tbuckley/cabot-search huggingface dataset:
Cancer clinical trial acronyms presented at ASCO Annual Meetings.
Authors: D. Wallace, Y. Ko
Journal: Journal of Clinical Oncology (2010)

e16558 Background: A recent review of clinical trials found that trials with acronym names were more likely to have industry involvement, enroll more patients and have less follow up time. Given the rapidly evolving landscape of cancer drugs over the last ten years, we performed a review of ASCO abstracts to identify trends in the coerciveness of trial names over time. Methods: Abstracts from the ASCO Annual Meetings from 2000-2009 were reviewed. Abstracts were included if the title contained a study name with an acronym. Details of each study including the number of abstracts, industry involvement, type of cancer, number of subjects, randomization, and type of primary endpoint, were collected. Coerciveness of the acronym was determined by assigning acronyms to not coercive (NC) or probably coercive (PC) categories based on past literature. Results: Of the 117,675 abstracts reviewed, 329 abstracts were identified with acronyms in the title. Of these, 219 studies were identified with 193 separate study names. Of these 219 trials, 14 represented the same trial and 3 shared the same name but were unrelated. 157 of the acronyms could be deemed real words, 53 could be read as possible words, and 9 were basic acronyms which could not be classified as words. 128 acronyms were considered NC and 91 were considered PC. There was no trend toward more frequent acronym use over time (approximately 0.1% each year). Industry involvement appeared to be more prevalent in PC trials with 38.5% (n = 35) trials having involvement compared to only 25.8% (n = 33) for NC trials. 20.8% (n = 19) of these PC titles first appeared from 2000-2004 compared to 79.2% (n = 72) titles appearing first from 2005- 2009. Breast cancer was the most common cancer for NC acronyms 29.7% (n = 36) while colorectal cancer was the most common cancer with a PC trial name 24.2 % (n = 22). The most common trial designs were phase II for NC trials (28.9%, n = 37), and phase III for PC trials with (35.2%, n = 32). Conclusions: This study demonstrates that although the proportion of clinical trials in oncology with acronym names has not increased over the past ten years, there has been an increase in the proportion of studies with possibly coercive titles and that those studies are more often industry sponsored. No significant financial relationships to disclose.
A Single Injection of Pegylated Murine Megakaryocyte Growth and Development Factor (MGDF ) Into Mice Is Sufficient to Produce a Profound Stimulation of Megakaryocyte Frequency, Size, and Ploidization
Authors: Julie T. Arnold, Najat C. Daw, Paula E. Stenberg, Deepthi Jayawardene, Deo Kumar Srivastava, Carl W. Jackson
Journal: Blood (1997)
Abstract 16434: Repaired Tetralogy of Fallot With Coexisting Unrepaired Partial Anomalous Pulmonary Venous Connection is Associated With Diminished Right Ventricular Ejection Fraction and More Severe Right Ventricular Dilation
Authors: Sherwin S Chan, Kevin K Whitehead, Timothy S Kim, Gregory L Fu, Marc S Keller, Mark A Fogel, Matthew A Harris
Journal: Circulation (2014)

Introduction: There is a known association between Tetrology of Fallot (ToF) and partial anomalous pulmonary venous connection (PAPVC).

Hypothesis: We hypothesize that patients with ToF and PAPVC have diminished right ventricular ejection fraction (RVEF) in comparison to ToF patients without PAPVC.

Methods: We reviewed all cardiac magnetic resonance imaging (CMR) at our institution for ToF from 1/1/2004 to 5/1/2014. We included patients with repaired ToF and unrepaired PAPVC. We used sex and age matched repaired ToF patients without PAPVC as controls. We performed comparative statistics to find differences between the groups.

Results: There were 9 patients with repaired ToF and unrepaired PAPVC and 18 controls. In all 9 cases, the PAPVC was not detected on preoperative echocardiography. There were no significant differences in surgical course and body surface area between the two groups (Table 1). Repaired ToF patients with unrepaired PAPVC showed significantly higher indexed RVEDV, RV to LV size ratios and a higher incidence of reduced RVEF compared to controls (Table 1). There were three pediatric patients with reduced RVEF (range 3 months to 16 years) which normalized on echocardiography after returning to the operating room for PAPVC repair. One of these patients had their RV function measured with CMR after PAPVC repair (Figure 1).

Conclusions: Repaired ToF with unrepaired PAPVC is associated with reduced RVEF and more significant RV dilation. Therefore, it is important to assess for PAPVC in repaired ToF patients with reduced RVEF and disproportionate RV dilation.

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ErbB/Her dimerization profiles and targeted therapy in breast and lung cancer
Authors: S. Singh
Journal: Journal of Clinical Oncology (2005)

808 Background: Aberrant signaling pathway drives cancer. This is because of the dysregulation of signaling by the erbB family of transmembrane receptor tyrosine kinases. The EGFR family includes human erbB1 (EGFR or Her1), erbB2 (Her2 or neu), erbB3 (Her3), and erbB4 (Her4). The aberrant signaling can be due to various reasons, like for example ligand overproduction, over-expression of the receptors on the cell surface, mutations or defective internalization of the receptor from the cell surface. Whatever the reason, these pathways become active in cancer and it is important to shut them down using appropriate therapy. Employing eTag assays, we can identify the active pathways in each cancer patient in a quantitative manner and provide a dimerization profile for targeted therapy. Materials and Method: We have measured the total Her1, Her2 and Her3 receptor expression levels and Her1/2, Her2/3 Her1/1 and Her2/2 dimerization profiles in 73 breast and 37 lung tissues using the proximity-based multiplexed eTag assays. Results: Our results indicate that the total receptor expression levels are different in different tumor samples. Moreover, the dimerization profiles may or may not correlate with the total receptor expression levels. ErbB/Her dimerization was detected only in tumor tissues but not in normal tissues, whether matched with the same donor or not. We also found that in breast tissues, all tumor samples had higher Her-2 levels compared to normal tissues. These results suggest that targeting therapy based on individual needs is the way to go in the treatment of breast and lung cancer. Conclusion: eTag technology can be a very useful tool in determining the total receptor expression levels and dimerization profiles in individual cancer patients, thereby providing a valuable prognostic tool for stratifying cancer patients for targeted therapy. In addition, eTag technology can also help in monitoring the patient response to targeted therapy during the course of drug treatment. No significant financial relationships to disclose.
Impact of positive peritoneal cytology on the survival of early stage endometrial cancer
Authors: P. M. Tebeu, Y. Popowski, H. M. Verkooijen, C. Bouchardy, F. Ludicke, M. Usel, A. L. Major
Journal: Journal of Clinical Oncology (2004)

5032 Background: The value of peritoneal cytology for stage I endometrial cancer remains controversial. According to the FIGO classification system, early stage endometrial tumors with positive peritoneal cytology are classified as stage IIIA, implying that their prognosis is similar to that of tumors with histological serosal or adnexal invasion. The aim of this study was to assess the prognostic importance of positive peritoneal cytology in early stage endometrial cancer. Methods: All 278 stage I and 53 stage IIIA (without cervical involvement) endometrial cancer patients operated between 1980–1996, recorded at the Geneva Cancer registry, were included. Stage lllA cancers were re-categorised into ‘cytological’ stage lllA (positive peritoneal cytology alone, n=33) and ‘histological’ stage lllA (serosal or adnexal infiltration, n=20). Survival according to stage was analysed by Kaplan Meier method and compared using log-rank test. The prognostic importance of cytology was analysed by Cox Proportional Hazards analysis, taking into account other prognostic factors. Results: The 5-year disease specific survival of cytological stage IIIA cancer was similar to stage I (91% versus 92% respectively) and better than histological stage IIIA cancer (50%, p<0.001). After adjustment for other prognostic factors (age, differentiation, myometrial invasion and use of adjuvant radiotherapy), cytological stage IIIA patients were still at similar risk to die from endometrial cancer as stage I patients (HR 0.7, 95%CI: 0.18–2.3), while histological stage IIIA patients were at a four fold increased risk to die from their disease (HR 4.2, 95%CI: 1.7–10.3). Conclusions: This population based study shows that positive peritoneal cytology in itself has no impact on survival of patients with localised endometrial cancer. Based on the present and previous studies, FIGO might consider reviewing its classification system. No significant financial relationships to disclose.
Chromosome Studies in Human Leukemia. III. Acute Granulocytic Leukemia
Authors: David A. Hungerford, Peter C. Nowell
Journal: JNCI Journal of the National Cancer Institute (1962)

Chromosome studies are reported in 9 cases of acute granulocytic leukemia in adults. In 5 of these, no significant chromosome abnormality was found. In one individual, the leukemic cells had 45 chromosomes including an abnormally large acrocentric chromosome. In the remaining 3 individuals, the leukemic cells all had 47 chromosomes with the extra chromosome in the #7 to 12 group. Clinically and hematologically these S patients did not constitute a recognizable subgroup. The findings indicate that acute granulocytic leukemia is not characterized by a consistent specific chromosome abnormality, but that in some of these individuals remarkably similar chromosome changes may occur.
HbA<sub>1c</sub>in the Evaluation of Diabetes Mellitus
Authors: Derek T. O’Keeffe, Spyridoula Maraka, Robert A. Rizza
Journal: JAMA (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 HomeNew OnlineCurrent IssueFor Authors Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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 journal
TG101348, a potent, highly selective JAK2 inhibitor, inhibits colony formation in stem cells from polycythemia vera patients and prevents JAK2V617F-mediated splenomegaly and death in a mouse model
Authors: J. Hood, J. Doukas, M. Martin, G. Noronha, C. Jamieson, R. Soll
Journal: Journal of Clinical Oncology (2007)

7031 Background: The molecular pathogenesis of the myeloproliferative disorders (MPDs) polycythemia vera, essential thrombocythemia, and myelofibrosis with myeloid metaplasia has been strongly linked to an activating mutation of JAK2 (Janus Associated Kinase 2). A G-T transversion event in exon 14 that translates into a substitution of phenylalanine for valine at amino acid residue 617 leads to constitutive activation of JAK2 V617F in a majority of these MPD cases. Methods: In order to address this unmet clinical need we designed, synthesized and performed preclinical evaluations on a series of structurally novel compounds optimized for JAK2 inhibition. Results: TG101348, a compound which potently inhibits JAK2 V617F enzymatically and in human cells, was selected as a clinical development candidate from this medicinal chemistry campaign. TG101348 displays remarkable kinase specificity as shown by 83X selectivity versus JAK3 and potent inhibition of &lt;2% of the kinases evaluated in a commercial, phylogenetically diverse panel of 212 kinases. TG101348 potently inhibits erythroid colony formation in patient-derived cells from polycythemia patients at doses 2–3X lower than in normal control patients. Consistent with this observation TG101348 inhibits JAK2-driven STAT5 phosphorylation, cell proliferation and cell survival in JAK2 V617F -expressing cell lines. In vivo, TG101348 exhibits promising pharmacokinetic profiles in species ranging from mouse to monkey including oral availabilities &gt;20%, and half-lives consistent with once or twice daily dosing. TG101348 reduces the number of circulating mutant JAK2 cells, inhibited splenomegaly and improved survival without significantly impacting normal hematocrit in an aggressive JAK2-driven circulating cell model of disease in rodents. Conclusion: TG101348 has considerable potential for the treatment of JAK2- driven myeloproliferative disorders based on its promising preclinical potency, selectivity and pharmaceutical properties. [Table: see text]
ECOG 1308: A phase II trial of induction chemotherapy followed by cetuximab with low dose versus standard dose IMRT in patients with HPV-associated resectable squamous cell carcinoma of the oropharynx (OP).
Authors: Shanthi Marur, Ju-Whei Lee, Anthony Cmelak, Weiqiang Zhao, William H. Westra, Christine H. Chung, Maura L. Gillison, Jill Gilbert, Julie E. Bauman, Lynne I. Wagner, Robert L. Ferris, David R. Trevarthen, A. Dimitrios Colevas, Balkrishna N. Jahagirdar, Barbara Burtness
Journal: Journal of Clinical Oncology (2012)

5566 Background: Human papillomavirus (HPV) infection is now recognized as a risk factor of oropharyngeal squamous cell carcinoma (OPSCC) and approximately 60% of OPSCC are HPV positive (+). ECOG 2399 using induction chemotherapy (IC) followed by chemoradiation demonstrated significantly improved 2-yr progression-free survival (PFS; 85% vs. 50%, p=0.05) and overall survival (OS; 94% vs. 58%p=0.004). These results have generated interest in development of less toxic regimens for HPV(+) patients with lower dose radiation. Methods: Design: This is a phase II clinical trial .The primary objective is the estimation of the 2-year PFS in the reduced dose RT arm. Secondary objectives include toxicity, OS, objective response, quality of life (QOL) and correlative studies of biomarkers. Eligibility Criteria: Patients with Stage III or IV resectable HPV(+) OPSCC. HPV(+) disease is defined as p16 IHC strongly (+) on at least 70% of cells, and/or HPV-16 ISH (+).Treatment : Patients received IC with a combination of paclitaxel 90mg/m 2 on days 1,8, and 15, cisplatin 75mg/m 2 on day 1, and cetuximab loading dose of 400 mg/m 2 on day 1, cycle 1 followed by cetuximab 250 mg/m 2 weekly, thereafter. Each cycle was 21 days for a total of 3 cycles. After completion of IC, patients were assessed clinically with a complete head and neck exam and imaging studies. Those with clinical CR at primary site received radiation to 54Gy plus cetuximab. Patients with clinical PR or SD at primary site received standard dose RT with cetuximab. Correlative Studies: The expression of biomarkers on tumor and blood samples and QOL parameters will be correlated with the clinical outcomes. Results: Current enrollment: Target accrual was 83 patients. The study accrued 90 patients from March 17, 2010 to accrual on October 19, 2011. Baseline characteristics reveal; median age 57 years, 94% male, 95% white, 47% never smokers, 10% &lt;10 pack year (pyr) smoking, 38% &gt;10 pyr smoking, 84% not current smokers, 39% node (N) stage N2b and 29% N2c, 22% tumor (T) stage T1, 52% T2, 16% T3, and 10% T4. Conclusions: Enrollment has just completed with no data analysis available.
Targeted rescue of a polycystic kidney disease mutation by lysosomal inhibition
Authors: Alexis Hofherr, Claudius J. Wagner, Terry Watnick, Michael Köttgen
Journal: Kidney International (2016)

Autosomal dominant polycystic kidney disease (ADPKD) is the most common monogenic cause of end-stage renal disease. The molecular pathogenesis of ADPKD is not completely known, and there is no approved therapy. To date, there is limited knowledge concerning the molecular consequences of specific disease-causing mutations. Here we show that the ADPKD missense variant TRPP2(D511V) greatly reduces TRPP2 protein stability, and that TRPP2(D511V) function can be rescued in vivo by small molecules targeting the TRPP2 degradation pathway. Expression of the TRPP2(D511V) protein was significantly reduced compared to wild-type TRPP2. Inhibition of lysosomal degradation of TRPP2(D511V) by the US Food and Drug Administration (FDA)-approved drug chloroquine strongly increased TRPP2 protein levels in vitro. The validation of these results in vivo requires appropriate animal models. However, there are currently no mouse models harboring human PKD2 missense mutations, and screening for chemical rescue of patient mutations in rodent models is time-consuming and expensive. Therefore, we developed a Drosophila melanogaster model expressing the ortholog of TRPP2(D511V) to test chemical rescue of mutant TRPP2 in vivo. Notably, chloroquine was sufficient to improve the phenotype of flies expressing mutant TRPP2. Thus, this proof-of-concept study highlights the potential of directed therapeutic approaches for ADPKD, and provides a rapid-throughput experimental model to screen PKD2 patient mutations and small molecules in vivo.
The impact of cetuximab on the gemcitabine/cisplatin combination in first-line treatment of EGFR-positive advanced pancreatic cancer (APC): A randomized phase II trial of GISCAD
Authors: S. Cascinu, R. Berardi, S. Siena, R. Labianca, A. Falcone, E. Aitini, S. Barni, F. Di Costanzo, L. Frontini, G. Tonini, A. Zaniboni
Journal: Journal of Clinical Oncology (2007)

4544 Background: Cetuximab, an EGFR antibody inhibitor, has been shown to increase the activity of gemcitabine (GEM) in APC. Based on data from randomised trials and meta-analyses suggesting that the combination of a GEM with a platinum analog significantly improves survival as compared to GEM alone, we assessed the activity and feasibility of a combination of GEM/cisplatin (CDDP) plus cetuximab. Methods: Multicenter, randomised two-arm phase II trial: GEM 1,000 mg/m 2 day 1,8 and CDDP 35 mg/m 2 day 1,8 every 21 days alone or in combination with cetuximab 250 mg/m 2 weekly after a loading dose of 400 mg/m 2 . Treatment was limited to a maximum of 9 cycles. With 37 patients in each arm the power was 90% to select the truly better arm if the true between arm difference in response rate (RECIST) is at least 15%. The study was open for accrual until June 2005. Results: We present here the results of 74 patients including in the study. In all the patients, the first response rate are available (investigators’ assessment after 3 cycles) as well as toxicity data. Conclusions: Cetuximab does not seem to positively interact with GEM/CDDP combination in terms of activity especially concerning time to progression. Although toxicity was not increased by cetuximab, this combination should not be assessed in a phase III trial.The trial was supported in part by by Merck KGaA. [Table: see text] No significant financial relationships to disclose.
Abstract 353: New Technique of Gas Adiabatic Expansion for Brain and General Hypothermia in Pig
Authors: Guy Fontaine, Benoit Lécuelle, Jean Philippe Didon, Johan Jacob Schmid, Juan Carlos Chachques
Journal: Circulation (2013)

Objective: The purpose of this work was to confirm on a pig model the previous work performed on a rabbit model (ReSS 2012) to demonstrate induction of both brain and general hypothermia on a beating heart. Material and method: 8 Landrace pigs 39.4 ± 3.9 kg (mean ± SD) were studied under general anesthesia according to the WICCM protocol. Temperatures were measured by thermocouples every minute, after each injection: close to the injector inserted up to the nasopharynx without contact to the posterior wall, in the retrograde jugular vein, in the tympanic area, in the esophagus and in the rectum. After stabilization of temperatures, CO2 regulated at 580 psi (40 bar) was delivered for periods of 10 min. Valid data were obtained from 14 injections. We compared the drops in temperatures recorded until stabilization. In these pigs 2 ± 1.5 injections of CO2 were delivered. Results: The initial 90% drop in temperature was detected after 4.7 ± 1.4 min for tympanic and 9.4 ± 4 min p=0.02 for the core temperature. Temperatures recorded from the tympanic/jugular probes were identical p=1. Return to stable temperature was observed in 10-15 mn. Esophagus drop in temperature was 23 ± 10 °C n=6. The drop in temperature was significantly higher in the tympanic area 0.69 ± 0.4 °C than in the core temperature 0.36 ± 0.15 p = 0.02. The amount of extracted calories was 14.9 ± 6.7 kilocalories. Discussion: Core temperature drop was similar to that reported in pigs after nasopharynx PFC evaporation (Yu et al Crit Care Med. 2010). In our experiments the lowest temperature (-30°C) was recorded, as expected, at the exit point for the gas. Significant decrease in temperature of 26°C in the esophagus was always observed. Conclusion: This study confirms that CO2 expansion in the nasopharynx is effective for brain and body hypothermia in a pig model. This new technique which is simple, inexpensive and easy to use opens new vistas for the treatment of OHCA which, mixed with oxygen, can be started intra-arrest before CPR.
Association between age and risk of stroke or death from carotid endarterectomy and carotid stenting: a meta-analysis of pooled patient data from four randomised trials
Authors: George Howard, Gary S Roubin, Olav Jansen, Jeroen Hendrikse, Alison Halliday, Gustav Fraedrich, Hans-Henning Eckstein, David Calvet, Richard Bulbulia, Leo H Bonati, Jean-Pierre Becquemin, Ale Algra, Martin M Brown, Peter A Ringleb, Thomas G Brott, Jean-Louis Mas
Journal: The Lancet (2016)
Abstract 10704: microRNA-495 Mediates Cell Differentiation via DNA Methylation in P19 Stem Cells: An Endothelial Cell Model System
Authors: Jialiang Liang, Wei Huang, Wenfeng Cai, Yuhua Wang, Dehua Chang, Zhili Wen, Kai Kang, Ronald W Millard, Meifeng Xu, Muhammad Ashraf, Xiyong Yu, Yigang Wang
Journal: Circulation (2013)

Background and Objective: The molecular basis for the relatively low efficiency of endothelial cell differentiation is not well understood. The present study uses microRNA-495 (miR-495) to promote the endothelial differentiation and investigate the mechanism in P19 embryonic carcinoma stem cells as a cell differentiation model system. Methods: A miRNA expression profile was performed on original P19 cells after spontaneous differentiation (7-day) using a PCR array. Then miR-495 was overexpressed in P19 cells via lentivirus (P19miR-495, P19Null as control). The expression of endothelial cell marker genes (CD31 and CDH5) and pluripotent markers (Oct4 and Nanog) was analyzed by qPCR. The percentages of CD31+ and CDH5+ cells were assayed by flow cytometer. The methylation status of endothelial genes was analyzed by sodium bisulfite sequencing. DNMT3a, analyzed by luciferase reporter assay and qPCR, was predicted as a target of miR-495. Results: Surprisingly we found that miR-495 expression was significantly i...