tbuckley/cabot-search huggingface dataset:
Assessment of quality improvement efforts by ASCO’s Quality Oncology Practice Initiative (QOPI) participants.
Authors: Anne C. Chiang, Kristen McNiff, Pamela Kadlubek, Michael N. Neuss, Jacobson Joseph
Journal: Journal of Clinical Oncology (2013)

55 Background: More than 600 practices have participated in ASCO’s QOPI since 2006. 192 have achieved certification through the QOPI Certification Program (QCP) since 2010. QOPI assesses greater than 150 performance metrics, organized into modules; QCP evaluates 20 chemotherapy-related standards. QI efforts resulting from QOPI/QCP participation have not been assessed, e.g. which measure areas or standards are preferentially selected by practices for local QI projects. Methods: A survey was sent to 1,450 participants at 850 practices to assess which measure modules/standards were selected by QOPI/QCP participants as the basis for local QI efforts and to understand the nature of the improvement initiatives. Results: 89 participants responded. 96% (85/89) respondents reported QOPI/QCP led to QI efforts. Respondents were asked to select module/s that spurred subsequent QI activities: core measures (57%; n=45), symptom/toxicity management (48%; n=38), end-of-life care (38%; n=29), breast cancer (13%; n=10), colorectal cancer (10%; n=8), NHL (6%; n=5) and NSCLC (4%; n=3). Related to the QCP structural safety standards, participants reported QI projects as follows: chemotherapy planning/chart documentation (39%; n=31), general chemotherapy standards (30%; n=24), monitoring and assessment (29%; n=23), chemotherapy administration (27%; n=21), chemotherapy orders (23%; n=18), staffing (16%; n=13), drug preparation (9%; n=7). Practices reported that QOPI measures improved in subsequent rounds as a result of specific projects (n=22/25, or 88%); 100% felt that these QI projects impacted their practices for the better. QI project results were presented primarily in practice meetings (74%; n=26), hospital or community forums (17%; n=6), ASCO Quality Symposium or other meeting (9%; n=3). No projects reached publication. Of note, 17 of 31 respondents who reported practice status indicated achieving QOPI certification. Conclusions: QOPI participants select improvement targets throughout QOPI modules and standards. QOPI and QCP have succeeded in spurring local QI efforts that have led to score improvements, increased discussion of quality and standards, and a positive impact on practices.
Review of E. N. Dorff and L. Zoloth, eds.,<i>Jews and Genes: The Genetic Future in Contemporary Jewish Thought</i><sup>1</sup>
Authors: Y. M. Barilan
Journal: The American Journal of Bioethics (2016)

"Review of E. N. Dorff and L. Zoloth, eds., Jews and Genes: The Genetic Future in Contemporary Jewish Thought1." The American Journal of Bioethics, 16(4), pp. W10–W11
Efficacy and safety of bortezomib-rituximab (VCR) vs rituximab® in patients (PTS) with relapsed, R-naive/-sensitive follicular lymphoma (FL): outcome according to prior therapy
Authors: M Crump, A Scheliga, J Mayer, Fritz Offner, A Teixeira, K Kuliczkowski, AM Liberati, CY Okada, DL Esseltine, C Enny, E Zhu, H Van de Velde, YA Elsayed, B Coiffier
Journal: Annals of Oncology (2011)
Expression Level Of p-STAT5, c-MYC and IKZF1 By Immunohistochemistry Might Correlate With Adverse Clinic Outcome In Adult B- Lymphoblastic Leukemia (B-ALL)
Authors: Jiangchuan Tao, Bijal D. Shah, Xiaohui Zhang, Prerna Rastogi, Jianguo Tao, Jeffrey E Lancet, Michael Nieder, Hui-Yi Lin, Eduardo M. Sotomayor, Lynn Moscinski, Ling Zhang
Journal: Blood (2013)
Warfarin for small-cell lung cancer: why not?
Authors: L R Zacharski, W G Henderson
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.1990.8.7.1282 Journal of Clinical Oncology - published online before print September 22, 2016 PMID: 2162913 Warfarin for small-cell lung cancer: why not? L R ZacharskixL R ZacharskiSearch for articles by this author , W G HendersonxW G HendersonSearch for articles by this author https://doi.org/10.1200/JCO.1990.8.7.1282 PDF "Warfarin for small-cell lung cancer: why not?." Journal of Clinical Oncology, 8(7), pp. 1282–1283© 1990 by American Society of Clinical Oncology
Etoposide, doxorubicin, and cisplatin chemotherapy for advanced gastric cancer: an old lesson revisited.
Authors: M J O'Connell
Journal: Journal of Clinical Oncology (1992)

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.1992.10.4.515 Journal of Clinical Oncology - published online before print September 21, 2016 PMID: 1548514 Etoposide, doxorubicin, and cisplatin chemotherapy for advanced gastric cancer: an old lesson revisited. M J O'ConnellxM J O'ConnellSearch for articles by this author https://doi.org/10.1200/JCO.1992.10.4.515 PDF "Etoposide, doxorubicin, and cisplatin chemotherapy for advanced gastric cancer: an old lesson revisited.." Journal of Clinical Oncology, 10(4), pp. 515–516© 1992 by American Society of Clinical Oncology
Oncogenes and tumor progression.
Authors: R A Weinberg
Journal: Journal of Clinical Oncology (1986)

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.1986.4.9.1293 Journal of Clinical Oncology - published online before print September 22, 2016 PMID: 3746374 Oncogenes and tumor progression. R A WeinbergxR A WeinbergSearch for articles by this author https://doi.org/10.1200/JCO.1986.4.9.1293 PDF "Oncogenes and tumor progression.." Journal of Clinical Oncology, 4(9), pp. 1293–1294© 1986 by American Society of Clinical Oncology
Dextroamphetamine Poisoning
Authors: Beale H. Ong
Journal: New England Journal of Medicine (1962)

DEXTROAMPHETAMINE sulfate (d-Amfetasul, Dexedrine sulfate) is a compound that, in recent years, has been used in the therapy of many clinical conditions — exogenous obesity, enuresis and depressive states, to name but a few. In addition, its stimulating effect on the central nervous system is becoming widely known to the public. In 1959, 75,000 pounds of this compound were produced, or enough to provide 20 tablets for each man, woman and child in the United States. Illicit traffic has become of national concern to the United States Public Health Service because the drug is being sold without prescription to various . . .
p53 stimulates recombination on chromosomes via topoisomerase I
Authors: Lisa Wiesmüller
Journal: Cancer Research (2006)

Proc Amer Assoc Cancer Res, Volume 47, 2006

3352 

So far, repression of homologous recombination (HR) has been the best established direct function of p53 in DNA repair. Several groups demonstrated that p53 activities in transcriptional transactivation and checkpoint control are separable from its HR regulatory functions and provided convincing evidence for fidelity control during HR as the mechanistic basis of the anti-recombinogenic effect. Surprisingly, however, when using an SV40-based recombination assay that was adapted to the analysis of different leukemia-related sequences, we previously discovered that p53 directly enhances HR at the RARalpha breakpoint cluster region (bcr) comprising topoisomerase I recognition sites. Applying siRNA-mediated knockdown, we newly show that p53 can stimulate HR in a manner strictly depending on topoisomerase I, which is consistent with our previous data revealing a similar degree of recombination enhancement by either p53 expression or camptothecin treatment. Similar to recombination on viral minichromosomes, enhancement of HR by exogenous p53 was seen, when the DNA substrates were localized on cellular chromosomes of p53-negative K562 cells. However, p53 exerted anti-recombinogenic rather than stimulatory activities, when the RARalpha bcr element was part of an episomal recombination plasmid, which was introduced into K562 cells by transient transfection, or when chromosomally integrated substrate was subjected to I-Sce I-meganuclease-mediated cleavage. Thus, the stimulatory effect was detectable only if the DNA recombination substrate was localized on viral or cellular chromosomes, i.e. was depending on chromatin structure. Our observations further suggest that p53 and topoisomerase I cooperate in a pathway increasing the recombinogenicity of the DNA substrate which becomes irrelevant upon availability of highly recombinogenic DNA, such as naked plasmid or cleaved DNA. Previously, p53 was reported to stimulate the formation of a double cleavage complex with two topoisomerase I molecules encompassing a DNA lesion. After the introduction of certain types of DNA lesions, such as caused by gamma-irradiation, p53 may, therefore, maintain genomic stability by this topoisomerase I-dependent lesion excision mechanism involving recombinative gap repair. These data describe a biological role of the biochemical interactions between p53 and topoisomerase I and have implications for a gain-of-function phenotype of certain p53 mutants in genetic destabilization.
Tanespimycin (T) + bortezomib (BZ) in multiple myeloma (MM): Pharmacology, safety and activity in relapsed/refractory (rel/ref) patients (Pts)
Authors: P. G. Richardson, A. Chanan-Khan, S. Lonial, A. Krishnan, M. Carroll, G. F. Cropp, M. Albitar, R. G. Johnson, A. Hannah, K. Anderson
Journal: Journal of Clinical Oncology (2007)

3532 Background: Tanespimycin (17-AAG/KOS 953) disrupts Hsp90, a molecular chaperone of MM client proteins including IL-6 and IGF-1R that are key to MM growth, survival and drug resistance. Single agent T was well tolerated with modest anti- MM activity. Preclinical studies suggest potential synergy with BZ. Methods: Pts received BZ as IVB followed by 1-hr infusion of T on D1,4,8,11 q 21d. Results: 49 pts were enrolled in 7 cohorts (T 100- 340 mg/m 2 ; BZ 0.7 - 1.3 mg/m 2 ). PK of T was similar with or without BZ. Inhibition of 20S proteasome with T+BZ was not different vs. historical BZ single agent data. PBLs showed induction of Hsp70 4h post-infusion with maintenance of induction prior to T infusion across the dosing interval; pAKT plus total AKT were also reduced 4 and 72h following infusion. CD138 but not CD4 or CD8 cells from serial BM aspirates showed induction of apoptosis by flow cytometry. In addition, ↓expression of IGR-1R and IL-6R client proteins was seen after treatment. Safety: In Cohort 7, 19 pts received T 340 / BZ 1.3 mg/m 2 . Common all-grade (G) drug-related toxicity (n=19) included diarrhea (42%), nausea (32%), vomiting (26%), ↑ AST/ALT/Alk Phos (26%/21%/21%), myalgias (16%), and dizziness (16%). G3 thrombocytopenia was noted in 16% with no other G3 toxicity observed in more than 1 pt. DLT was seen in 2 pts: G3 myalgias/cramps and dehydration (reversible in both). G1–2 only treatment-emergent peripheral neuropathy was recorded in 15%. Activity: Responses have been seen across dose levels in BZ-naïve, pre-treated and ref pts (“ref” defined as no response to or disease progression within 60d of last dose of BZ-containing regimen). Specifically, 1 BZ-ref pt with 3 prior regimens had confirmed PR after 2 cycles and continues in Cycle 9 (M-spike ↓92%); a 2nd pt with 2 prior regimens achieved PR after 2 cycles and continues in Cycle 7; a 3rd pt with 7 prior regimens with confirmed PR after 3 cycles continues in Cycle 6. Conclusions: Treatment with T 340/ BZ 1.3 combination had generally manageable toxicity. Durable Hsp90 inhibition and similar proteasome inhibition (vs single-agent BZ) was seen. Importantly, anti-MM activity in BZ-ref pts was observed and further investigation of this combination in rel/ref MM is therefore warranted. No significant financial relationships to disclose.
Flare in axial spondyloarthritis. The dark side of the outcome
Authors: Daniel Wendling, Clément Prati
Journal: Annals of the Rheumatic Diseases (2016)

Spondyloarthritis (SpA) is a chronic inflammatory rheumatic disease with many phenotypes,1 but the frame of the disease is still a matter of debate, particularly regarding the non-radiographic forms of axial SpA.2 ,3 The disease evolution may have several profiles, mainly related to the treatment strategy, balancing from periods of remission or low disease activity to flares of the disease. The recommended treatment strategies are supposed to be tailored to the disease activity, aiming to reach remission or low disease activity in a T2T strategy,4 with management of remission (reduction of dosage or increase in interval of administration), as well as treatment intensification in case of flares.

Definition of a flare may be difficult, particularly in a multifaceted disease like SpA, and in fact there is currently no clear, universally recognised, definition of a flare in axial SpA. This is part of the research agenda of recent recommendations.5 Looking at a medical dictionary, flare is defined as a sudden intensification in disease. In first analysis, one may propose that flare represents a worsening of symptoms with an increase in disease activity. Taking this into consideration, many questions arise: should we consider relative variation or absolute value above a significant threshold? Should we consider only generalised increase in activity? Should we include extra rheumatic manifestations such as uveitis or inflammatory bowel disease (IBD)? Are synovitis and enthesitis also part of this evaluation? Should we include biological markers (but reliable biomarkers are lacking in …
Loss of B Cells in Patients with Heterozygous Mutations in IKAROS
Authors: Hye Sun Kuehn, Bertrand Boisson, Charlotte Cunningham-Rundles, Janine Reichenbach, Asbjørg Stray-Pedersen, Erwin W. Gelfand, Patrick Maffucci, Keith R. Pierce, Jordan K. Abbott, Karl V. Voelkerding, Sarah T. South, Nancy H. Augustine, Jeana S. Bush, William K. Dolen, Betty B. Wray, Yuval Itan, Aurelie Cobat, Hanne Sørmo Sorte, Sundar Ganesan, Seraina Prader, Thomas B. Martins, Monica G. Lawrence, Jordan S. Orange, Katherine R. Calvo, Julie E. Niemela, Jean-Laurent Casanova, Thomas A. Fleisher, Harry R. Hill, Attila Kumánovics, Mary Ellen Conley, Sergio D. Rosenzweig
Journal: New England Journal of Medicine (2016)

Common variable immunodeficiency (CVID) is characterized by late-onset hypogammaglobulinemia in the absence of predisposing factors. The genetic cause is unknown in the majority of cases, and less than 10% of patients have a family history of the disease. Most patients have normal numbers of B cells but lack plasma cells.
Novel Gene Signatures Observed in the Nonlesional Skin from European American Atopic Dermatitis Subjects Who Are Colonized with Staphyloccoccus Aureus
Authors: Takeshi Yoshida, Jason R. Myers, John M. Ashton, Anna De Benedetto, Steven R. Gill, Catherine Philpot, Gloria David, Donald Y. Leung, Lisa A. Beck
Journal: Journal of Allergy and Clinical Immunology (2016)
In Vivo Isolation of a Metastatic Tumor Cell Variant Involving Selective and Nonadaptive Processes&lt;xref ref-type="fn" rid="fn2"&gt;2&lt;/xref&gt;, &lt;xref ref-type="fn" rid="fn3"&gt;3&lt;/xref&gt;
Authors: A Raz, N Hanna, I J Fidler
Journal: JNCI Journal of the National Cancer Institute (1981)

An investigation was done to determine whether spontaneous metastases that develop in a C3H mouse bearing the syngeneic UV-2237 fibrosarcoma are derived from specialized subpopulations of cells or represent an adaptation process to a local (organ) environment. Inbred C3H mice received sc injections of parent tumor and, 9 weeks later, 5 individual pulmonary metastases were harvested and established in culture. Cells from each of these metastases colonized in the lungs of normal recipient mice with significantly greater efficiency than did cells from the parent tumor. Mice received injections iv of cells from a cloned line of UV-2237 that produced few lung metastases. Cells from these metastases did not colonize in the lungs at a dramatically higher rate than did the parent clone. The growth per se of tumor cells into colonies in the lung is not sufficient by itself to endow cells with metastatic properties. The selection in vivo of cells with enhanced lung colonization does not require that the lung be used as a selective organ. A cell variant was selected for enhanced capacity to grow in the peritoneal cavity of normal recipients. This cell line was also found to have a high capacity to colonize in the lungs following introduction into the circulation. It was concluded that the growth of metastases in this murine tumor system was not due to adaptive processes but rather to selection by intrinsic properties of tumor cells.
Photodynamic therapy for palliation of locally recurrent breast carcinoma.
Authors: M Schuh, U O Nseyo, W R Potter, T L Dao, T J Dougherty
Journal: Journal of Clinical Oncology (1987)

Fourteen women with locally recurrent breast carcinoma on the chest wall following mastectomy were given 30 courses of photodynamic therapy (PDT). All patients had been heavily pretreated with conventional modes of therapy (radiation therapy, chemotherapy, hormonal therapy, surgical resection). Twenty-two courses yielded a partial response; two courses yielded a complete response; four courses showed no response; one patient was treated as an adjunct to surgery; and one patient was lost to follow-up. Duration to response was variable, ranging from 6 weeks to 8 months. Several women had chest wall disease controlled for prolonged periods of time using repeated courses of PDT. Two women had re-epithelialization of ulcerated lesions. Complications were minimal and included pain (two patients), sunburn (two), and infection (one). These results suggest that treatment with PDT can aid in local control of chest wall recurrence following mastectomy in selected patients.
Sofosbuvir in combination with simeprevir +/- ribavirin in genotype 4 hepatitis C patients with advanced fibrosis or cirrhosis: a real-life experience from Belgium
Authors: C Moreno, L Lasser, Jean Delwaide, P Starkel, W Laleman, P Langlet, H Reynaert, S Bourgeois, S Negrin Dastis, T Gustot, S Francque, A Geerts, C Van Steenkiste, C de Galocsy, C Assene, H Orlent, M Nkuize, D Degre
Journal: Hepatology (2015)

patients with advanced fibrosis or cirrhosis: real-life experience from Belgium Christophe Moreno1, Luc Lasser2, Jean Delwaide3, Peter Starkel4, Wim Laleman5, Philippe Langlet6, Hendrik Reynaert7, Stefan Bourgeois8, Sergio Negrin9, Thierry Gustot1, Sven Francque10, Anja Geerts11, Christophe Van Steenkiste12, Chantal de Galocsy13, Collins Assene13, Hans Orlent14, Thomas Serste1,15, Delphine Degre1 1. Department of Gastroenterology, Hepatopancreatology and digestive Oncology. Erasme hospital, ULB , Brussels, Belgium. 2.Department of Gastroenterology, Brugmann Hospital, Brussels, Belgium. 3.Department of HepatoGastroenterology, CHU Liege, Liege, Belgium. 4. Department of Hepato-Gastroenterology, Clinique Universitaire Saint-Luc, Brussels, Belgium. 5. Department of Gastroenterology and Hepatology. University Hospital Gasthuisberg, Leuven, Belgium. 6. Department of Hepato-Gastroenterology, CHIREC, Brussels, Belgium. 7. Department of Gastroenterology and Hepatology, VUB, UZ Brussels, Belgium. 8. Department of Gastroenterology and Hepatology, ZNA, Antwerpen, Belgium. 9.Department of Gastroenterology and Hepatology, CHdC, Charleroi, Belgium. 10. Division of Gastroenterology and Hepatology, University Hospital Antwerp, Edegem, Belgium. 11. Department of Gastroenterology and Hepatology, University Hospital Ghent, Belgium. 12. Department of Gastroenterology and Hepatology, AZ Maria Middelares, Ghent, Belgium, 13. Department of Gastroenterology and Hepatology, hopitaux IRIS sud, Brussels, Belgium. 14. Department of Gastroenterology and Hepatology, AZ Bruges, Belgium. 15. Department of Hepato-Gastroenterology, CHU Saint-Pierre, Brussels, Belgium.
Sixty seconds on . . . the NHS Bill
Authors: Clare Dyer
Journal: BMJ (2016)

This is a private member’s bill sponsored in the UK parliament by the Green Party MP Caroline Lucas. Backed by health service campaigners, it aims to reverse Conservative NHS reforms and stop the “creeping privatisation” of the service over decades by Labour and Tory governments.

Extremely unlikely. Few private members’ bills—those put forward by backbench MPs—get anywhere unless …
IMCT-03SAFETY AND ACTIVITY OF NIVOLUMAB MONOTHERAPY AND NIVOLUMAB IN COMBINATION WITH IPILIMUMAB IN RECURRENT GLIOBLASTOMA: UPDATED RESULTS FROM CHECKMATE-143
Authors: John Sampson, Antonio Omuro, Gordana Vlahovic, Solmaz Sahebjam, Joachim Baehring, David A. Hafler, Alfredo Voloschin, Jason Simon, Robert Latek, Vlad Coric, Timothy Cloughesy, Michael Lim, David Reardon
Journal: Neuro-Oncology (2015)

INTRODUCTION: Following progression after first-line therapies, patients with glioblastoma (GBM) have a poor prognosis. Immune checkpoint inhibitors have shown antitumor activity in patients with several types of solid tumors and also in preclinical glioma models. The Phase 1 portion of CHECKMATE-143 was designed to evaluate the safety and tolerability of nivolumab, a fully human IgG4 monoclonal antibody targeting the programmed death-1 (PD-1) immune checkpoint pathway, as monotherapy and in combination with ipilimumab, a monoclonal antibody that inhibits CTLA-4, in patients with a first recurrence of GBM. All patients in Cohort 1 had prior surgical resection, radiation, and temozolomide. Median age was 57 years (range: 37–73), and KPS ≥70. Preliminary results from the study were previously presented and showed nivolumab monotherapy 3 mg/kg was well tolerated in patients with recurrent GBM, with no reported treatment-related grade 3–4 adverse events (AEs). Nivolumab 1 mg/kg in combination with ipilimumab 3 mg/kg was associated with a higher incidence of treatment-related grade 3 (n = 7/10) and grade 4 AEs (n = 2/10). Histopathologic and neuroimaging detected antitumor activity within the tumor site, and the preliminary overall survival (OS) rate at 9 months was 6/10 for both the monotherapy and combination arms. METHODS: Patients (n = 20) were randomized 1:1 to receive either nivolumab 3 mg/kg Q2W or nivolumab 1 mg/kg + ipilimumab 3 mg/kg Q3W followed by nivolumab 3 mg/kg Q2W. Eligible patients had no prior bevacizumab treatment and Karnofsky Performance Status ≥70. The primary endpoint was safety/tolerability. RESULTS: This report will provide updated follow-up data including safety and OS at 12 months.
Monitoring Egfr T790M Using Plasma Dna in Lung Cancer Patients Treated with Egfr Tyrosine Kinase Inhibitor in a Prospective Observational Study
Authors: Y. Urata, N. Sueoka-Aragane, N. Katakami, M. Satouchi, S. Yokota, K. Aoe, K. Iwanaga, K. Otsuka, S. Kimura, S. Negoro
Journal: Annals of Oncology (2014)