tbuckley/cabot-search huggingface dataset:
Writing Out Loud
Authors: Mehak Dhande
Journal: JAMA Cardiology (2016)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Cardiology 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 Cardiology journal
MOPP dose intensity and survival: flawed analysis.
Authors: M H Cohen
Journal: Journal of Clinical Oncology (1990)

Article Tools Article Tools OPTIONS & TOOLS Export Citation Track Citation Add To Favorites Rights & Permissions COMPANION ARTICLES No companion articles ARTICLE CITATION DOI: 10.1200/JCO.1990.8.4.756 Journal of Clinical Oncology - published online before print September 22, 2016 PMID: 2313341 MOPP dose intensity and survival: flawed analysis. M H CohenxM H CohenSearch for articles by this author https://doi.org/10.1200/JCO.1990.8.4.756 PDF "MOPP dose intensity and survival: flawed analysis.." Journal of Clinical Oncology, 8(4), pp. 756–757© 1990 by American Society of Clinical Oncology
Novel surface-enhanced Raman scattering-based assays for ultra-sensitive detection of human pluripotent stem cells
Authors: Jingjia Han, Ximei Qian, Qingling Wu, Rajneesh Jha, Jinshuai Duan, Zhou Yang, Kevin O. Maher, Shuming Nie, Chunhui Xu
Journal: Biomaterials (2016)

Human pluripotent stem cells (hPSCs) are a promising cell source for regenerative medicine, but their derivatives need to be rigorously evaluated for residual stem cells to prevent teratoma formation. Here, we report the development of novel surface-enhanced Raman scattering (SERS)-based assays that can detect trace numbers of undifferentiated hPSCs in mixed cell populations in a highly specific, ultra-sensitive, and time-efficient manner. By targeting stem cell surface markers SSEA-5 and TRA-1-60 individually or simultaneously, these SERS assays were able to identify as few as 1 stem cell in 106 cells, a sensitivity (0.0001%) which was ∼2000 to 15,000-fold higher than that of flow cytometry assays. Using the SERS assay, we demonstrate that the aggregation of hPSC-based cardiomyocyte differentiation cultures into 3D spheres significantly reduced SSEA-5+ and TRA-1-60+ cells compared with parallel 2D cultures. Thus, SERS may provide a powerful new technology for quality control of hPSC-derived products for preclinical and clinical applications.
Abstract 1547: Circulating tumor cells from a syngeneic mouse model of hepatocellular carcinoma demonstrate epithelial-mesenchymal transition, decreased MHC I expression, and increased CCR7 expression
Authors: Jeannette A. Huaman, Ubayed Muhith, Dibash K. Das, Michelle Naidoo, Olorunseun O. Ogunwobi
Journal: Cancer Research (2016)

Abstract Metastasis is the leading cause of death in cancer patients, worldwide. A better understanding of how cancer cells detach from the primary tumor, escape from immunosurveillance while in circulation, and successfully colonize distant parts of the body, is needed. Circulating tumor cells (CTCs) are excellent tools to study this process. Using a syngeneic hepatocellular carcinoma mouse model, we were able to isolate cancer cells from the primary tumor and CTCs from the blood and establish novel primary tumor-derived cell lines and novel CTC lines. Wound healing assays revealed that CTCs have greater migratory capacity than the cancer cells from the primary tumors. However, MTT assays revealed that CTCs had less proliferative capacity than the cancer cells from the primary tumors. Furthermore, molecular characterization of the cancer cells from primary tumors and CTCs using Western blotting showed a decreased expression of E-cadherin and an increased expression of fibronectin by CTCs, suggesting that epithelial-to-mesenchymal transition (EMT) takes place in CTCs in comparison to cancer cells from primary tumors. To address the question of how CTCs may evade immunosurveillance, we investigated the profile of expression of two cell surface proteins involved in immune system function: the major histocompatibility complex class I (MHCI)- required for cytotoxic T cell activation and subsequent cancer cell killing, and chemokine receptor 7 (CCR7)- exploited by cancer cells for immune evasion. Our analysis revealed that there is decreased cell surface expression of MHCI and increased expression of CCR7 in the CTCs in comparison to the cancer cells from primary tumors. These findings indicate that although CTCs are not more proliferative, they have acquired significantly increased migratory capacity than cancer cells in primary tumors. This may be explained by their demonstration of EMT. Furthermore, their loss of MHC I expression and their gain of CCR7 expression may help with evasion of killing by cytotoxic T cells and result in enhanced metastasis. Citation Format: Jeannette A. Huaman, Ubayed Muhith, Dibash K. Das, Michelle Naidoo, Olorunseun O. Ogunwobi. Circulating tumor cells from a syngeneic mouse model of hepatocellular carcinoma demonstrate epithelial-mesenchymal transition, decreased MHC I expression, and increased CCR7 expression. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 1547.
A systematic in vitro investigation on poly-arginine modified nanostructured lipid carrier: Pharmaceutical characteristics, cellular uptake, mechanisms and cytotoxicity
Authors: Mingshuang Sun, Yunyun Gao, Zhihong Zhu, Huixin Wang, Cuiyan Han, Xinggang Yang, Weisan Pan
Journal: Asian Journal of Pharmaceutical Sciences (2016)

The aim of the present study was to develop a poly-arginine modified nanostructured lipid carrier (R-NLC) by fusion-emulsification method and to test its pharmaceutical characteristics. The influence of R-NLC on A549 cells like cellular uptake and cytotoxicity was also appraised using unmodified NLC as the controlled group. As the results revealed, R-NLC had an average diameter of about 40 nm and a positive zeta potential of about +17 mv, the entrapment efficiency decreased apparently, and no significant difference on the in vitro drug release was found after R8-modification. The cellular uptake and cytotoxicity increased obviously compared with unmodified NLC. The cellular uptake mechanisms of R-NLC involved energy, macropinocytosis, clathrin-mediated endocytosis, and caveolin-mediated endocytosis. The outcomes of the present study strongly support the theory that cell penetrating peptides have the ability of enhancing the cellular uptake of nanocarriers.
대한간학회지 제8차 춘계학술대회 초록집 : 구연 ; 알코올대사효소의 유전적 다형성이 알코올성 간경변의 발생과 음주습관에 미치는 영향
Authors: 기주영 ( Gi Ju Yeong ), 채희복 ( Chae Ui Bog ), 윤세진 ( Yun Se Jin ), 김헌 ( Kim Heon )
Journal: Clinical and Molecular Hepatology (2002)
Fecal Immunochemical Test Detects Sessile Serrated Adenomas and Polyps With a Low Level of Sensitivity
Authors: Li-Chun Chang, Chia-Tung Shun, Weng-Feng Hsu, Chia-Hong Tu, Pei-Yu Tsai, Been-Ren Lin, Jin-Tung Liang, Ming-Shiang Wu, Han-Mo Chiu
Journal: Clinical Gastroenterology and Hepatology (2016)
Induced superficial chondrocyte death reduces catabolic cartilage damage in murine posttraumatic osteoarthritis
Authors: Minjie Zhang, Sriniwasan B. Mani, Yao He, Amber M. Hall, Lin Xu, Yefu Li, David Zurakowski, Gregory D. Jay, Matthew L. Warman
Journal: Journal of Clinical Investigation (2016)

Joints that have degenerated as a result of aging or injury contain dead chondrocytes and damaged cartilage. Some studies have suggested that chondrocyte death precedes cartilage damage, but how the loss of chondrocytes affects cartilage integrity is not clear. In this study, we examined whether chondrocyte death undermines cartilage integrity in aging and injury using a rapid 3D confocal cartilage imaging technique coupled with standard histology. We induced autonomous expression of diphtheria toxin to kill articular surface chondrocytes in mice and determined that chondrocyte death did not lead to cartilage damage. Moreover, cartilage damage after surgical destabilization of the medial meniscus of the knee was increased in mice with intact chondrocytes compared with animals whose chondrocytes had been killed, suggesting that chondrocyte death does not drive cartilage damage in response to injury. These data imply that chondrocyte catabolism, not death, contributes to articular cartilage damage following injury. Therefore, therapies targeted at reducing the catabolic phenotype may protect against degenerative joint disease.
PWE-306 Rationalisation of two week wait referrals in suspected colorectal cancer: Abstract PWE-306 Table 1
Authors: DG Couch, JH Murphy, KM Boyle, DM Hemingway
Journal: Gut (2015)

<h3>Introduction</h3> The 2-week wait pathway was designed to decrease the time from presentation to primary care with “red flag” symptoms of suspected cancer to review by a specialist for diagnosis or exclusion of cancer. Within our tertiary referral centre 968 colonoscopies per year are required to satisfy the demand for the 2-week wait at the expense of other services. We sought to determine yields of colorectal cancer found at colonoscopy in reference to original red flag symptoms in order to select the most efficacious primary investigation based upon presenting symptoms. <h3>Method</h3> Electronic records were retrospectively analysed. All patients who went through the 2-week wait system for suspicion of colorectal cancer in 2013 found to have colorectal cancer at colonoscopy were included. Patients not undergoing colonoscopy as first investigation were excluded. The splenic flexure was deemed within the range of a flexible sigmoidoscope. <h3>Results</h3> 2950 referrals were made. 968 colonoscopies were performed as the primary investigation. 35 patients were found to have colorectal cancer. No patients referred with rectal bleeding and another symptom had a tumour outside the range of a flexible sigmoidoscope. Eighty percent of tumours proximal to the splenic flexure were suitable for CT diagnosis alone. <h3>Conclusion</h3> Our data supports the use of flexible sigmoidoscopy alone as an initial investigation for patients presenting with rectal bleeding with or without additional colorectal symptoms within our local population. Patients with anaemia (without bleeding) or change in bowel habit (without bleeding) may be investigated with CT colonography alone; colonoscopy may then be used selectively prior to surgery. <h3>Disclosure of interest</h3> None Declared.
Warning As Defiened By European Leukemia Net 2013 (ELN 2013) In Chronic Phase Chronic Myeloid Leukemia (CP-CML) Corresponds To Warning In The Clinical Practice?
Authors: Laura Fogliatto, Marcelo Capra, Mariza Shaan, Tito Vanelli Costa, Raquel Breunig, Christina G S Fraga, Mayde Seadi Torriani, Lucia Silla, Liane Esteves Daudt, Mario Sérgio Fernandes, Denise Almeida, Marco Antônio Schilling, Tânia Hellwig, Katia Fassina, Sabrina Wisintainer, Mariangela Moschen, Tiago Daltoe, Adriana Zardo, Juliana Kratochvil, Viviane Magagnin Fernandes, Cheila Eickhoff, Moema Nene, Saozan Ahmad, Andréia Dias Almeida, Vitor Lenz
Journal: Blood (2013)
OC-041 Reduced Hospital Admission And Rapid Access To Specialist Services Through The Introduction Of A Gastroenterology And Hepatology Ambulatory Care Service: Abstract OC-041 Table 1
Authors: J Fielding, A Hawley, S Hardcastle, K Drew, D Gleeson, M Karajeh, D Sanders, A Hopper, R Sidhu, M McAlindon, AJ Lobo
Journal: Gut (2014)

<h3>Introduction</h3> Ambulatory care sensitive conditions are those where intervention may limit hospital admissions. Improvements in the management of these conditions may save the NHS £96–£238 million per annum and alleviate pressures on Accident and Emergency. This is directly applicable in Gastroenterology but few gastrointestinal (GI) conditions are conventionally listed as suitable for this approach. This study examined the effect of such a service providing rapid access to specialist services in a UK Gastroenterology Unit. <h3>Methods</h3> A Gastroenterology ambulatory care service was established as part of an investigation unit with on-ward endoscopy facilities. General practitioners (GPs) were given written guidelines and referred to a senior nurse via telephone. Patients considered suitable were those requiring urgent assessment but where admission might be avoided. Exclusion criteria: hypotension, suspected acute abdomen, or GP concern about potential for deterioration. <h3>Results</h3> 224 patients were referred by their GP from June 2011 to January 2013. 12 did not attend. Presentation and outcome are described in Table 1. 179 patients (84%) were seen on arrival by a consultant. 96 patients (45%) were admitted; 116 were discharged on the same day – of whom 94 (91%) were offered either same day (n = 67 (58%)) or outpatient (n = 27 (23%)) investigations. 30 day readmission rate was only 4% (n = 5). 51 patients had low risk GI bleeds (Rockall score 0–1). 30 (59%) of these were discharged the same day and 90% (n = 27) had an OGD within 24 h of assessment, either same day or returning the following morning. <h3>Conclusion</h3> The Ambulatory Care Service provides direct, rapid access to specialist opinion and investigation for a range of GI presentations, avoiding hospital admission for the majority referred. In contrast to other UK studies those with low risk GI bleeding were managed as out-patients but with gastroscopy undertaken. This is a model for a tiered approach to emergency care in Gastroenterology. <h3>Disclosure of Interest</h3> None Declared.
Abstract 40: Metabolic rewiring in Rb deficient cells during cancer progression
Authors: Susumu Kohno, Nobuyuki Okahashi, Shunsuke Kitajima, Sawako Suzuki, Tomoaki Tanaka, Fumio Matsuda, Hiroshi Shimizu, Chiaki Takahashi
Journal: Cancer Research (2016)

Abstract Tumor suppressors control critical steps of cellular metabolism and its inactivation induces cancer specific-metabolic features including aerobic glycolysis. Glycolysis contributes to energy generation and supplying precursors of biomass, e.g., nucleotide, amino sugar, amino acid and lipids. These macromolecules were required for proliferation and cancer survival. Although aerobic glycolysis is now widely accepted as a metabolic feature of cancer, its causal relationship with cancer progression is still unclear. In common type cancers, inactivation of RB tumor suppressor is prevalently observed during tumor progression. Previous studies demonstrated RB inactivation induces inflammation, angiogenesis, drug resistance, etc., as well as cell cycle progression. We currently focus on the impact of RB deficiency on the central carbon metabolism, e.g., glycolysis, TCA cycle and glutamine metabolism. To address this point, we established a mouse model in which RB depletion in p53-null soft tissue sarcoma cells induced undifferentiated phenotype associated with “glycolytic to glutaminolytic” switch (metabolic rewiring) most probably due to down-regulation of Pgam2 activity. Up-regulation of Pgam2 in these cells antagonized the metabolic rewiring, and suppressed spherogenic and tumorigenic activities of RB deficient cells, however did not affect cell proliferation in 2D culture conditions. Moreover, Pgam2 depletion suppressed RB-dependent myogenic differentiation. These findings suggest that RB controls tumorigenicity and differentiation by influencing central carbon metabolism via Pgam2. Citation Format: Susumu Kohno, Nobuyuki Okahashi, Shunsuke Kitajima, Sawako Suzuki, Tomoaki Tanaka, Fumio Matsuda, Hiroshi Shimizu, Chiaki Takahashi. Metabolic rewiring in Rb deficient cells during cancer progression. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 40.
The Broad Kinase Inhibitor Dasatinib in Combination with Fludarabine in Patients with Refractory Chronic Lymphocytic Leukemia
Authors: Arnon P. Kater, Marjolijn Spiering, Rob D. Liu, Marielle M. Beckers, Sanne H. Tonino, Simon Daenen, Jeanette K. Doorduijn, Nienke A. Lankheet, Dieuwertje M. Luijks, Doreen te Raa, Eric Eldering, Marinus H. J. Van Oers
Journal: Blood (2012)
EGFR C797S mutation mediates resistance to third-generation inhibitors in T790M-positive non-small cell lung cancer
Authors: Shuhang Wang, Stella T. Tsui, Christina Liu, Yongping Song, Delong Liu
Journal: Journal of Hematology & Oncology (2016)

T790M mutation is the most common mechanism for resistance to first- and second-generation tyrosine kinase inhibitors (TKI) for epidermal growth factor receptor (EGFR). Several third-generation EGFR mutant selective TKIs are being explored to conquer this resistance. AZD9291 (osimertinib, tagrisso) has been approved for treatment of the metastatic EGFR T790M mutation-positive non-small cell lung cancer. Resistance to AZD9291 has been described. C797S mutation was reported to be a major mechanism for resistance to T790M-targeting EGFR inhibitors. This review summarizes the latest development in identifying the C797S mutation and EAI045, the novel selective inhibitor overcoming the C797S mutant.
Correlation of WNT/β-catenin pathway activation with immune exclusion across most human cancers.
Authors: Jason John Luke, Riyue Bao, Stefani Spranger, Randy F. Sweis, Thomas Gajewski
Journal: Journal of Clinical Oncology (2016)

3004 Background: The presence of intra-tumoral CD8+T cells has been associated with clinical benefit to immunotherapy and patients can be categorized based on the presence or absence of a T cell-inflamed tumor microenvironment. Molecular mechanisms underpinning the absence of a T cell response are beginning to be understood with identification of the WNT/β-catenin pathway playing a major role in melanoma. Methods: Gene expression data from TCGA was segregated using a T cell-inflamed gene expression signature to identify patient samples by immune phenotype. Within the subset of each tumor histology lacking the T cell signature, exomic sequencing data was interrogated for mutations and pathway analysis was performed to identify gene expression changes predicted to activate the β-catenin signaling pathway. Immunohistochemistry was performed on human primary and metastatic specimens of multiple tumor histologies to correlate the presence of nuclear β-catenin with the lack of a T cell infiltrate. Results: Predicted activating mutations in CTNNB1 or inactivating mutations in Axin1, Axin2, APC1, APC2 were observed within 13 tumor histologies ranging in frequency of 9% (esophageal) to 67% (colon) of tumor specific samples. Pathway analysis identified 12 further histologies harboring increased expression of β-catenin pathway elements such as WNT ligands. Only 3 tumors (pancreatic, thyroid, paraganlioma) showed no activation correlating with absence of immune signatures. Immunohistochemistry demonstrated inverse correlations between β-catenin and CD8+T cells. Conclusions: WNT/β-catenin pathway signaling correlates with T cell exclusion and is activated in most human solid tumors. Clinical development of β-catenin pathway inhibitors that combine with immunotherapies should be prioritized. Pathway activation by mutation Pathway activation by increased expression Colon Kidney – clear cell Melanoma (metastatic) Mesothelioma Glioma – low grade Head and Neck Testicular Gastric Lung – Squamous Breast Sarcoma Ovarian Lung – Adenocarcinoma Cervical Uveal Melanoma Bladder Hepatocellular Adrenocortical Kidney – Papillary Uterine Uterine Sarcoma Prostate Kidney – Chromophobe Glioblastoma
A Phase Ib Dose Escalation Trial of SAR650984 (Anti-CD-38 mAb) in Combination with Lenalidomide and Dexamethasone in Relapsed/Refractory Multiple Myeloma
Authors: Thomas G. Martin, Rachid Baz, Don M. Benson, Nikoletta Lendvai, Frank Campana, Eric Charpentier, Ravi Vij
Journal: Blood (2014)
Early PET assessment and therapy de-escalation in patients with advanced Hodgkin’s lymphoma treated with escalated BEACOPP regimen
Authors: D. Krochmalczyk, W. Jurczak, A. Giza, D. Zimowska-Curylo, M. Sobocinski, B. Malkowski, T. Pietrzak, J. Szefer, E. Senkus-Konefka, B. Kumiega, A. B. Skotnicki
Journal: Journal of Clinical Oncology (2008)

8541 Background: In Europe both ABVD and escalated BEACOPP regimens are considered as a “standard therapies”. In our previous analysis (ASCO 2007, Abstract No. 8063), patients with advanced disease treated outside clinical trials, chose the first line therapy, after being informed about possible advantages and side effects. De-escalation of therapy after the first 3 cycles in good responders (based on PET or CT scan) didn’t make OS and EFS inferior, while in poor responders to 3 initial ABVD cycles, even early treatment intensification, didn’t improve the outcome. Methods: 31 patients with advanced HD IIBX-IV (43,3% of pts in IV-th clinical stage, 66% with ≥ 3 EORTC risk factors, 33% ≥3 GHSG risk factors) where staged with PET scans at diagnosis (average SUV 13.2), after the second cycle for early response assessment and at the end of treatment. De-escalation of chemiotherapy (escalated BEACOPP ⋄ ABVD) was considered after the 3-rd cycle, if an early response assessment PET scan confirmed adequate regression. Results: Early response assessment PET scan allowed for treatment de-escalation in 20/31 patients (64%). Further 10/31 patients completed the full course of 6 escalated BEACOPP cycles. Additional radiotherapy was allowed for IIBX patients with a large residual masses. With the relatively short observation time of 19,7 months (range 12-32) overall survival (OS) and event free survival (EFS) were both 100%. There were no treatment related mortality, nor relapses within the first year after negative PET scan results. Conclusions: The early treatment assessment PET scans may allow for better identification of responders, leading to limitation of toxicity of upfront escalated BEACOPP regimen without limiting it’s efficiency. No significant financial relationships to disclose.