tbuckley/cabot-search huggingface dataset:
Mitoxantrone and Cytarabine Combination in Untreated Elderly Patients with Acute Myeloid Leukemia (AML): A Retrospective Single-Centre Analysis.
Authors: Theodore Marinakis, Vasilios Xanthopoulos, Athanasios Galanopoulos, Evrydiki Michalis, George Gortzolidis, Athanasios Zomas, Ioannis Tsourveloudis, Ioanna Savvidou, Myrsini Pergaminou, Antonios Angelidis, Ioanna Michail, Helen Goumakou, Elpiniki Griva, Alexandra Tsakri, Maria Georgiakaki, George Paterakis, Nikolaos I. Anagnostopoulos
Journal: Blood (2007)
P3-130: A large Spanish experience with erlotinib in advanced non–small cell lung cancer
Authors: Luis Paz-Ares, José-Luis González-Larriba, Nùria Viñolas, Alberto Arízcum, David Gutiérrez-Abad, Caterina Madroñal, José Ramón Delgado, Purificación Martínez Del Prado, Maria Luz Amador, Bartomeu Massutí
Journal: Journal of Thoracic Oncology (2007)
Survival for Chronic Lymphocytic Leukaemia (CLL) Patients in Hungary from 2000 to 2014 Based on the Single Payer's Database: A Nationwide Study
Authors: Maren Gaudig, István Vályi-Nagy, Peter Takacs, Miklos Bacskai, Petra Kozma, Pal Rakonczai, Julianna Püspöki
Journal: Blood (2014)
BRAF and KRAS mutations as additional risk factors in the context of clinical parameters of patients with colorectal cancer.
Authors: Vlad Calin Popovici, Eva Budinska, Arnaud Roth, Fred Bosman, Sabine Tejpar, Mauro Delorenzi
Journal: Journal of Clinical Oncology (2013)

3522 Background: The BRAF and KRAS mutations have been proposed as prognostic markers in colorectal cancer (CRC). Of them, only the BRAF V600E mutation has been validated as prognostic for overall survival and survival after relapse, while the value of KRAS mutation is still unclear. Methods: In a cohort of 1423 stage II-III patients from the PETACC-3 clinical trial, the prognostic value of the BRAF and KRAS mutations was retrospectively assessed in all possible stratifications defined by the 5 factors (T and N stage, tumor site and grade, and microsatellite instability status), by log rank test for overall survival (OS), relapse-free survival (RFS), and survival after relapse (SAR). The presence of interactions was tested by Wald test. The significance level was set to 0.01 for Bonferroni-adjusted p-values (P*), and a second level for a trend towards statistical significance was set at 0.05 for unadjusted p-values (P). Results: BRAF mutation was a marker of poor OS only in microsatellite stable (MSS) and left-sided tumors, with no prognostic value in microsatellite instable (MSI-H) or right-sided tumors. In MSS/left-sided tumors, BRAF mutation represents a marker of higher risk than previously reported: OS HR=6.4 [95% CI: 3.6-11.5], P* &lt; 0.0001. For SAR, BRAF was prognostic in more stratifications, with higher risk in MSS/left-sided tumors (HR=3.9 [95% CI: 2.1-7.2], P* = 0.0002) than in MSS/right-sided (HR=2.3 [95% CI: 1.2-4.4], P=0.01). A novel observation was that BRAF mutation was prognostic also for RFS, but only in MSS/left-sided tumors (HR=3.6 [95% CI:2-6.3], P*=0.0005]). Additionally, heterogeneity in OS and RFS among BRAF mutants was observed. In general, KRAS mutation did not reach the significance level required, but showed a trend to become a prognostic marker for RFS in MSS tumors with early lymph node involvement (N1) (HR=1.6 [95% CI:1.1-2.2], P=0.01). Conclusions: The prognostic utility of the BRAF and KRAS mutations has to be interpreted in the context of other factors. For the BRAF mutation, a clear interaction with MSI status and tumor site was observed, with BRAF mutation indicating a much higher risk in MSS/left-sided tumors than previously considered.
Promoting patient adherence with imatinib treatment in chronic myeloid leukemia: Physicians’ perceptions of utility (effectiveness, feasibility, cost) and rankings of clinical applicability of 13 adherence-enhancing strategies – Results from the ADAGIO Study
Authors: MA van Lierde, E Strobbe, L De Rop, F Serra, K MacDonald, S Vancayzeele, Sabina De Geest, L Letvak, T Albrecht, I Abraham
Journal: Blood (2007)
Are ER+PR+ and ER+PR- breast tumors genetically different? An array CGH study
Authors: Alma Carracedo, Marta Salido, Josep Maria Corominas, Bibiana Ferreira, Ignasi Tusquets, Cristina Corzo, Marcel Segura, Blanca Espinet, Juan Cruz Cigudosa, Joan Albanell, Sergi Serrano, Francesc Sole
Journal: Cancer Research (2008)

1685   Traditionally, clinical observations have indicated that estrogen receptor positive and progesterone receptor negative (ER+/PR-) breast cancers could present a different pattern of hormone sensibility than ER+/PR+ tumors. Furthermore, it seems that ER+/PR- tumors are more likely to have an agressive phenotype. The aim of this study is to investigate the pattern of DNA copy number aberrations (CNAs) of these two subtypes of breast carcinomas, and try to identify differences between them using a high-resolution array CGH. The Agilent 44K oligonucleotide array-based comparative genomic hybridization (CGH) has been applied to 25 ER+/PR+ and 25 ER+/PR- ductal infiltrating carcinomas (DIC) of the breast (histological grades I, II and III, negative ERBB2 status). Data analysis and chromosome segmentation were performed with InSilicoArray CGH software. Currently, we are analysing the last 14 ER+/PR- tumors, and stablishing the smallest overlapping regions of imbalance (SORIs) for each chromosome. The present results correspond to a preliminary analysis of 25 ER+/PR+ and 11 ER+/PR- tumors. On average, there were 12,1 altered regions in the ER+/PR- tumors vs 6,84 in the ER+/PR+ ones. Preliminary analysis of the 36 cases (25 ER+/PR+ vs 11 ER+/PR-) shows that chromosomal regions most commonly gained in both subtypes of tumors were: 1q (61%), 16p (47%), 11q12.1-q14.1 (36%), 8p11-p12 (33%), 8q (33%), 20q (33%), 17q (27%), 5q (27%) and 5p (22%). On the other hand, chromosomal regions most commonly lost were: 16q (69%), 17p (44%), 11q14.2-qter (39%), 8p21-pter (33%), 9p12-p21.3 (25%), 22q (30%) and 13q (22%). Despite their similar CNAs, we have found that gains in the 17q region, and the lost of 22q were more frequent in the ER+/PR- subgroup (64% and 54% respectively), than in the ER+/PR+ (12% and 20% respectively). In our knowledge, this is the first study focused on the genetic comparison of ER+/PR+ and ER+/PR- breast tumors by aCGH technology. In the analysis of 36 DICs, CNAs were consistent with the results previously reported on CGH and aCGH studies. Taking into account our preliminary results, ER+/PR- tumors seemed to present a higher chromosomal instability. Moreover, gains in the 17q region -that do not induce an overexpression of ERRB2- and the lost of 22q were more frequently observed in the ER+/PR- ones. Finally, our results indicate that array CGH can be useful for the better understanding of the DIC genetic profile, as well as for the possibility of identifying some differences in the genomic alterations between subtypes of breast cancer, that may be useful for the seeking for new drugs or treatments. Definitively results will be presented on the AACR conference. ACKNOWLEDGEMENTS: This study has been supported by the grant #FIS PIOP50961 from the Ministerio de Sanidad y Consumo.
Clinical Benefit with Regorafenib Across Subgroups and Post-Progression in Patients with Advanced Gastrointestinal Stromal Tumor (GIST) After Progression on Imatinib (IM) and Sunitinib (SU): Phase 3 Grid Trial Update
Authors: P.G. Casali, P. Reichardt, Y. Kang, J. Blay, P. Rutkowski, H. Gelderblom, P. Hohenberger, M. Leahy, M. von Mehren, H. Joensuu, G. Badalamenti, M. Blackstein, A. Le Cesne, P. Schöffski, R. Maki, J. Xu, T. Nishida, I. Kuss, D. Laurent, G.D. Demetri
Journal: Annals of Oncology (2012)
Long-Term Prognostic Value of Coronary CT Angiography in Asymptomatic Type 2 Diabetes Mellitus
Authors: Se Hun Kang, Gyung-Min Park, Seung-Whan Lee, Sung-Cheol Yun, Young-Hak Kim, Young-Rak Cho, Hyun Woo Park, Jon Suh, Dong Hyun Yang, Joon-Won Kang, Tae-Hwan Lim, Chang Hee Jung, Eun Hee Koh, Woo Je Lee, Min-Seon Kim, Ki-Up Lee, Joong-Yeol Park
Journal: JACC. Cardiovascular imaging (2016)
P2-045: Increased and sustained expression of p-Akt in HCC827 cells with the acquired resistance to gefitinib
Authors: Jae Cheol Lee, Yun Jung Choi, Jin Kyung Rho, Im Il Na, Bae-Yeol Ryoo, Jin Kyung Lee, Sung Hyun Yang, Cheol Hyeon Kim
Journal: Journal of Thoracic Oncology (2007)
A phase III randomized controlled trial of short-course radiotherapy with or without concomitant and adjuvant temozolomide in elderly patients with glioblastoma multiforme
Authors: J. R Perry, C. J O'Callaghan, K Ding, A. A Brandes, C Phillips, Johan Menten, M Fay, R Nishikawa, C Winch, N Laperriere
Journal: Neuro-Oncology (2010)

A PHASE III RANDOMIZED CONTROLLED TRIAL OF SHORT-COURSE RADIOTHERAPY WITH OR WITHOUT CONCOMITANT AND ADJUVANT TEMOZOLOMIDE IN ELDERLY PATIENTS WITH GLIOBLASTOMA (NCIC CTG CE.6, EORTC 26062-22061, TROG 08.02, NCT00482677) James R. Perry MD, FRCPC, Christopher J. O’Callaghan, Keyue Ding, Wilson Roa, Warren P. Mason, J. Gregory Cairncross, Alba Ariela Brandes, Johan Menten, Claire Phillips, Michael F. Fay, Ryo Nishikawa, Chad Winch, and Normand Laperriere; University of Toronto, Odette Cancer Centre
Angiotensin receptors and β-catenin regulate brain endothelial integrity in malaria
Authors: Julio Gallego-Delgado, Upal Basu-Roy, Maureen Ty, Matilde Alique, Cristina Fernandez-Arias, Alexandru Movila, Pollyanna Gomes, Ada Weinstock, Wenyue Xu, Innocent Edagha, Samuel C. Wassmer, Thomas Walther, Marta Ruiz-Ortega, Ana Rodriguez
Journal: Journal of Clinical Investigation (2016)

Cerebral malaria is characterized by cytoadhesion of Plasmodium falciparum-infected red blood cells (Pf-iRBCs) to endothelial cells in the brain, disruption of the blood-brain barrier, and cerebral microhemorrhages. No available antimalarial drugs specifically target the endothelial disruptions underlying this complication, which is responsible for the majority of malaria-associated deaths. Here, we have demonstrated that ruptured Pf-iRBCs induce activation of β-catenin, leading to disruption of inter-endothelial cell junctions in human brain microvascular endothelial cells (HBMECs). Inhibition of β-catenin-induced TCF/LEF transcription in the nucleus of HBMECs prevented the disruption of endothelial junctions, confirming that β-catenin is a key mediator of P. falciparum adverse effects on endothelial integrity. Blockade of the angiotensin II type 1 receptor (AT1) or stimulation of the type 2 receptor (AT2) abrogated Pf-iRBC-induced activation of β-catenin and prevented the disruption of HBMEC monolayers. In a mouse model of cerebral malaria, modulation of angiotensin II receptors produced similar effects, leading to protection against cerebral malaria, reduced cerebral hemorrhages, and increased survival. In contrast, AT2-deficient mice were more susceptible to cerebral malaria. The interrelation of the β-catenin and the angiotensin II signaling pathways opens immediate host-targeted therapeutic possibilities for cerebral malaria and other diseases in which brain endothelial integrity is compromised.
Tell women IUD is more effective than emergency contraceptive pill, says NICE
Authors: Anne Gulland
Journal: BMJ (2016)

Women seeking emergency contraception should be told that an intrauterine device (IUD, or coil) is more effective than the emergency contraceptive pill, new guidelines say.

As well as urging health professionals to talk about emergency contraception, the new quality standard from the National Institute for Health and Care Excellence (NICE) states that women should be told about long acting, reversible methods such …
A phase II study of BIBW 2992, a novel irreversible dual EGFR and HER2 tyrosine kinase inhibitor (TKI), in patients with adenocarcinoma of the lung and activating EGFR mutations after failure of one line of chemotherapy (LUX-Lung 2)
Authors: J. Shih, C. Yang, W. Su, T. Hsia, C. Tsai, Y. Chen, H. Chang, E. Terlizzi, M. Shahidi, V. A. Miller
Journal: Journal of Clinical Oncology (2009)

8013 Background: EGFR mutations are associated with exquisite sensitivity to EGFR TKIs in NSCLC. A phase II trial evaluating the efficacy of BIBW 2992 (Tovok), a novel, potent, irreversible, dual EGFR and HER2 TKI with preclinical activity in cell lines harboring activating (H3255, IC 50 =0.7 nM) and resistant (H1975, IC 50 =99 nM) EGFR mutations, is reported. Methods: Objective response rate is the primary endpoint of this 2-stage trial. Based on 16 or more unconfirmed PRs in an interim analysis of the first 40 2 nd line patients (pts) completing 1 course (28 days), accrual will continue to a total of 120 1 st and 2 nd line pts (expected completion of accrual by May 2009. Data on 2 nd line pts only are presented). Eligible pts have stage IIIB/IV lung adenocarcinoma, EGFR mutation in exons 18–21 (tested by direct sequencing), measurable disease, ECOG PS 0–2 and adequate end organ function. Pts receive 50 mg BIBW 2992 qd until progression. Tumor assessments are performed every 4 weeks for 12 weeks, then every 8 weeks. Results: Since Oct 2007, samples from 289 pts (222 from Taiwan and 67 from the US) have been sequenced. 100 had detectable EGFR mutations including del19 (n=39), L858R (n=45) and others (n=16). 69 pts have started treatment. The trial was moved to stage 2 after 21 of the first 38 treated pts had objective response at 28 days. Of 55 evaluable 2 nd line pts, 29 (53%) had PR, and 23 (42%) had SD. Median follow up is 5.1 months. Most common related AEs were diarrhea and skin-related AEs, reported in 87% and 88% of pts, respectively. 27 pts (42.9 %) had dose reduction to 40 mg and 7 pts (11%) to 30 mg but only 1 pt permanently discontinued due to AEs. Diarrhea and rash were main causes of dose reduction. Conclusions: In the 2 nd line setting, BIBW 2992 shows efficacy in NSCLC harboring EGFR activating mutations. Diarrhea and skin disorders, the most frequently observed AEs, are manageable with supportive care and dose reduction. Updated response and disease control rates and preliminary progression-free survival data will be presented. An international Phase III trial program investigating BIBW 2992 in NSCLC, LUX-Lung, is now recruiting. [Table: see text]
Mechanical Dispersion Predicts Ventricular Arrhythmias After Myocardial Infarction
Authors: Kristina H Haugaa, Bjornar L Grenne, Jens-Uwe Voigt, Anca-Rezeda Florian, Benthe Sjoli, Harald Brunvand, Christian H Eek, Walter Desmet, Jesper H Svendsen, Otto A Smiseth, Thor Edvardsen
Journal: Circulation (2011)
P1-119: Tissue and serum EGFR as prognostic factors in malignant pleural mesothelioma
Authors: Rabab M. Gaafar, Abeer A. Bahnassy, Ibrahim Abdel-Salam, Amani Helal, Abdelrahman Abdelrahman, Nelly Hassan, Hoda Ismail, Nadia Mokhtar
Journal: Journal of Thoracic Oncology (2007)
Call for coordinated and systematic training load measurement (and progression) in athlete development: a conceptual model with practical steps
Authors: Mark Booth, Rhonda Orr, Stephen Cobley
Journal: British Journal of Sports Medicine (2016)

The recent IOC consensus statement1 on youth athletic development highlights how the careers of many youth athletes are often temporarily halted or derailed by overuse injuries, resulting from disproportionate training loads along with insufficient rest and recovery. Training volume and intensity2 as well as excessive training doses predict specific injury types.3 Recently, the acute: chronic workload ratio has shown how inappropriate short-term increases in training load are associated with heightened injury risk.4 Further, chronic exposure to inappropriate training volume is associated with further deleterious outcomes.2 ,5 ,6

Empirical evidence exists suggesting that systematic regulation of training loads across the various stages of development occurs in some sport contexts. However, we suspect disparity and inconsistency in the quality of training load regulation across sport contexts and organisations. In some it may be inadequate, possibly lead by intuitive dogmatic approaches (ie, the ‘more is better’ ethos), whereas in other contexts or organisations such monitoring may simply not exist. …
Clinical Activity and Pharmacokinetics (PK) of Cabozantinib (XL184) in Patients with Progressive Medullary Thyroid Carcinoma (MTC)
Authors: E.E.W. Cohen, R. Elisei, M.J. Schlumberger, S.P. Müller, P. Schöffski, M. Brose, M. Shah, D.R. Miles, L.T. Nguyen, S. Sherman
Journal: Annals of Oncology (2012)
Colchicine and Prevention of Cardiovascular Events
Authors: Lars G. Hemkens, Hannah Ewald, Matthias Briel
Journal: JAMA (2016)

<h3>Clinical Question</h3> Is continuous long-term treatment with colchicine associated with lower rates of all-cause mortality and myocardial infarction and higher rates of adverse events? <h3>Bottom Line</h3> Continuous long-term treatment with colchicine may be associated with lower rates of myocardial infarction, but may be associated with higher rates of gastrointestinal adverse events.
Abstract 1020: Latent membrane protein 1 N-C interaction of EBV facilitates (nuclear factor kappa-light-chain-enhancer of activated B cells transcriptional activity
Authors: Cheng-Lung Hsu, Hsin-Pai Li, Yung-Chia Kuo, Ngan-Ming Tsang, Yu-Sun Chang
Journal: Cancer Research (2015)

Abstract Background: Epstein-Barr virus latent membrane protein 1 (LMP1) is known to be involved in the carcinogenesis of numerous cancers, including nasopharyngeal carcinoma and lymphoma. The C-terminus of LMP1 can recruit a spectrum of host cell cytosolic signaling molecules to exert its effects on downstream pathways. However, the function of the cytosolic N-terminus of LMP1 is not clear. Methods: Partial deletion or point mutation of the N-terminus of LMP1 were made. Results: Sequence analysis showed that not only were the lengths of LMP1 N- and C-termini different, so too were their distributions of charged amino acid side chains, with negatively charged amino acids being abundant in the C-terminus and positively charged amino acids dominating in the N-terminus. We found that deletion or mutation of N-terminal positively charged amino acids weakened the effects of LMP1 on nuclear factor NF-κB transcriptional activity. Furthermore, co-expressing a short N-terminal peptide of LMP1 enhanced the effect of full-length LMP1 on NF-κB transcriptional activity. We further demonstrated that the LMP1 N- and C-termini interact, which facilitated downstream signal transduction. Mutation of N-termial positively charged side chain amino acid could weaken LMP1 effect on cell motility. Conclusion: LMP1 N- and C-termini could interact and facilitate NF-κB transcriptional activity and cell motility. Citation Format: Cheng-Lung Hsu, Hsin-Pai Li, Yung-Chia Kuo, Ngan-Ming Tsang, Yu-Sun Chang. Latent membrane protein 1 N-C interaction of EBV facilitates (nuclear factor kappa-light-chain-enhancer of activated B cells transcriptional activity. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 1020. doi:10.1158/1538-7445.AM2015-1020
P2-190: The number of residual metastatic lymph nodes following neoadjuvant chemotherapy predicts survival in patients with stage III NSCLC
Authors: Se Hyun Kim, Byoung Chul Cho, Hye Jin Choi, Sang Joon Shin, Joo Hyuk Sohn, Joo-Hang Kim
Journal: Journal of Thoracic Oncology (2007)
Targeted Pre-Emptive Anti-Aspergillus Therapy in Neutropenic Patients Not Receiving Empirical Antifungal Therapy.
Authors: Johan A. Maertens, Koen Theunissen, Gregor Verhoef, Johnny Verschaekelen, Katrien Lagrou, Eric Verbeken, Jan Verhaegen, Wouter Meersseman, Alexander Wilmer, Marc Boogaerts, Johan Van Eldere
Journal: Blood (2004)
High Frequency of P53 Mutations Detected by a Microarray Resequencing Assay, the AmpliChip P53 Test, in AML with a Complex Aberrant Karyotype.
Authors: Nancy Patten, Sim Truong, Jeff Fu, Frank Dicker, Susanne Schnittger, Wolfgang Kern, Alexander Kohlmann, Torsten Haferlach, Claudia Schoch, Lin Wu
Journal: Blood (2006)
A novel gene, MSI2, encoding a putative RNA-binding protein is recurrently rearranged at disease progression of chronic myeloid leukemia
Authors: A Barbouti, M Hoglund, B Johansson, C Lassen, PG Nilsson, I Winquist, Anne Hagemeijer-Hausman, F Mitelman, T Fioretos
Journal: Blood (2002)
Physical declines occurring after hospital discharge in ARDS survivors: a 5-year longitudinal study
Authors: Elizabeth R. Pfoh, Amy W. Wozniak, Elizabeth Colantuoni, Victor D. Dinglas, Pedro A. Mendez-Tellez, Carl Shanholtz, Nancy D. Ciesla, Peter J. Pronovost, Dale M. Needham
Journal: Intensive Care Medicine (2016)
P3-008: Identification of DNA methylation markers for NSCLC and adjacent normal lung tissue using Hpall-Mspl Methylation chip
Authors: Meehye Kwon, Eu Gene Choi, Moon Jun Na, Hyun Min Cho, Young Jin Kim, Jung Uee Lee, Hye Jung Sul, Yoon Mee Kim, Bum Kyeong Kim, Ji Woong Son
Journal: Journal of Thoracic Oncology (2007)
Deficiency of <i>ATP6V1H</i> Causes Bone Loss by Inhibiting Bone Resorption and Bone Formation through the TGF-β1 Pathway
Authors: Xiaohong Duan, Jin Liu, Xueni Zheng, Zhe Wang, Yanli Zhang, Ying Hao, Tielin Yang, Hongwen Deng
Journal: Theranostics (2016)

Vacuolar-type H + -ATPase (V-ATPase) is a highly conserved, ancient enzyme that couples the energy of ATP hydrolysis to proton transport across vesicular and plasma membranes of eukaryotic cells.Previously reported mutations of various V-ATPase subunits are associated with increased bone density.We now show that haploinsufficiency for the H subunit of the V 1 domain (ATP6V1H) is associated with osteoporosis in humans and mice.A genome-wide SNP array analysis of 1625 Han Chinese found that 4 of 15 tag SNPs (26.7%) within ATP6V1H were significantly associated with low spine bone mineral density.Atp6v1h +/-knockout mice generated by the CRISPR/Cas9 technique had decreased bone remodeling and a net bone matrix loss.Atp6v1h +/- osteoclasts showed impaired bone formation and increased bone resorption.The increased intracellular pH of Atp6v1h +/-osteoclasts downregulated TGF-β1 activation, thereby reducing induction of osteoblast formation but the bone mineralization was not altered.However, bone formation was reduced more than bone resorption.Our data provide evidence that partial loss of ATP6V1H function results in osteoporosis/osteopenia.We propose that defective osteoclast formation triggers impaired bone formation by altering bone remodeling.In the future, ATP6V1H might, therefore, serve as a target for the therapy of osteoporosis.