tbuckley/cabot-search huggingface dataset:
Finding the Balance of Less Is More
Authors: Chester B. Good, Mark McConnell, John R. Downs
Journal: JAMA Internal Medicine (2016)

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Mortality after COPD-exacerbations: Learning from epidemiology
Authors: Enrique Stazzone, Sol Pinasco, Daniel Piñeiro, Horacio di Fonzo, Mariano Mazzei
Journal: European Respiratory Journal (2014)

Chronic obstructive pulmonary disease (COPD) is characterized by exacerbations during the course of the disease. Many patients die during the admission. We had previously reported the mortality and epidemiological characteristics of those patients (ATS 2014). Many patients who survive the hospitalization die during the following year. We wanted to know the mortality at 1 year of the hospitalization and the epidemiological characteristics.  We analyzed all patients admitted to our hospital from January 2008 to December 2012. In that time period there were 340 patients admitted with the diagnosis of COPD-E. After reviewing the hospital course, 142 had COPD-E, 63 patients had pneumonia (COPD-P), all the other had a different diagnosis (heart failure, thromboembolic disease, etc).  Of those 142 patients, many had several admissions, that left us with 108 patients. Of those 108 patients, 10 died during the hospitalization, so we had 98 patients discharged after a COPD-E. We had no follow up data of 22 (22%). So we have 86 admited patients for our analisis, of those 10 died during the hospitalization.  From the 86 patients admited for COPD-E, 26 are dead at 1 year, 10 during the hospitalization, and 16 during the 1 year follow up, so the  1 year mortality in our cohort is 30.2%  (Male 32.7%/females 25.8%). If we analize only those 76 patients discharged after a COPD-E, 16 died at 1 year, so the 1 year mortality after a COPD-E is 21% ( males 21.3%/ female 20.7%).  Conclusion: Hospitalization for COPD-E has a high 1 year mortality, despite maximizing efforts to change the course of the disease.
Development of a 9L Rat Brain Tumor Cell Multicellular Spheroid System and Its Response to 1,3-Bis(2-chloroethyl)-1-nitrosourea and Radiation2
Authors: Dennis F. Deen, Takao Hoshino, Mary E. Williams, Isao Muraoka, Kathy D. Knebel, Marvin Barker
Journal: JNCI Journal of the National Cancer Institute (1980)

Rat brain tumor cells (9L cells) were cultured in suspension as multicellular spheroids. When individual spheroids with diameters of approximately 200 μm were transferred to test wells, their diameters increased by about 25 μm/day; colony-forming efficiencies were routinely 40–50%. The durations of the S-phase (8.0–8.5 hr), the G2 phase (3.0–4.0 hr), and the cell cycle time (20.1–20.5 hr) in spheroids with diameters from 200 to 500 μm were similar to those determined earlier for monolayer and intracerebral 9L cells. The growth fraction of spheroids was approximately 0.5, also similar to that of 9L intracerebral tumors. Autoradiographic studies showed that 30 minutes were sufficient for [3H]thymidine to penetrate to the center of the spheroids and that after prolonged periods of exposure, both labeled and unlabeled cells existed throughout the spheroid. Cells cultured and treated as spheroids with approximate diameters of 200–600 μm were more sensitive to 1,3-bls(2-chloroethyl)-1-nitrosourea (BCNU) than were cells grown as spheroids but treated as suspended single cells. The most prominent change between percent labeled mitoses curves of control and BCNU-treated spheroids was the absence of a prominent second wave in the treated groups. Flow cytometry studies showed a gradual increase in the G2-M population 12 hours after BCNU treatment; a maximum was attained 30 hours after treatment. However, approximately 50% of the population remained in the 2C DNA position up to 56 hours after treatment. Radiation survival curves were obtained for spheroids having approximate diameters of 200–400 μm. In each case, intact spheroids were slightly more resistant to radiation than was the single cell suspension. Resistance was not displayed as a plateau region on the survival curves but rather as a shifting of the entire curve to the right. The amount of resistance over this size range was similar.
A Carcinogenicity Assay of Mirex in Charles River CD Rats2
Authors: Borge M. Ulland, Norbert P. Page, Robert A. Squire, Elizabeth K. Weisburger, Robert L. Cypher
Journal: JNCI Journal of the National Cancer Institute (1977)

Journal Article A Carcinogenicity Assay of Mirex in Charles River CD Rats Get access Borge M. Ulland, Borge M. Ulland Search for other works by this author on: Oxford Academic PubMed Google Scholar Norbert P. Page, Norbert P. Page Search for other works by this author on: Oxford Academic PubMed Google Scholar Robert A. Squire, Robert A. Squire Search for other works by this author on: Oxford Academic PubMed Google Scholar Elizabeth K. Weisburger, Elizabeth K. Weisburger Search for other works by this author on: Oxford Academic PubMed Google Scholar Robert L. Cypher Robert L. Cypher Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 58, Issue 1, January 1977, Pages 133–140, https://doi.org/10.1093/jnci/58.1.133 Published: 01 January 1977 Article history Received: 12 July 1976 Accepted: 27 September 1976 Published: 01 January 1977
Sunitinib for patients (pts) with advanced imatinib (IM)-refractory GIST: Early results from a “treatment-use” trial
Authors: J. A. Morgan, C. R. Garrett, H. J. Schutte, H. Hurwitz, L. S. Rosen, W. Ruka, J. Picus, P. Kaiser, C. M. Baum, G. D. Demetri
Journal: Journal of Clinical Oncology (2006)

9540 Background: Pts with advanced or metastatic GIST are typically treated first with IM, but many GISTs develop resistance to IM over time or are initially resistant this agent, and a small fraction of GIST pts are intolerant of IM therapy. Sunitinib malate (previously known as SU11248) is an oral, multitargeted tyrosine kinase inhibitor of KIT, PDGFR, VEGFR, FLT3, and RET that has demonstrated efficacy in extensive prior trials involving IM-refractory GIST pts. Since GIST pts who were ineligible for participation in sunitinib clinical trials might derive significant benefit from this therapy, a treatment-use program was implemented for this purpose. Methods: This on-going, multicenter, open-label trial was designed to grant access to sunitinib for treatment use in pts who were ineligible for other sunitinib trials and who had advanced IM-resistant GIST or documented intolerance to IM. Pts on sunitinib are monitored closely to assess clinical benefit as judged by the investigator. Sunitinib is administered at a starting dose of 50 mg/day on a 4/2 schedule (4 consecutive weeks on, 2 weeks off treatment). Clinical endpoints include safety and tolerability, as well as disease control (TTP), response rates, and survival. Results: Of 268 GIST pts enrolled in this treatment-use trial at the time of this analysis, 247 had received at least one dose of sunitinib. The median number of cycles completed was 2 (range, 0–9), and the median number of days on treatment was 83 (range, 1–385). The most frequently reported treatment-related AEs were fatigue (36%), diarrhea (31%), nausea (27%), and hand-foot syndrome (15%), which were generally grade 1/2. At the time of analysis, preliminary efficacy data were available for 152 pts. Of these, 123 pts remain on therapy and have received a median of 3 (range, 2–7) cycles of sunitinib. Based on initial investigator assessments, one pt achieved a CR, 14% achieved PR and 63% have noted SD as best response. Conclusions: Sunitinib was associated with acceptable tolerability in this population of IM-refractory GIST pts enrolled in this treatment-use trial. Consistent with previous results, promising clinical activity was seen, and expanded tolerability and efficacy data will be presented. [Table: see text]
Human Granulocyte Colony-Stimulating Factor (G-CSF) Stimulates the In Vitro and In Vivo Development But Not Commitment of Primitive Multipotential Progenitors From Transgenic Mice Expressing the Human G-CSF Receptor
Authors: Feng-Chun Yang, Sumiko Watanabe, Kohichiro Tsuji, Ming-jiang Xu, Azusa Kaneko, Yasuhiro Ebihara, Tatsutoshi Nakahata
Journal: Blood (1998)
A randomized open-label comparison of aprepitant (A) versus gabapentin (G) in the prevention of the refractory nausea and vomiting associated with moderately and severely emetogenic chemotherapy
Authors: A. Pacheco, C. F. Verschraegen, A. Mangalik, S. Cheshire, M. E. Royce
Journal: Journal of Clinical Oncology (2008)

20509 Background: The purpose of study is to compare the effectiveness of A versus G in treating refractory nausea and/or vomiting for patients receiving chemotherapy treatment. A is approved by the FDA for nausea and vomiting (N/V). G is approved by the FDA for the treatment of seizures, but it may be effective in controlling N/V due to chemotherapy (Guttuso, Lancet 2003). Methods: During the second course of chemotherapy associated with level 3, 4 or 5 emetogenic potential, patients received A (125 mg on day 1 and 80 mg on days 2 and 3) or G (300 mg tid days -2 to 5) in addition to the standard dexamethasone and odansetron if these drugs failed to control emesis during the first course of chemotherapy. A validated N/V self reported scoring system was used, with 0 being no N/V, and 15 being the worse N/V. Safety profile and subject satisfaction were also assessed. Results: 156 patients (123 Females and 33 Males; 79 Whites, 38 Hisp, 20 Native Am, 15 Unknown, and 3 Other) were screened and 87 signed a consent form during a 2 year period (2005- 2007) (25 were not interested, 16 were not eligible, and 28 had other reasons to not participate). Of 87 enrolled patients, 7 were not eligible, and 3 withdrew consents. Seventy-seven patients received 2 courses of chemotherapy. Of these, 17% (13 patients) (12F, 1M; 8W, 2NA, 2U, 1O) needed salvage antiemetic regimen. Six patients were randomized to A and 7 to G. Mean nausea scores/pt after the first cycle (control) were 7.0 for A and 7.43 for G and after the second cycle (post A or G treatment) were 2.66 for A and 1.0 for G. There were no differences in toxicity profile and satisfaction levels. Conclusions: G might be as efficacious as A to control refractory emesis. A front line study is planned. The lowest cost of G for 1 course of treatment is about $21 (21 pills at $1/pill) and for A $255 (3 pills at $85/pill). No significant financial relationships to disclose.
Trimetrexate: a second generation folate antagonist in clinical trial.
Authors: J T Lin, J R Bertino
Journal: Journal of Clinical Oncology (1987)

Trimetrexate is a promising new lipophilic antifolate with antitumor and antimicrobial activity, which is currently undergoing clinical trials. It differs from methotrexate in its transport and intracellular retention, and may be useful against tumors resistant to methotrexate because of impaired transport or deficient polyglutamylation. In preclinical studies, it has demonstrated a broader spectrum of antitumor activity than methotrexate, and appears to have synergistic antitumor activity when combined with a number of other agents. In clinical trials, the primary toxicity has been hematologic, with rapid recovery and no evidence of cumulative dose effect. Nonhematologic toxicity has been sporadic. Preliminary results of phase II trials indicate activity against breast, non-small-cell lung, and head and neck tumors. In addition, trimetrexate with simultaneous leucovorin rescue appears to be a promising new treatment for pneumocystis pneumonia in AIDS patients, with minimal toxic side effects.
Randomized Trial of Hepatic Artery Embolization for Hepatocellular Carcinoma Using Doxorubicin-Eluting Microspheres Compared With Embolization With Microspheres Alone
Authors: Karen T. Brown, Richard K. Do, Mithat Gonen, Anne M. Covey, George I. Getrajdman, Constantinos T. Sofocleous, William R. Jarnagin, Michael I. D’Angelica, Peter J. Allen, Joseph P. Erinjeri, Lynn A. Brody, Gerald P. O’Neill, Kristian N. Johnson, Alessandra R. Garcia, Christopher Beattie, Binsheng Zhao, Stephen B. Solomon, Lawrence H. Schwartz, Ronald DeMatteo, Ghassan K. Abou-Alfa
Journal: Journal of Clinical Oncology (2016)

Transarterial chemoembolization is accepted therapy for hepatocellular carcinoma (HCC). No randomized trial has demonstrated superiority of chemoembolization compared with embolization, and the role of chemotherapy remains unclear. This randomized trial compares the outcome of embolization using microspheres alone with chemoembolization using doxorubicin-eluting microspheres.At a single tertiary referral center, patients with HCC were randomly assigned to embolization with microspheres alone (Bead Block [BB]) or loaded with doxorubicin 150 mg (LC Bead [LCB]). Random assignment was stratified by number of embolizations to complete treatment, and assignments were generated by permuted blocks in the institutional database. The primary end point was response according to RECIST 1.0 (Response Evaluation Criteria in Solid Tumors) using multiphase computed tomography 2 to 3 weeks post-treatment and then at quarterly intervals, with the reviewer blinded to treatment allocation. Secondary objectives included safety and tolerability, time to progression, progression-free survival, and overall survival. This trial is currently closed to accrual.Between December 2007 and April 2012, 101 patients were randomly assigned: 51 to BB and 50 to LCB. Demographics were comparable: median age, 67 years; 77% male; and 22% Barcelona Clinic Liver Cancer stage A and 78% stage B or C. Adverse events occurred with similar frequency in both groups: BB, 19 of 51 patients (38%); LCB, 20 of 50 patients (40%; P = .48), with no difference in RECIST response: BB, 5.9% versus LCB, 6.0% (difference, -0.1%; 95% CI, -9% to 9%). Median PFS was 6.2 versus 2.8 months (hazard ratio, 1.36; 95% CI, 0.91 to 2.05; P = .11), and overall survival, 19.6 versus 20.8 months (hazard ratio, 1.11; 95% CI, 0.71 to 1.76; P = .64) for BB and LCB, respectively.There was no apparent difference between the treatment arms. These results challenge the use of doxorubicin-eluting beads for chemoembolization of HCC.
Abstract 17536: Association Between Chronic Obstructive Pulmonary Disease and Risk of Coronary Vasospastic Angina: a National Database Study
Authors: Ming-jui Hung, Ming-Yow Hung, Shuo-Ju Chiang, Li-Hsuan Wang, Nen-Chung Chang, Hsiu-Chen Lin
Journal: Circulation (2014)

Background:  Although chronic obstructive pulmonary disease (COPD) increases the risk of cardiovascular disease, little is known about the relation of COPD to coronary vasospastic angina (CVsA)   Methods:  The case-control study applied a longitudinal health insurance database (LHID) from the National Health Insurance program. LHID was a retrospective cohort as a population of 1,073,891 and randomly sampled from the entire population of 22,717,053 that were from 1996 to 2008. Patients who had at least one admission claim with an International Classification of Diseases Ninth Revision, Clinical Modification (ICD-9-CM) code of 4131 were identified as CVsA. The control group I was established by identifying other ischemic heart disease )ICD-9-CM codes 410 to 414 except 4131). The remaining subjects with matched age, gender and entry year from the LHID were defined as the control group II. Multivariate logistic regression analyses were performed and simultaneously adjusted for potential confounders to evaluate the association of COPD with CVsA.   Results:  We found 697 patients if CVsA (prevalence = 69.7/100,000 persons), and the mean age was 55 years old, male to female was 0.97:1. There were 115,433 and 2,788 patients in the group I and II, respectively. Compared with other ischemic heart disease group, CVsA patients were more likely to have prior COPD [adjusted odds ratio (OR) = 2.13, 95% confidence interval (CI) = 1.65 - 2.73], had more COPD hospitalization frequency (>= 3 times in 1 year) (adjusted OR = 5.25, 95% CI = 1.93 - 14.29), be younger and had hyperlipidemia (adjusted OR = 1.82, 95% CI = 1.54 - 2.14), even after adjusting for the confounders and co-morbidities.   Conclusions:  COPD was independently associated with a higher incidence of CVsA. Endothelial dysfunction and low-grade inflammation might play a role on CVsA.
Patterns of hepatotoxicity after chemotherapy for colorectal cancer metastases: Effect of bevacizumab
Authors: M. Klinger, S. Kandutsch, S. Hacker, B. Gruenberger, T. Gruenberger
Journal: Journal of Clinical Oncology (2008)

4082 Background: Combining bevacizumab with XELOX/FOLFOX4 is inreasingly being recognized as state of the art in the neoadjuvant treatment of colorectal cancer liver metastases. Our group has recently shown that bevacizumab does not increase perioperative morbidity after surgical resection of colorectal cancer liver metastases. Futhermore, we have shown recently that XELOX/FOLFOX4 causes profound morphological changes in liver parenchyma with Sinusiodal Dilatation and Liverfibrosis as its pathohistological correlate. The aim of this study was to determine if the addition of bevacizumab does change the injury pattern of XELOX/FOLFOX4. Methods: Liver specimen of 56 patients receiving biweekly bevacizumab plus capecitabine and oxaliplatin for six cycles (the sixth cycle of therapy did not including bevacizumab) and liver specimen of 50 patients solely receiving capecitabine and oxaliplatin (XELOX) or 5-fluorouracil, leucovorin plus oxaliplatin (FOLFOX4) for six cycles were analyzed. Results: Steatosis, fibrosis, concomitant necroinflammation, as well as sinusoidal injury were evaluated according to widely accepted pathohistological scores. We found no difference in grading of steatohepatitis among the two groups. The incidence of sinusoidal dilation of any grade was significantly lower in patients treated with bevacizumab. Furthermore, the incidence of moderate or severe sinusoidal dilation was significantly higher in patients treated without bevacizumab. Conclusions: We conclude that the addition of bevacizumab to XELOX/FOLFOX4 therapy has a protective effect with respect to Sinusiodal Injury. No significant financial relationships to disclose.
Late-breaking abstract: Postmenopausal hormone replacement therapy is associated with increased risk of asthma hospitalization
Authors: Klaus Bønnelykk, Ole Raaschou-Nielsen, Hans Bisgaard, Anne Tjønneland, Kim Overvad, Zorana J. Andersen
Journal: European Respiratory Journal (2011)

Background: Postmenopausal hormone replacement therapy (HRT) has been associated with asthma, but is not yet an established risk factor.

Aim: To investigate, for the first time, the association between HRT use and risk of severe asthma exacerbations requiring hospitalization in a prospective study. COPD was analyzed simultaneously to account for potential misclassification.

Methods: Intake of HRT and potential confounders, including smoking status, occupational exposure, educational level, body mass index, and hysterectomy, were assessed in 1993-1997 in 23 138 postmenopausal women from the Danish Diet, Cancer and Health cohort. Incident (first-ever) asthma and COPD hospitalizations were registered prospectively in Danish Hospital Discharge Register between 1993 and 2006. Association with HRT was analyzed with Cox's regression analyses.

Results: We observed 446 (1.9%) incident asthma hospitalizations in 23 138 women over 9.9 years mean follow-up. 11 575 (50.0%) women ever used HRT. Ever using HRT was positively associated with asthma hospitalization (hazard ratio [95% confidence interval]: 1.37 [1.14-1.65]). The risk was highest with the longest duration of HRT use (≥ 10 years: 1.51 [1.15-1.98], 3-10 years: 1.34 [1.05-1.72], < 3years: 1.29 [1.00-1.67], reference never users). Effect modification was detected by smoking, indicating strongest effect in never smokers (1.84 [1.32-2.56]) and no effect in current smokers (1.08 [0.79-1.45]). HRT was also associated with COPD hospitalization, with a smaller effect (1.19 [1.05-1.35]).

Conclusion: HRT use may cause asthma onset or worsening with severe exacerbation.
Partial Characterization of &lt;italic&gt;n&lt;/italic&gt;-Butanol-Solubilized Rejection-Type Antigens of Syngeneic Murine Colon Tumors
Authors: N Sato, K Kikuchi
Journal: JNCI Journal of the National Cancer Institute (1985)

Previous investigation of the transplantation immunity of 2 cultured murine colon lines of BALB/c origin, C-C36 and C-C26, showed these tumor lines to be immunogenic against individual tumors and to have possibly cross-reactive, tumor-rejection-type antigens. For characterization of the molecular features of tumor-rejection antigens expressed on the colon tumor cells, n-butanol was used for the extraction of rejection-type antigens from tumor cells and immunogenic molecules were analyzed on transplantation immunity. The data demonstrated that extraction of the rejection-type antigens from C-C36 and C-C26 surface membrane without cellular lysis was possible with n-butanol treatment of these cells, and immunogenic activities of these extracts from C-C36 and C-C26 cells were more potent than those of nonionic detergent Nonidet P40 extracts in the tumor-rejection assays. The extracts were partially characterized by chromatographic separation on Sephadex G-200 gel filtration and lectin-affinity chromatography. It was suggested that the C-C36 antigens responsible for tumor-rejection activity against the same tumor cells had a molecular weight range of approximately 150,000 to 250,000 (fraction II) in the presence of 5 mM EDTA and had been eluted into unbound fractions to lens culinaris lectin on affinity chromatography. Moreover, immunization of mice with antigens from the same fractions (fraction II) of n-butanol extracts of C-C26 tumor on the gel filtration could induce the resistance against challenged C-C36 as well as against challenged C-C26 tumor growth. These results may indicate that solubilized tumor-rejection-type antigens found in C-C36 and C-C26 colon tumors have a size similar to that of the molecules and that cross-reacting, rejection-type antigens between these cells are the products of the same gene clusters or somatic derivatives of a single gene.