tbuckley/cabot-search huggingface dataset:
Development of the functional capacity screening tool (FCST): A brief instrument to identify functional capacity deficits in anemic cancer patients
Authors: D. Cella, H. Viswanathan, R. D. Hays, T. Mendoza, K. Stein, D. Pasta, L. Potter, S. Vadhan-Raj, J. Kallich
Journal: Journal of Clinical Oncology (2006)

8593 Background: Existing fatigue measures are long and often difficult to incorporate in practice. The objective of this study was to develop a short tool (Functional Capacity Screening Tool [FCST]) to identify functional capacity deficits related to fatigue in anemic cancer patients (pts) using self-report and performance-based measures of functional capacity. Methods: Data were obtained from a multicenter, open-label, single-arm study of darbepoetin alfa therapy (3.0 μg/kg every 2 weeks) in cancer pts (n=1558) who were ≥ 18 years of age with nonmyeloid malignancies receiving cyclic chemotherapy and anemia (hemoglobin [Hb] ≤ 11 g/dL). The Modified Harvard Step Test (MHST) was used as a performance-based measure of functional capacity to assess adjusted VO 2max . Pts who contributed data for the development of FCST completed the following: MHST, baseline and ≥ 1 follow-up Hb measurement, baseline and ≥ 1 follow-up Functional Assessment of Cancer Therapy-Fatigue (FACT-F), and fatigue assessed within 3 days of MHST. Items from FACT-F, Brief Fatigue Inventory (BFI), Fatigue Symptom Inventory (FSI) and Medical Outcomes Study physical functioning scale were tested for inclusion in the FCST. Individual item scores were transformed to a 100-point scale. Item selection was based on identifying best predictors of adjusted VO 2max , Hb, and global FACT-F scores using linear regression and the r-square selection method. FCST scores were calculated by summating item scores and dividing by number of items. Results: Data from401 pts contributed to the development of the FCST. Eight items were identified for the FCST with a Cronbach’s coefficient alpha of 0.92. Construct validity was supported by correlations of FCST with FSI (r = 0.80, P &lt; .0001) and BFI (r = 0.86, P &lt; .0001). Correlations between FCST and energy (r = 0.75, P &lt; .0001), productivity (r = 0.72, P &lt; .0001), and Hb (r = 0.24, P &lt; .0001) further supported construct validity. Conclusions: FCST holds promise as a short screening tool for identifying functional capacity deficits in cancer pts. This new instrument was reliable, easy to score, and completed quickly by pts, making it suitable for incorporation in clinical practice. Further validation is required in different cancer populations. [Table: see text]
In-Vivo T-Cell Depletion with Rabbit Anti-Thymocyte Globulin (r-ATG) Prevents Severe Acute and Chronic Graft Versus Host Disease (GVHD) and Allows Safe Allogeneic Stem Cell Transplantation (allo-SCT) From Mismatched, Unrelated Donors
Authors: James L. Slack, Jose F. Leis, Craig B. Reeder, Joseph R. Mikhael, Pierre Noel, Ruben A. Mesa, Raoul Tibes, Jeffrey A. Betcher, Mary E Peterson, Meagan S. Higgins, Ginger Gillette-Kent, Lisa D. Tremblay, Jane J. Olson, Roberta H. Adams
Journal: Blood (2011)
Preferred reporting of case series in surgery; the PROCESS guidelines
Authors: Riaz A. Agha, Alexander J. Fowler, Shivanchan Rajmohan, Ishani Barai, Dennis P. Orgill, Raafat Afifi, Raha Alahmadi, Joerg Albrecht, Abdulrahman Alsawadi, Jeffrey Aronson, M. Hammad Ather, Mohammad Bashashati, Somprakas Basu, Patrick Bradley, Mushtaq Chalkoo, Ben Challacombe, Trent Cross, Laura Derbyshire, Naheed Farooq, Jerome Hoffman, Huseyin Kadioglu, Veeru Kasivisvanathan, Boris Kirshtein, Roberto Klappenbach, Daniel Laskin, Diana Miguel, James Milburn, Oliver Muensterer, James Ngu, Iain Nixon, Ashraf Noureldin, Benjamin Perakath, Nicholas Raison, Kandiah Raveendran, Timothy Sullivan, Achilleas Thoma, M.A. Thorat, Andy Petroianu, Ashwini Rao, Michele Valmasoni, Samuele Massarut, Anil D’cruz, Baskaran Vasudevan, Salvatore Giordano, Donagh Healy, David Machado-Aranda, Frederick H. Millham, Bryan Carroll, Indraneilm Mukherjee, Peter McCulloch, Yasuhiko Sugawara, David Rosin
Journal: International Journal of Surgery (2016)

Case series have been a long held tradition within the surgical literature and are still frequently published. Reporting guidelines can improve transparency and reporting quality. No guideline exists for reporting case series, and our recent systematic review highlights the fact that key data are being missed from such reports. Our objective was to develop reporting guidelines for surgical case series.A Delphi consensus exercise was conducted to determine items to include in the reporting guideline. Items included those identified from a previous systematic review on case series and those included in the SCARE Guidelines for case reports. The Delphi questionnaire was administered via Google Forms and conducted using standard Delphi methodology. Surgeons and others with expertise in the reporting of case series were invited to participate. In round one, participants voted to define case series and also what elements should be included in them. In round two, participants voted on what items to include in the PROCESS guideline using a nine-point Likert scale to assess agreement as proposed by the Grading of Recommendations, Assessment, Development and Evaluations (GRADE) working group.In round one, there was a 49% (29/59) response rate. Following adjustment of the guideline with incorporation of recommended changes, round two commenced and there was an 81% (48/59) response rate. All but one of the items were approved by the participants and Likert scores 7-9 were awarded by >70% of respondents. The final guideline consists of an eight item checklist.We present the PROCESS Guideline, consisting of an eight item checklist that will improve the reporting quality of surgical case series. We encourage authors, reviewers, editors, journals, publishers and the wider surgical and scholarly community to adopt these.
Erlotinib customization based on epidermal growth factor receptor (EGFR) mutations in stage IV non-small-cell lung cancer (NSCLC) patients (p)
Authors: R. Porta, C. Queralt, F. Cardenal, C. Mayo, M. Provencio, C. Camps, D. Isla, J. González-Larriba, M. Tarón, R. Rosell
Journal: Journal of Clinical Oncology (2008)

8038 Background: EGFR-mutant "oncogene-addicted" cancers are a distinct form of NSCLC that can be targeted with erlotinib (Paz-Ares et al. ASCO 2006). Methods: From April 2005 to December 2007, tumor biopsies from 2,312 stage IV NSCLC p from 43 centers were screened in one central laboratory in Badalona, Spain for EGFR exon 19 Δ746–750 deletion and exon 21 L858R mutation. Results were available within 8 days. p with EGFR mutations were selected for erlotinib therapy. Results: 307 p had EGFR mutations; data available on 165/307. 48 (29.1%) male; 112 (67.9%) never-smokers; 124 (75.2%) adenocarcinoma; 103 (62.8%) exon 19 deletion, 62 (37.6%) L858R mutation; 89 (53.9%) first-line, 76 (46.1%) second-line. Response in 111 p (73.1%); complete response in 20 p (13.2%); progressive disease in 16 p (10.5%). Odds ratio for response: 2.3 for p receiving first-line erlotinib and 2 for p with exon 19 deletion. Median survival: 24 months (m) overall; 27 m in responders vs 10 m in non-responders (P<0.001); not reached in females vs 16 m in males (P=0.04); 27 m for p with exon 19 deletion vs 16 m for p with L858R mutation (P=0.03). Results of the multivariate analysis are shown in the table. Conclusions: Customized erlotinib in EGFR-mutant NSCLC p results in longer survival in p with exon 19 deletion, PS 0, and no brain metastases. Updated information on all 307 p will be presented. The Spanish Lung Cancer Group has initiated a randomized trial of first- line erlotinib vs chemotherapy for stage IV NSCLC p. Hazard Ratio 95% CI p ECOG PS 0 1 (ref.) 1 2.20 0.91–5.36 0.08 ≥2 3.74 1.26–11–1 0.02 EGFR mutation Exon 19 deletion 1 (ref.) Exon 21 L858R mutation 2.12 1.10–4.53 0.03 Prior chemotherapy No 1 (ref.) Yes 0.84 0.41–1.73 0.64 Brain metastasis No 1 (ref.) Yes 2.8 1.16–6.76 0.02 No significant financial relationships to disclose.
A Phase I Study of Sequential Azacitidine and Lenalidomide for Elderly Patients with Acute Myeloid Leukemia (AML)
Authors: Daniel A Pollyea, Holbrook E Kohrt, Leonel Gallegos, Caroline Berube, Steven Coutre, Jason Gotlib, Michaela Liedtke, Beverly S. Mitchell, Bruno C. Medeiros
Journal: Blood (2010)
Abstract B38: F317i mutation-associated nilotinib resistance in a child with CML: A first report.
Authors: Heidi Tucker, Paul Kent
Journal: Clinical Cancer Research (2015)

Abstract Background: Philadelphia chromosome, t(9;22), positive (Ph+) chronic myelogenous leukemia (CML) accounts for only 2-2.5% of childhood leukemia cases or about 60 cases per year in the US. Tyrosine kinase inhibitors (TKIs) have dramatically changed the prognosis and treatment of CML in adults and children. Failure of TKIs is often due to mutations. In adult CML, the F317i mutation has been implicated in resistance to first and second line TKIs (imatinib/dasatinib) without affecting sensitivity to the third line TKI, nilotinib. The F317i mutation has been documented a handful of times in adult CML and in childhood Ph+ALL cases. We describe what we believe to be a first report of F317i mutation in a child with Ph+ CML who, after initial major molecular responses, rapidly developed resistance to first, second and third line TKIs. The current Childrens Oncology Group trial of oral nilotinib (COG AAML1321) does not recognize F317i as a mutation associated with nilotinib resistance. Case: An 11-year old female with classic chronic phase (CP) CML was found to have the F317i mutation after initially achieving an MMR during the first 3 months of treatment while on dasatinib. After results of the F317i mutation were received, the patient was switched to nilotinib and again achieved an MMR in the first 2 months before rapidly decompensating with a pre B cell ALL blast crisis. The child was then treated with ALL induction and consolidation and allogeneic stem cell transplant and again achieved an MMR which has been sustained for 5 months. Methods: Cases of the F317i mutation have been documented in adults, however, we did an extensive literature search of PubMed, Ovid, and Google Scholar using keywords “F317” as well as F317i, ” and we were unable to find another report of this mutation in a child. Discussion: CML in children is rare and to our knowledge the F317i mutation in children has not been previously reported. In contrast to how the F317i mutation is expected to behave in adult Ph+ CML, our patient developed resistance to nilotinib. Conclusion: Our CML patient failed nilotinib. The F317i mutation in a child may warrant closer molecular monitoring and the consideration of early stem cell transplantation. Citation Format: Heidi Tucker, Paul Kent. F317i mutation-associated nilotinib resistance in a child with CML: A first report. [abstract]. In: Proceedings of the AACR Special Conference on Hematologic Malignancies: Translating Discoveries to Novel Therapies; Sep 20-23, 2014; Philadelphia, PA. Philadelphia (PA): AACR; Clin Cancer Res 2015;21(17 Suppl):Abstract nr B38.
The Proteasome Inhibitor Bortezomib Affects Osteoblastogenesis and Bone Formation In Vitro and In Vivo in Multiple Myeloma Patients.
Authors: Nicola Giuliani, Francesca Morandi, Sara Tagliaferri, Mirca Lazzaretti, Sabrina Bonomini, Monica Crugnola, Daniela Petrò, Cristina Mancini, Eugenia Martella, Vittorio Rizzoli
Journal: Blood (2006)
Magnetic resonance imaging of infarct-induced canonical wingless/integrated (Wnt)/β-catenin/T-cell factor pathway activation,<i>in vivo</i>
Authors: Marco Matteucci, Valentina Casieri, Khatia Gabisonia, Giovanni Donato Aquaro, Silvia Agostini, Giuseppe Pollio, Daniela Diamanti, Marco Rossi, Massimiliano Travagli, Valentina Porcari, Fabio A. Recchia, Vincenzo Lionetti
Journal: Cardiovascular Research (2016)

Combined magnetic resonance imaging (MRI) of molecular and morpho-functional changes might prove highly valuable for the elucidation of pathological processes involved in the development of cardiac diseases. Our aim was to test a novel MRI reporter gene for in vivo assessment of the canonical Wnt/β-catenin/TCF pathway activation, an important regulator of post-ischaemic cardiac remodelling. We designed and developed a chimeric construct encoding for both of iron-binding human ferritin heavy chain (hFTH) controlled by the β-catenin-responsive TCF/lymphoid-enhancer binding factor (Lef) promoter and constitutively expressed green fluorescent protein (GFP). It was carried by adeno-associated virus serotype 9 (rAAV9) vectors and delivered to the peri-infarct myocardium of rats subjected to coronary ligation (n = 11). By 1.5 T MRI and a multiecho T2* gradient echo sequence, we detected iron accumulation only in the border zone of the transduced infarcted hearts. In the same cardiac area, post-mortem histological analysis confirmed the co-existence of iron accumulation and GFP. The iron signal was absent when rats (n = 6) were chronically treated with SEN195 (10 mg/kg/day), a small-molecular inhibitor of β-catenin/TCF-dependent gene transcription. Canonical Wnt pathway inhibition attenuated the post-ischaemic remodelling process, as demonstrated by the significant preservation of cardiac function, the 42 ± 1% increase of peri-infarct arteriolar density and 43 ± 3% reduction in infarct scar size compared with untreated animals. The TCF/Lef promoter-hFTH construct is a novel and reliable MRI reporter gene for in vivo detection of the canonical Wnt/β-catenin/TCF activation state in response to cardiac injury and therapeutic interventions.
Risk Factors for Cardiovascular Events in Myeloproliferative Syndromes.
Authors: Iolanda Vincelli, Esther N. Oliva, Roberto Latagliata, Giorgina Specchia, Giuliana Alimena, Massimo Breccia, Caterina Alati, Ida Carmosino, Grazia Iaria, Antonio Marino, Natale Ranieri, Vincenzo Liso, Francesca Ronco, Bruno Martino, Francesco Nobile
Journal: Blood (2006)
The effects of a brief relaxation program on heart rate variability in cancer patients
Authors: A. Asher
Journal: Journal of Clinical Oncology (2009)

e20713 Background: Objectives were: (1) To characterize the physiologic changes of the autonomic nervous system, demonstrated by heart rate variability (HRV) high frequency (HF) spectral analysis, before and after a 15 minute, one-time, guided relaxation program for cancer patients. (2) To assess whether changes of HRV correlate with subjective feeling for anxiety, based on the Edmonton Symptom Assessment Scale (ESAS), and the summed ESAS score. Methods: 20 patients with any cancer diagnosis and normal cognition were recruited for the study. The ECG electrodes were attached and a 5-minute period of heart rate variability was recorded (HRV before ) after 15 minutes of supine resting. The patient then began the brief relaxation program via recorded audio. Another 5 minute period of HRV was then recorded (HRV after ). The ESAS was completed before and immediately after the relaxation program. Parasympathetic activity assessed by heart rate variability, as measured by high frequency spectral analysis, was the primary outcome measure. The differences between the pre and post values of low and high frequency HRV, of the ESAS anxiety score, and of the summed ESAS score were compared using a Wilcoxan signed rank test. Results: No statistically significant differences were found in HF HRV power between the pre and post relaxation program. However, the summed ESAS scores were significantly lower after the relaxation program (p &lt;0.001). There was also a trend of decrease in the ESAS anxiety score (p = 0.086). There was no correlation between the change in HRV HF and change in the ESAS anxiety score. Conclusions: A brief guided relaxation program can significantly improve symptoms as measured by ESAS, but not HF HRV power. No significant financial relationships to disclose.
A phase I study of chronically dosed, single-agent veliparib (ABT-888) in patients (pts) with either BRCA 1/2-mutated cancer (BRCA+), platinum-refractory ovarian cancer, or basal-like breast cancer (BRCA-wt).
Authors: Shannon Leigh Huggins-Puhalla, Jan Hendrik Beumer, Leonard Joseph Appleman, Hussein Abdul-Hassan Tawbi, Ronald G. Stoller, Yan Lin, Brian Kiesel, Antoinette R. Tan, Darlene Gibbon, Yixing Jiang, Agustin Garcia, Helen K. Chew, Robert Morgan, Stacie Peacock Shepherd, Vincent L. Giranda, Alice P. Chen, Chandra Prakash Belani, Edward Chu
Journal: Journal of Clinical Oncology (2012)

3054 Background: Veliparib (ABT-888) is an oral, potent inhibitor of PARP 1/2. Preclinically, PARP inhibitors have activity in tumors with defective homologous recombination (HR), particularly those that are BRCA+. Reduced levels of BRCA expression have been observed in ovarian cancer and basal-like breast cancer, which share genotypic and phenotypic similarities with BRCA+ cancers. We postulated that these tumors types may be similarly sensitive to single-agent PARP inhibition. This study sought to establish the maximum tolerated dose (MTD), dose limiting toxicities (DLT), pharmacokinetic and pharmocodynamic properties, and preliminary efficacy of chronically-dosed veliparib. Methods: A 3+3 dose escalation phase I trial was performed. Nine dose levels (DL) were planned, and dose escalation started at 50 mg BID to a maximum of 500 mg BID. Veliparib was administered orally continuously on a 28 day cycle. Results: 63 pts have been enrolled to date. Thirty-eight were BRCA+ (20 ovary, 12 breast, 2 pancreas, and one each - prostate, peritoneal, fallopian tube, endometrial); 25 BRCA-wt. (21 breast, 4 ovarian). DLTs occurred at the following dose levels: BRCA+: gr. 2 thrombocytopenia at 50 mg BID; BRCA+: gr.3 Nausea/vomiting at 400 mg BID; BRCA-wt: gr 2 seizure at 400 mg BID. The MTD has not been determined and 500 mg BID is presently enrolling. Notable toxicities have included low-grade fatigue and nausea. PK was linear and non-saturable with t ½ of 5 h. The number of cycles administered ranged from 1- 15, median 2. In BRCA+ pts, there were 2 partial responses (breast, ovarian) and 10 pts had evidence of prolonged SD ≥ 4 months. In BRCA-wt pts, there was 1 PR (breast) and 7 pts with SD≥ 4 months. Correlative studies, including assessment of PAR inhibition and BRCA methylation status, are ongoing. Conclusions: Veliparib is tolerable on a continuous oral dosing schedule with evidence of anti-tumor activity seen in BRCA+ and BRCA-wt tumors. A mandatory biopsy expansion cohort is planned at the recommended phase II dose, which will allow further insights regarding efficacy and mechanisms of resistance to PARP inhibition.
Phase 1 Study of Talabostat and Rituximab in Patients with Indolent Non-Hodgkin’s Lymphoma with Primary Resistance to or Progression Following Rituximab.
Authors: Ayad Al-Katib, David D. Hurd, Robert Raju, Joe Stephenson, Francis Giles, Eric Haltom, Margaret J. Uprichard
Journal: Blood (2004)
Low intensity pulsed ultrasound for fractures of the tibial shaft.
Authors: X L Griffin
Journal: BMJ (2016)

We now have sound evidence that it doesn’t work

The key characteristic of a clinical researcher is probably the determination to deliver high quality studies despite all the inevitable bumps along the road. As well as the difficulties around funding and maintaining large collaborations that can deliver high impact multicentre studies, there are also more worrying challenges that threaten the robustness of the science. Some are widely recognised, such as publication bias, others are less overt; the reluctance of sponsors to complete some industry funded studies if the results aren’t going their way and the distorting effect of regulatory policies on study design, such as regulatory demand for placebo controlled designs rather than more useful comparative research.

In a linked paper, Busse and colleagues (doi:10.1136/bmj.i5351) report findings from a trial of low intensity pulsed ultrasound (LIPUS) in tibial fracture healing.1 They are to be congratulated …
Colorectal Cancer Screening Recommendations
Authors: Klaus Mergener, Nicholas T. Potter
Journal: JAMA (2016)

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Use of Cytarabine for Mantle Cell Lymphoma Treatment: 10 Years of Experience of a French Haematology Department
Authors: Marie-Pierre Gourin, Julie Abraham, Franck Trimoreau, Barbara Petit, Stephane Girault, Agnes Olivrie-Gamaury, Arnaud Jaccard, Jean Feuillard, Dominique Bordessoule
Journal: Blood (2010)
Design and Printing Strategies in 3D Bioprinting of Cell‐Hydrogels: A Review
Authors: Jia Min Lee, Wai Yee Yeong
Journal: Advanced Healthcare Materials (2016)

Bioprinting is an emerging technology that allows the assembling of both living and non‐living biological materials into an ideal complex layout for further tissue maturation. Bioprinting aims to produce engineered tissue or organ in a mechanized, organized, and optimized manner. Various biomaterials and techniques have been utilized to bioprint biological constructs in different shapes, sizes and resolutions. There is a need to systematically discuss and analyze the reported strategies employed to fabricate these constructs. We identified and discussed important design factors in bioprinting, namely shape and resolution, material heterogeneity, and cellular‐material remodeling dynamism. Each design factors are represented by the corresponding process capabilities and printing parameters. The process‐design map will inspire future biomaterials research in these aspects. Design considerations such as data processing, bio‐ink formulation and process selection are discussed. Various printing and crosslinking strategies, with relevant applications, are also systematically reviewed. We categorized them into 5 general bioprinting strategies, including direct bioprinting, in‐process crosslinking, post‐process crosslinking, indirect bioprinting and hybrid bioprinting. The opportunities and outlook in 3D bioprinting are highlighted. This review article will serve as a framework to advance computer‐aided design in bioprinting technologies.
GW26-e2155 Best Predictor of Metabolic Syndrome: Comparison of Various Anthropometric and Atherogenic Parameters in the Kazakh Population in Xinjiang Province
Authors: Chunhui He, You Chen, Yining Yang, Xiang Ma, Zhenyan Fu, Xiaomei Li, Xiang Xie, Zixiang Yu, Fen Liu, Bangdang Chen, Yingying Zheng, Yitong Ma
Journal: Journal of the American College of Cardiology (2015)
GW26-e5434 The study of relationships between intra-abdominal obesity and high sensitive C-reactive protein, tissue inhibitor of metalloproteinase-1 in patients with coronary heart disease
Authors: Xingshan Zhao, Jihong Wang, Jinjin Zhai, Yonghao Lan, Mei Zheng, Xiaoguang Cheng
Journal: Journal of the American College of Cardiology (2015)
Prolonged Survival and Carcinoma as Frequent Cause of Death in Patients Treated with Sustained Imatinib Mesylate for Advanced Chronic Phase CML Intolerant or Refractory to Interferon.
Authors: M.A. Capucci, M. Micheletti, E. Borlenghi, M. Rigno, L. Consoli, G. Ruggeri, D. Marocolo, D. Bellotti, G. Rossi
Journal: Blood (2005)