Great Mimicker—Tuberculosis Involving Prostate and Vertebrae Posing as Metastatic Prostate Carcinoma on FDG PET/CT
Authors: Prathamesh Vijay Joshi, Balaji Shewalkar, Thomas George, Shrikant Sahasrabudhe, Sujit Joshi, Mukta Kulkarni
Journal: Clinical Nuclear Medicine (2019)

Abstract A 65-year-old man underwent FDG PET/CT for evaluation of vertebral lesions, radiologically suspected to be metastases. The scan showed hypermetabolism in D8 to D9 vertebrae, retroperitoneal lymph nodes, and both the lobes of prostate. Transrectal ultrasound-guided biopsy of prostate was performed with suspicion of prostate malignancy. The biopsy revealed caseating granulomatous lesions in prostate suggestive of tuberculosis. Post antitubercular treatment patient showed excellent clinical response. Possibility of infective pathologies mimicking malignancy should be kept in mind while evaluating hypermetabolic foci seen on PET/CT. Although rare, tuberculosis of prostate needs consideration in differential diagnosis of FDG-avid foci seen in prostate.
Effect of DNA methyltransferase and histone deacetylase inhibitors on tumorigenicity and MHC1 expression in a murine non-small cell lung cancer cell line
Authors: Thiru V. Lakshman, Joshua P. Cantor, Atul S. Rao, Joshua E. Collins, Joseph S. Friedberg
Journal: Cancer Research (2006)

1612  Background: Epigenetic alterations, such as DNA hypermethylation, are commonly seen in many malignancies including non-small cell lung cancer (NSCLC). DNA methyltransferase (DNMT) inhibitors, in conjunction with histone deacetylase (HDAC) inhibitors, have been shown to reverse these epigenetic events and result in antitumor activity through numerous mechanisms, including tumor suppressor gene reactivation. These pharmacologic inhibitors may also confer increased immunogenicity via upregulated expression of key immune recognition proteins, such as MHC1. Objectives: The purpose of this study was to determine whether treatment with pharmacologic inhibitors of DNMT and HDAC results in increased MHC1 expression and decreased tumorigenicity of a poorly immunogenic murine NSCLC cell line. Methods: The activated k-ras murine adenocarcinoma cell line, LKR13 was used in this study. Cells were treated in vitro with varying doses of 5-Aza-2’-deoxycytidine (AZA), a DNMT inhibitor, and trichostatin A (TSA), an HDAC inhibitor. MTS assays were performed in order to determine the dosage necessary to maintain a metabolically active population of cells. FACS analysis was performed to quantify the expression of MHC1 before and after in vitro treatment. In vivo tumorigenicity studies were carried out in three groups of immunocompetent B6SF129/1 mice (5 mice per group). Group 1 and group 2 were injected with 1x105 LKR13 cells subcutaneously (s.c.) in the right flank. Group 1 was subsequently treated with intraperitoneal (i.p.) injections of phosphate buffered saline (PBS) and group 2 was treated with i.p. injections of 5mg/kg AZA and 500μg/kg TSA. Treatments began 1 week after tumor challenge and continued weekly for a total of 3 treatments. Group 3 mice were injected s.c. in the right flank with 1x105 LKR13 cells that had been pre-treated in vitro with AZA and TSA. Results: MTS assays revealed that the majority of LKR13 cells remained metabolically active following in vitro treatment with AZA (2.5μΜ) for 3 days followed by 1 day of treatment with TSA (0.5μΜ). Flow cytometry demonstrated an increase in MHC1 expression from 18% to 50% after in vitro treatment. Tumorigenicity studies revealed that by day 30, mean tumor volume of group 1 mice (PBS) was 540mm3, group 2 mice (in vivo AZA/TSA) was 125mm3, and group 3 mice (in vitro AZA/TSA) was 175mm3. By day 45, 5/5 group 1 mice, 0/5 group 2 mice, and 1/5 group 3 mice had tumor volumes >500mm3. Conclusions: These initial studies demonstrate that pharmacologic inhibition of DNMT and HDAC decreases tumorigenicity in an immunocompetent murine NSCLC model. This could be partly due to an immunostimulatory effect, which may work in conjunction with other epigenetic phenomena to decrease tumorigenicity. Further studies are warranted to determine the specific tumor suppressor genes and immune mechanisms involved.
On the valid publication of names of mycobacteria
Authors: Enrico Tortoli
Journal: European Respiratory Journal (2019)

We are grateful to A. Oren and M.E. Trujillo for their precise clarifications. I admit that my knowledge about the complex rules governing the nomenclature of prokaryotes is very limited and dates back to no more than an year ago when, in reply to a manuscript of mine, a reviewer for the International Journal of Systematic and Evolutionary Microbiology invited me to read the papers of B.J. Tindall and co-workers [1, 2]. The complex taxonomic rules do not affect the legitimacy of using the conventional nomenclature of mycobacteria based on the single genus Mycobacterium <http://bit.ly/2L3mpKi>
P1.17-08 mRNA Expression Level of Receptor Tyrosine Kinases and Non-Receptor Tyrosine Kinases as a Recurrence Risk in Resected Adenocarcinoma of the Lung
Authors: M. Ito, M. Serra, R. Rami-Porta, J. Belda-Sanchis, I. Chaib, M. Okada, N. Karachaliou, R. Rosell
Journal: Journal of Thoracic Oncology (2019)
P2.04-32 Comparison of Clinicopathological and Genomic Characteristics Between NSCLCs with a PD-L1 Tumor Proportion Score of ≥90% vs <1%
Authors: G. Lamberti, Y. Li, L. Spurr, B. Ricciuti, G. Recondo, R. Umeton, L. Sholl, A. Cherniak, M. Awad
Journal: Journal of Thoracic Oncology (2019)
Thyroid function and life expectancy with and without noncommunicable diseases: A population-based study
Authors: Arjola Bano, Layal Chaker, Francesco U. S. Mattace-Raso, Natalie Terzikhan, Maryam Kavousi, M. Arfan Ikram, Robin P. Peeters, Oscar H. Franco
Journal: PLoS Medicine (2019)

Background Variations in thyroid function within reference ranges are associated with increased risk of diseases and death. However, the impact of thyroid function on life expectancy (LE) with and without noncommunicable diseases (NCDs) remains unknown. We therefore aimed to investigate the association of thyroid function with total LE and LE with and without NCD among euthyroid individuals. Methods and findings The study was embedded in the Rotterdam Study, a prospective population-based study carried out in the Netherlands. In total, 7,644 participants without known thyroid disease and with thyroid-stimulating hormone (TSH) and free thyroxine (FT4) levels within reference ranges were eligible. NCDs were defined as presence of cardiovascular disease, diabetes mellitus type 2, or cancer. We used the demographic tool of multistate life tables to calculate LE estimates at the age of 50 years, using prevalence, incidence rates, and hazard ratios for three transitions (healthy to NCD, healthy to death, and NCD to death). The total LE and LE with and without NCD among TSH and FT4 tertiles were calculated separately in men and women. Analyses were adjusted for sociodemographic and cardiovascular risk factors. The mean (standard deviation) age of the participants was 64.5 (9.7) years, and 52.3% were women. Over a median follow-up of 8 years (interquartile range 2.7–9.9 years), 1,396 incident NCD events and 1,422 deaths occurred. Compared with those in the lowest TSH tertile, men and women in the highest TSH tertile were expected to live 1.5 years (95% confidence interval [CI] 0.8–2.3, p < 0.001) and 1.5 years (CI 0.8–2.2, p < 0.001) longer, respectively, of which 1.4 years (CI 0.5–2.3, p = 0.002) and 1.3 years (CI 0.3–2.1, p = 0.004) with NCD. Compared with those in the lowest FT4 tertile, the difference in LE for men and women in the highest FT4 tertile was −3.7 years (CI −5.1 to −2.2, p < 0.001) and −3.3 years (CI −4.7 to −1.9, p < 0.001), respectively, of which −1.8 years (CI −3.1 to −0.7, p = 0.003) and −2.0 years (CI −3.4 to −0.7, p = 0.003) without NCD. A limitation of the study is the observational design. Thus, the possibility of residual confounding cannot be entirely ruled out. Conclusions In this study, we found that people with low–normal thyroid function (i.e., highest tertile of TSH and lowest tertile of FT4 reference ranges) are expected to live more years with and without NCD than those with high–normal thyroid function (i.e., lowest tertile of TSH and highest tertile of FT4 reference ranges). These findings provide support for a re-evaluation of the current reference ranges of thyroid function.
EP1.03-06 POLD1 Mutations Define a Unique Molecular Class of Non-Small Cell Lung Cancer in Chinese Patients
Authors: W. Wang, C. Xu, Q. Zhang, W. Zhuang, Y. Zhu, Y. Huang, G. Chen, M. Fang, T. Lv, Y. Song
Journal: Journal of Thoracic Oncology (2019)
Prospective Countywide Surveillance and Autopsy Characterization of Sudden Cardiac Death
Authors: Zian H. Tseng, Jeffrey E. Olgin, Eric Vittinghoff, Philip C. Ursell, Anthony S. Kim, Karl Sporer, Clement Yeh, Benjamin Colburn, Nina M. Clark, Rana Khan, Amy P. Hart, Ellen Moffatt
Journal: Circulation (2018)

Background: Studies of out-of-hospital cardiac arrest and sudden cardiac death (SCD) use emergency medical services records, death certificates, or definitions that infer cause of death; thus, the true incidence of SCD is unknown. Over 90% of SCDs occur out-of-hospital; nonforensic autopsies are rarely performed, and therefore causes of death are presumed. We conducted a medical examiner–based investigation to determine the precise incidence and autopsy-defined causes of all SCDs in an entire metropolitan area. We hypothesized that postmortem investigation would identify actual sudden arrhythmic deaths among presumed SCDs. Methods: Between February 1, 2011, and March 1, 2014, we prospectively identified all incident deaths attributed to out-of-hospital cardiac arrest (emergency medical services primary impression, cardiac arrest) between 18 to 90 years of age in San Francisco County for autopsy, toxicology, and histology via medical examiner surveillance of consecutive out-of-hospital deaths, all reported by law. We obtained comprehensive records to determine whether out-of-hospital cardiac arrest deaths met World Health Organization (WHO) criteria for SCD. We reviewed death certificates filed quarterly for missed SCDs. Autopsy-defined sudden arrhythmic deaths had no extracardiac cause of death or acute heart failure. A multidisciplinary committee adjudicated final cause. Results: All 20 440 deaths were reviewed; 12 671 were unattended and reported to the medical examiner. From these, we identified 912 out-of-hospital cardiac arrest deaths; 541 (59%) met WHO SCD criteria (mean 62.8 years, 69% male) and 525 (97%) were autopsied. Eighty-nine additional WHO-defined SCDs occurred within 3 weeks of active medical care with the death certificate signed by the attending physician, ineligible for autopsy but included in the countywide WHO-defined SCD incidence of 29.6/100 000 person-years, highest in black men ( P &lt;0.0001). Of 525 WHO-defined SCDs, 301 (57%) had no cardiac history. Leading causes of death were coronary disease (32%), occult overdose (13.5%), cardiomyopathy (10%), cardiac hypertrophy (8%), and neurological (5.5%). Autopsy-defined sudden arrhythmic deaths were 55.8% (293/525) of overall, 65% (78/120) of witnessed, and 53% (215/405) of unwitnessed WHO-defined SCDs ( P =0.024); 286 of 293 (98%) had structural cardiac disease. Conclusions: Forty percent of deaths attributed to stated cardiac arrest were not sudden or unexpected, and nearly half of presumed SCDs were not arrhythmic. These findings have implications for the accuracy of SCDs as defined by WHO criteria or emergency medical services records in aggregate mortality data, clinical trials, and cohort studies.
A Compound L1196M/G1202R ALK Mutation in a Patient with ALK-Positive Lung Cancer with Acquired Resistance to Brigatinib Also Confers Primary Resistance to Lorlatinib
Authors: Geeta G. Sharma, Diego Cortinovis, Francesco Agustoni, Giulia Arosio, Matteo Villa, Nicoletta Cordani, Paolo Bidoli, William H. Bisson, Fabio Pagni, Rocco Piazza, Carlo Gambacorti-Passerini, Luca Mologni
Journal: Journal of Thoracic Oncology (2019)
A Model of Indirect Cell Death Caused by Tumor Vascular Damage after High-Dose Radiotherapy
Authors: Pedro Rodríguez-Barbeito, Pablo Díaz-Botana, Araceli Gago-Arias, Manuel Feijoo, Sara Neira, Jacobo Guiu-Souto, Óscar López-Pouso, Antonio Gómez-Caamaño, Juan Pardo-Montero
Journal: Cancer Research (2019)

There is increasing evidence that high doses of radiotherapy, like those delivered in stereotactic body radiotherapy (SBRT), trigger indirect mechanisms of cell death. Such effect seems to be two-fold. High doses may trigger an immune response and may cause vascular damage, leading to cell starvation and death. Development of mathematical response models, including indirect death, may help clinicians to design SBRT optimal schedules. Despite increasing experimental literature on indirect tumor cell death caused by vascular damage, efforts on modeling this effect have been limited. In this work, we present a biomathematical model of this effect. In our model, tumor oxygenation is obtained by solving the reaction-diffusion equation; radiotherapy kills tumor cells according to the linear-quadratic model, and also endothelial cells (EC), which can trigger loss of functionality of capillaries. Capillary death will affect tumor oxygenation, driving nearby tumor cells into severe hypoxia. Capillaries can recover functionality due to EC proliferation. Tumor cells entering a predetermined severe hypoxia status die according to a hypoxia-death model. This model fits recently published experimental data showing the effect of vascular damage on surviving fractions. It fits surviving fraction curves and qualitatively reproduces experimental values of percentages of functional capillaries 48 hours postirradiation, and hypoxic cells pre- and 48 hours postirradiation. This model is useful for exploring aspects of tumor and EC response to radiotherapy and constitutes a stepping stone toward modeling indirect tumor cell death caused by vascular damage and accounting for this effect during SBRT planning. SIGNIFICANCE: A novel biomathematical model of indirect tumor cell death caused by vascular radiation damage could potentially help clinicians interpret experimental data and design better radiotherapy schedules.
P2.18-18 Impact of Combined Evaluation Using Tumor Volume and Metastatic Nodal Extent in Stage III NSCLC Treated with CRT
Authors: Y. Tamiya, M. Morise, R. Matsuzawa, I. Tanaka, T. Okada, S. Iwano, T. Hase, N. Hashimoto, M. Sato, Y. Itoh, Y. Hasegawa
Journal: Journal of Thoracic Oncology (2019)
P2.04-27 Clinical Implementation of Multiplex Immunofluorescence to Characterize Tumor Immune Status in Lung Cancer Patients
Authors: L. Sholl, E. Gjini, K. Felt, P. Kumari, J. Lindsay, N. Lindeman, J. Nowak, E. Cerami, S. Rodig
Journal: Journal of Thoracic Oncology (2019)
Analyses of Physical Activity and Health—Are Our Methods Too Sedentary?
Authors: Pamela A. Shaw
Journal: JAMA Network Open (2019)

Michael J. LaMonte, PhD, MPH; Jean Wactawski-Wende, PhD; Joseph C. Larson, MS; Xiaodan Mai, PhD; John A. Robbins, MD, MHS; Meryl S. LeBoff, MD; Zhao Chen, PhD, MPH; Rebecca D. Jackson, MD; Andrea Z. LaCroix, PhD; Judith K. Ockene, PhD; Kathleen M. Hovey, MS; Jane A. Cauley, DrPH; for the Women’s Health Initiative (WHI)
Abstract 14961: Is Mental Stress-Induced Myocardial Ischemia a Silent Phenomenon?
Authors: Pratik M Pimple, Amit J Shah, Cherie Rooks, J. Douglas Bremner, Jonathon A Nye, Ijeoma Ibeanu, Nancy Murrah, Xinwei Hua, Paolo Raggi, Viola Vaccarino
Journal: Circulation (2013)

Objective: Mental stress-induced myocardial ischemia (MSMI) is a common phenomenon in CAD patients and an emerging prognostic factor. MSMI correlates with ambulatory ischemia, and in contrast to ph...
P1.14-17 Genomic Evolution During TKI Treatment in Non-Small Cell Lung Cancer Patients With or Without Acquired T790M Mutation
Authors: Y. Jin, H. Bao, X. Le, X. Fan, M. Tang, Y. Fan, Y. Zhang, X. Shi, J. Zhao, G. Lou, L. Shao, Q. He, C. Lin, J. Zhang, P.A. Futreal, I. Wistuba, J. Heymach, X. Wu, Y.W. Shao, J. Yan, Y. Chen, M. Chen, J. Zhang, X. Yu, Y. Xu
Journal: Journal of Thoracic Oncology (2019)
EP1.15-10 Survival Impact of Non-Surgical Treatment in Thymic Epithelial Tumours: A Retrospective Study
Authors: S. Ridai, N. Benchakroun, Z. Bouchbika, H. Jouhadi, N. Tawfik, S. Sahraoui, A. Benider
Journal: Journal of Thoracic Oncology (2019)
P1.06-07 Targeting Photo-Therapy for Malignant Pleural Mesothelioma; Near Infrared Photoimmunotherapy Targeting Podoplanin
Authors: Y. Nishinaga, Y. Isobe, H. Yasui, K. Takahashi, S. Taki, T. Matsui, K. Sato, Y. Hasegawa, Y. Kato
Journal: Journal of Thoracic Oncology (2019)
Reduced Intensity Allogeneic Stem Cell Transplantation for Follicular Lymphoma Results in An Improved Progression Free Survival When Compared to Autologous Stem Cell Transplantation. An Analysis from the Lymphoma Working Party of the EBMT
Authors: Stephen P Robinson, Carmen Canals, Didier Blaise, Kirsty Thomson, Robert Foa, Arturo Iriondo Atienza, Jean-Luc Harousseau, Catherine Cordonnier, Gordon Cook, Jean-Pierre Jouet, Jean-Yves Cahn, Charles Crawley, Michel Attal, Marek Trneny, H. Tilly, Anna Sureda
Journal: Blood (2008)
P2.03-05 PHLPP1 Expression Through AKT and ERK Dual Signaling Pathways May Slow Down the Resistance to TKI in EGFR-Mutated Lung Adenocarcinoma
Authors: W. Wang, D. Lv, Y. Meng, M. Ye, S. Zhou, F. Kong, H. Yang
Journal: Journal of Thoracic Oncology (2019)
EP1.13-02 Negative Predictive Value of EBUS-TBNA for Mediastinal Staging of Non-Small Cell Lung Cancer
Authors: N. Anagnostopoulos, K. Cholidou, D. Ampazis, D. Grapsa, R. Trigidou, V. Vitsas, G. Stratakos, P. Bakakos, I. Gkiozos
Journal: Journal of Thoracic Oncology (2019)
P1.13-06 Impact of Lymph Node Involvement and Tumor Location on Survival Following Resection for pN1/pN2 Non-Small Cell Lung Cancer
Authors: T. Tsitsias, I. Saftic, L. Harling, L. Veres, J. King, K. Harrison-Phipps, T. Routledge, J. Pilling, A. Bille
Journal: Journal of Thoracic Oncology (2019)
Microarray analysis of formalin-fixed paraffin-embedded specimens shows distinct gene expression patterns in tumors containing the transforming growth factor beta receptor 6A polymorphism (TGFBR1*6A)
Authors: A. Omori, C. Stephens, J. Cooc, P. V. Danenberg, K. Danenberg, H. Lenz, B. Pasche
Journal: Journal of Clinical Oncology (2007)

4111 Introduction: A frequent polymorphism of the type I transforming growth factor beta receptor (TGFBR1) is TGFBR1*6A (6A), which has a deletion of 3 CGC triplets coding for alanine within a 9-alanine (9A) repeat of TGFBR1 exon 1. 6A may act as a tumor susceptibility allele through switching TGF-beta growth inhibitory signals into growth stimulatory signals and also appears to be acquired in some cases by primary colon cancers and their liver metastases. Our aim in this study was to compare the gene expression profiles of colorectal tumors bearing the 6A and the more common 9A genotypes to discover pathways that might be differentially induced by the 6A polymorphism. Methods: 28 colorectal tumors with matched synchronous metastases and 23 non-metastatic colorectal tumors were analyzed for TGFBR1 exon 1 genotype by a PCR-based assay. Nine metastatic and 10 non-metastatic tumors were analyzed by gene expression microarrays. Following microdissection of paraffin-embedded specimens, RNA was isolated, amplified, labeled, and hybridized to Affymetrix U133 Plus 2.0 GeneChips. Results: Among the 28 primary metastatic tumors, 19 were 9A (68%), 8 were 9A/6A heterozygotes (29%) and 1 was a 6A homozygote (3%). There was 100% genotype correspondence with the matched metastases. Among the 23 non-metastatic tumors, 18 were 9A (78%), 3 were heterozygotes (13%) and 2 were 6A/6A (9%). Microarray analysis showed 578 differentially expressed genes in the metastatic tumors and 467 in the non-metastatic tumors between the 6A and 9A genotypes (p&lt;0.01). Significant pathway deregulation between 9A and 6A genotypes included estrogen receptor signaling and histidine metabolism in the non-metastatic tumors and B cell receptor, GM-CSF, SAPK/JNK and IL-4 signaling in the metastatic tumors. Conclusion: Microarray analysis shows differentially expressed genes in the 6A genotype compared to 9A, with different deregulated pathways in metastatic and non-metastatic tumors. This alludes to 6A-specific downstream signaling effects, which may contribute to tumor development and progression. No significant financial relationships to disclose.
EP1.01-45 Cisplatin Plus Gemcitabine Therapy Followed by Maintenance Gemcitabine for Advanced Squamous Cell Lung Cancer (KTORG1302)
Authors: T. Kaneda, S. Ikeda, H. Yoshioka, T. Yokoyama, T. Niwa, N. Sone, T. Ishida, M. Morita, H. Tomioka, C. Komaki, M. Hirabayashi, Y. Hasegawa, T. Noguchi, Y. Nakano, C. Sakaguchi, K. Yoshimura, T. Hirai
Journal: Journal of Thoracic Oncology (2019)
Acute Lymphoblastic Leukemia Blast Cells Stimulate the Autocrine Production of CCL2 and IL-8 in Bone Marrow Stromal Cells
Authors: Jaira Ferreira de Vasconcellos, Nilson Ivo Tonin Zanchin, Angelo A. Cardoso, Silvia Regina Brandalise, José Andrés Yunes
Journal: Blood (2008)
P2.01-15 Phase II Single Arm Study of CABozantinib in Non-Small Cell Lung Cancer Patients with MET Deregulation (CABinMET)
Authors: M. D'Arcangelo, D. Tassinari, F. De Marinis, A. Delmonte, D. Galetta, F. Cecere, S. Pilotto, F. Zanelli, L. Bonanno, L. Landi, F. D'Incà, F. Cappuzzo
Journal: Journal of Thoracic Oncology (2019)
Electronic Cigarette Use Among Populations of Women During Reproductive Years
Authors: Abhimanyu S. Ahuja, Vineet Pasam Reddy
Journal: JAMA Pediatrics (2019)

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Percutaneous traction via a novel endoscopic trocar facilitates endoscopic submucosal dissection
Authors: Diogo Turiani Hourneaux de Moura, Hiroyuki Aihara, Kelly E. Hathorn, Liam Patrick Burns, Christopher C. Thompson
Journal: Endoscopy (2019)

Minimally invasive endoscopic procedures are associated with fewer adverse events and shorter hospital stays compared with surgery [1]. However, some advanced endoscopic procedures, including endoscopic submucosal dissection (ESD), require specialized training and significant experience to achieve competency and are not widely performed in non-specialist centers [2].
EP1.01-37 Platinum-Based Chemotherapy (CT) Rechallenge in Advanced Non Small Cell Lung Cancer (NSCLC) Patients (p): A Single Institution Experience
Authors: E. Carcereny, A.M. Esteve, A. Estival, M. Domenech, L. Angelats, C. Erasun, A. Gonzalez, A. Plaja, N. Garcia, S. España, M. Cucurull, A. Ferrando, A. Pous, L. Notario, S. Sanchez Martin, C. Villacorta Garcia, T. Moran
Journal: Journal of Thoracic Oncology (2019)