tbuckley/cabot-search huggingface dataset:
Results with the intensive chemotherapy Mexican regimen in the treatment of pediatric high-grade osteosarcoma: Experience at the Instituto Nacional de Pediatria.
Authors: Araceli Castellanos-Toledo, Marta Zapata-Tarres, Humberto Peña-del-Castillo, Jose de Jesus Figueroa Carbajal
Journal: Journal of Clinical Oncology (2013)

10058 Background: In Mexico, pediatric high-grade osteosarcoma (HGO) occupies the fifth place of all pediatrics cancers, representing the 4.4%. It presents with a high incidence of metastatic pulmonary disease and large primary tumor volume at diagnosis, resulting in poor survival. The results of the named 2005 Chemotherapy Regimen are very promising. Methods: A retrospective, longitudinal, clinical study was performed from January 2005 to January 2012, including 55 patients (&lt;18 years old) with extremity HGO and no prior chemotherapy treatment. All patients received a 10-week neoadjuvant-chemotherapy regimen (6 curses), with cisplatino 120mg/m 2 plus doxorrubicina 75mg/m 2 and a 15-week adjuvant-treatment (5 curses) with ciclofosfamide 1800 mg/m 2 plus etoposide 900 mg/m 2 . Results: Median age was 12 years, 51% boys and 49% girls. There were 51% distal femur, 11% proximal humerus, 18.2% proximal tibia, 7.3% distal tibia, 5.4% fibula and 5.5% proximal femur. Thirty-two patients (58.2%) had pulmonary metastases at diagnosis. There were 76.4% osteoblastic tumors, 16% chondroblastic and 7.3% telangiectatic. Twenty patients (36.4%) had an amputation procedure and 15 (27%) a limb desarticulation, 18 by a great tumor volume at diagnosis and two by eventual local relapse. Twelve patients (22%) had limb-sparing surgery. There were 10 (18.2%) good-responder patients and 38 (69%) bad-responders to neoadjuvant-chemotherapy. The overall survival (OS) for non-metastatic patients was 70% and 35% for metastatic patients (p 0.016). The event-free survival for non-metastatic patients was 65% and 30% for metastatic patients (p 0.032). OS for good-responders was 80% and 50% for bad-responders (p 0.009). No important toxicity and no second malignancies were reported. Conclusions: In spite of the presence of significant unfavorable prognostic factors in our patients, this intensive chemotherapy regimen showed improved results in overall survival as compared to other standard regimens, being short, inexpensive and with relatively few adverse events. This regimen can be useful in other developing countries.
Soluble Syndecan-1 (sCD138) Is an Independent Prognostic Factor in Patients with Chronic Lymphocytic Leukemia.
Authors: I. Jilani, M. Keating, W. William, A. Ferrajoli, H. Kantarjian, S. M. O’Brien, F. J. Giles, M. Albitar
Journal: Blood (2005)
MPLW515L/K and JAK2V617F Mutations: Single Colony Studies, Lineage Restriction, and Chronology of Clonal Emergence.
Authors: Animesh Pardanani, Terra Lasho, Christy Finke, Ruben Mesa, William Hogan, Ross Levine, D. Gary Gilliland, Ayalew Tefferi
Journal: Blood (2006)
Survival in Oligometastatic Prostate Cancer—A New Dawn or the Will Rogers Phenomenon?
Authors: Martin J. Connor, Mathias Winkler, Hashim U. Ahmed
Journal: JAMA Oncology (2019)

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 Oncology HomeNew OnlineCurrent IssueFor Authors Podcast 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 Oncology journal
Simultaneously inactivating Src and AKT by saracatinib/capivasertib co-delivery nanoparticles to improve the efficacy of anti-Src therapy in head and neck squamous cell carcinoma
Authors: Liwei Lang, Chloe Shay, Xiangdong Zhao, Yuanping Xiong, Xuli Wang, Yong Teng
Journal: Journal of Hematology & Oncology (2019)

Abstract Background Src, an oncoprotein that drives progression of head and neck squamous cell carcinoma (HNSCC), is commonly hyperactivated in this disease. Unfortunately, the clinical benefit of targeting Src is significantly dampened in HNSCC patients, because the cytotoxic effects of anti-Src therapy and tumor resistance to it are less predictable. Thus, understanding the mechanism of tumor resistance to Src inhibition and seeking a way to overcome it are warranted. Methods Dual drug-loaded nanoparticles (NPs) were developed to co-deliver Src inhibitor saracatinib (AZD0530) and AKT inhibitor capivasertib (AZD5363) into the same population of tumor cells. An orthotopic tongue tumor model was generated to evaluate the in vivo therapeutic effects. Cell growth was determined by CellTiter-Glo® Luminescent Cell Viability Kit, colony formation, and 3D culture, and tumor growth was determined by bioluminescence and tumor size. The molecular changes induced by the treatments were assessed by Western blotting and immunohistochemistry. Results Capivasertib inactivated the AKT-S6 signaling and re-sensitized saracatinib-resistant HNSCC cells to saracatinib. Combination of capivasertib with saracatinib suppressed HNSCC growth more efficiently than either drug alone. Cathepsin B-sensitive NPs for co-delivering saracatinib and capivasertib significantly improved the efficacy of tumor repression without increasing side effects, which were due to highly specific tumor-targeting drug delivery system and synergistic anticancer effects by co-inactivation of AKT and Src in HNSCC cells. Conclusions Addition of AKT blockade improves anti-HNSCC efficacy of anti-Src therapy, and co-delivery of capivasertib and saracatinib by tumor-targeting NPs has the potential to achieve better treatment outcomes than the free drug combination.
Stem Cell Transplant (SCT) for Patients (pts) with Chronic Myeloid Leukemia (CML) Resistant to Tyrosine Kinase Inhibitors (TKI) with BCR-ABL Kinase Domain (KD) Mutation T315I.
Authors: Nikolai Velev, Jorge Cortes, Richard Champlin, Hagop M. Kantarjian, Gabriela Rondon, Sergio Giralt, Gautam Borthakur, Marcos De Lima
Journal: Blood (2008)
Platelet-Derived Microparticels Stimulate Proliferation of Colony-Forming Unit Granulocyte-Macrophage of Umbilical Cord Blood Hematopoietic Stem Cells.
Authors: Bao-An Chen, Fei Fei, Cheng-Yin Huang, Cui-Ping Li, Xiao-Ping Pei, Chong Gao, Jia-Hua Ding, Yun-Yu Sun, Feng Gao, Ning-Na Chen
Journal: Blood (2005)
High-Dose Myeloablative Zevalin Radioimmunotherapy with Tandem Stem-Cell Autografting Has Minimal Toxicity and Full Feasibility in an Outpatient Setting.
Authors: Liliana Devizzi, Ettore Seregni, Anna Guidetti, Chiara Forni, Angela Coliva, Michele Magni, Massimo Di Nicola, Carmelo Carlo-Stella, Paola Matteucci, Antonella De Pascale, Claudia Erminero, Marco Maccauro, Carlo Chiesa, Emilio Bombardieri, Alessandro M. Gianni
Journal: Blood (2005)
NFκB Activation in Primary Mediastinal Large B-Cell Lymphoma: Nuclear Localization of c-REL and Coordinate Upregulation of NFκB Target Genes.
Authors: Friedrich Feuerhake, Jeffery L. Kutok, Stefano Monti, Giorgio Cattoretti, Paul Kurtin, Geraldine S. Pinkus, Laurence de Leval, Nancy L. Harris, Kerry J. Savage, Thomas M. Habermann, Riccardo Dalla-Favera, Todd R. Golub, Jon C. Aster, Margaret A. Shipp
Journal: Blood (2004)
The microRNA144/451 Locus Enhances Nuclear FOXO3a Activity to Protect Erythroid Cells against Oxidant Stress
Authors: Camila O. dos Santos, Duonan Yu, Julio Amigo, Eugene Kandros, Eric R Valentine, Suresh Shelat, Louis C Dore, Yu Yao, Janine D’ Souza, Saghi Ghaffari, Barry H. Paw, Jordan S Orange, Mitchell J. Weiss
Journal: Blood (2008)
Something is changing in adherence to CPAP therapy: real world data after 1 year of treatment in patients with obstructive sleep apnoea
Authors: Elisa Morrone, Andrea Giordano, Sonia Carli, Dina Visca, Fabio Rossato, Massimo Godio, Elena Paracchini, Sabrina Rossi, Bruno Balbi, Carlo Sacco, Alberto Braghiroli
Journal: European Respiratory Journal (2019)

<b>Adherence to CPAP therapy is effective when applying a standard protocol consisting of a diagnostic procedure, accurate pressure setting and mask choice, a group educational session on sleep disorders and 1-yr follow up visit</b>http://bit.ly/352XPBH
The Novel Potent Pan-Deacetylase (DAC) Inhibitor, Panobinostat (LBH589), Markedly Enhances the Anti-Myeloma Effects of Chemotherapy In Vitro and In Vivo.
Authors: Richard A. Campbell, Eric Sanchez, Jeffrey Steinberg, Michael Share, Joseph Wang, Mingjie Li, Haiming Chen, Dror Shalitin, Shen Pang, Jonathan Said, James R. Berenson
Journal: Blood (2007)
biAb Mediated Restoration of the Linkage between Dystroglycan and Laminin-211 as a Therapeutic Approach for α-Dystroglycanopathies
Authors: Nathan Gumlaw, Leila M. Sevigny, Hongmei Zhao, Zhengyu Luo, Dinesh S. Bangari, Elizabeth Masterjohn, Yangde Chen, Barbara McDonald, Maureen Magnay, Tara Travaline, Takako Yoshida-Moriguchi, Wei Fan, David Reczek, James E. Stefano, Huawei Qiu, Christian Beil, Christian Lange, Ercole Rao, Michael Lukason, Elizabeth Barry, William H. Brondyk, Yunxiang Zhu, Seng H. Cheng
Journal: Molecular Therapy (2019)
Efficacy and Safety of Sevuparin, a Novel Non-Anti-Coagulant Heparinoid, in Patients with Acute Painful Vaso-Occlusive Crisis; A Global, Multicenter Double-Blind, Randomized, Placebo-Controlled Phase 2 Trial (TVOC01)
Authors: Bart J. Biemond, Anil Tombak, Yurdanur Kilinc, Murtadha Al-Khabori, Miguel R. Abboud, Mohammed Nafea, Adlette Inati, Yasser Ahmed Mohamed Soliman Wali, Jens Kristensen, Ellen Donnelly, John Ohd
Journal: Blood (2019)
Stereotactic radiosurgery for non-functioning pituitary adenomas: meta-analysis and International Stereotactic Radiosurgery Society practice opinion
Authors: Rupesh Kotecha, Arjun Sahgal, Muni Rubens, Antonio De Salles, Laura Fariselli, Bruce E Pollock, Marc Levivier, Lijun Ma, Ian Paddick, Jean Regis, Jason Sheehan, Shoji Yomo, John H Suh
Journal: Neuro-Oncology (2019)

This systematic review reports on outcomes and toxicities following stereotactic radiosurgery (SRS) for non-functioning pituitary adenomas (NFAs) and presents consensus opinions regarding appropriate patient management.Using the guidelines of the Preferred Reporting Items for Systematic Reviews and Meta-Analyses, a systematic review was performed from articles of ≥10 patients with NFAs published prior to May 2018 from the Medline database using the key words "radiosurgery" and "pituitary" and/or "adenoma." Weighted random effects models were used to calculate pooled outcome estimates.Of the 678 abstracts reviewed, 35 full-text articles were included describing the outcomes of 2671 patients treated between 1971 and 2017 with either single fraction SRS or hypofractionated stereotactic radiotherapy (HSRT). All studies were retrospective (level IV evidence). SRS was used in 27 studies (median dose: 15 Gy, range: 5-35 Gy) and HSRT in 8 studies (median total dose: 21 Gy, range: 12-25 Gy, delivered in 3-5 fractions). The 5-year random effects local control estimate after SRS was 94% (95% CI: 93.0-96.0%) and 97.0% (95% CI: 93.0-98.0%) after HSRT. The 10-year local control random effects estimate after SRS was 83.0% (95% CI: 77.0-88.0%). Post-SRS hypopituitarism was the most common treatment-related toxicity observed, with a random effects estimate of 21.0% (95% CI: 15.0-27.0%), whereas visual dysfunction or other cranial nerve injuries were uncommon (range: 0-7%).SRS is an effective and safe treatment for patients with NFAs. Encouraging short-term data support HSRT for select patients, and mature outcomes are needed before definitive recommendations can be made. Clinical practice opinions were developed on behalf of the International Stereotactic Radiosurgery Society (ISRS).
Undulating changes in human plasma proteome profiles across the lifespan
Authors: Benoit Lehallier, David Gate, Nicholas Schaum, Tibor Nanasi, Song Eun Lee, Hanadie Yousef, Patricia Moran Losada, Daniela Berdnik, Andreas Keller, Joe Verghese, Sanish Sathyan, Claudio Franceschi, Sofiya Milman, Nir Barzilai, Tony Wyss-Coray
Journal: Nature Medicine (2019)
Genetic Engineering and Significant Ex-Vivo Expansion of Cord Blood Natural Killer Cells: Implications for Post-Transplant Adoptive Cellular Immunotherapy
Authors: Jessica Hochberg, Brenton Mar, Janet Ayello, Nancy Day, Carmella van de Ven, Angela Ricci, Lalit Gurnani, Evan Cairo, Dario Campana, Mitchell S. Cairo
Journal: Blood (2008)
Abstract 141: Bicuspid Aortic Valve Hemodynamic Abnormalities Promote Early Development of Calcific Aortic Valve Disease
Authors: Ling Sun, Santanu Chandra, Philippe Sucosky
Journal: Circulation Research (2012)

INTRODUCTION: The bicuspid aortic valve (BAV) is the most common congenital cardiac anomaly and is frequently associated with calcific aortic valve disease (CAVD). Although CAVD also develops in the normal tricuspid aortic valve (TAV), its progression in the BAV is more rapid. While the accelerated calcification of BAV leaflets has been linked to genetic and atherogenic predispositions, hemodynamic abnormalities are increasingly pointed as potential pathogenic contributors. HYPOTHESIS: Supported by our previous work, which demonstrated the sensitivity of valve leaflets to the surrounding blood flow and associated wall-shear stress (WSS), we hypothesize that the abnormal WSS experienced by BAV leaflets contribute to CAVD development by promoting valvular inflammation, remodeling and osteogenic differentiation. OBJECTIVE: This study aims at comparing ex vivo the effects of TAV and BAV leaflet WSS on valvular pathogenesis. METHODS: The native, side-specific WSS experienced by TAV and type-I (i.e., fused and non-coronary) BAV leaflets were obtained computationally using fluid-structure interaction simulations. Fresh porcine leaflets were subjected for 48 hours to each of the three WSS conditions using a novel double-sided shear stress bioreactor. Tissue response was characterized via Western blot and immunohistochemistry in terms of markers of endothelial activation (VCAM-1, ICAM-1), paracrine expression (BMP-4), TGF-β/Wnt signaling pathways (TGF-β1, β-catenin), extracellular matrix remodeling (cathepsin L, MMP-2, MMP-9) and osteogenic differentiation (α-SMA, osteocalcin). RESULTS: No significant differences in VCAM-1 and ICAM-1 expressions were detected between tissue exposed to TAV and BAV WSS. While the native WSS experienced by the TAV and non-coronary BAV leaflets maintained tissue homeostasis, tissue exposure to the fused BAV leaflet WSS resulted in a significant pathological response marked by the upregulations of BMP-4, β-catenin, MMP-2 and osteocalcin expressions. CONCLUSION: This study demonstrates the pathological nature of the native BAV hemodynamics and confirms the higher susceptibility of the fused BAV leaflet to calcify. The results provide new insights into the hemodynamic theory of BAV calcification.
Sex-based differences in the prevalence of acute mountain sickness: a meta-analysis
Authors: Yun-Peng Hou, Jia-Lin Wu, Chao Tan, Yu Chen, Rui Guo, Yong-Jun Luo
Journal: Military Medical Research (2019)

When lowlanders rapidly ascend to altitudes > 2500 m, they may develop acute mountain sickness (AMS). The individual susceptibility, ascending velocity, time spent at altitude, activity levels and altitude reached are considered risk factors for AMS. However, it is not clear whether sex is a risk factor. The results have been inconclusive. We conducted a meta-analysis to test whether there were sex-based differences in the prevalence of AMS using Lake Louise Scoring System.Systematic searches were performed in August 2019 in EMBASE, PubMed, and Web of Science for prospective studies with AMS data for men and women. The titles and abstracts were independently checked in the primary screening step, and the selected full-text articles were independently assessed in the secondary screening step by the two authors (YPH and JLW) based on pre-defined inclusion criteria. The meta-analysis was performed using by the STATA 14.1 software program. A random-effects model was employed.Eighteen eligible prospective studies were included. A total of 7669 participants (2639 [34.4%] women) were tested. The results showed that there was a statistically significant higher prevalence rate of AMS in women than in men (RR = 1.24, 95%CI 1.09-1.41), regardless of age or race. Howerver, the heterogeneity was significant in the analysis (Tau2 = 0.0403, Chi2 = 50.15, df = 17; I2 = 66.1%, P = 0.000), it was main caused by different numbers of subjects among the studies (coefficient = - 2.17, P = 0.049). Besides, the results showed that there was no evidence of significant publication bias in the combined studies on the basis of Egger's test (bias coefficient = 1.48, P = 0.052) and Begg's test (P = 0.130).According to this study, the statistically significant finding emerging from this study was that women have a higher prevalence of AMS. However, the authors could not exclude studies where patients were on acetazolamide. Our analysis provided a direction for future studies of the relationship of sex and the risk of AMS, such as the pathological mechanism and prevention research.
Clinical trial risk reduction in non-small cell lung cancer though the use of biomarkers and receptor-targeted therapies.
Authors: Adam Falconi, Gilberto Lopes, Jayson L. Parker
Journal: Journal of Clinical Oncology (2013)

8040 Background: We analyzed the risk of clinical trial failure duringnon-small cell lung cancer (NSCLC) drug development between 1998 and 2012. Methods: NSCLC drug development was investigated using trial disclosures from publically available resources. Compounds were excluded from the analysis if they began phase I clinical testing before 1998 and if they did not use treatment relevant endpoints. Analysis was conducted in regards to treatment indication, compound classification and mechanism of action. Costs of clinical drug development for advanced NSCLC were calculated using industry data and assumptions, a 9% yearly discount rate and assuming a clinical trial length of 2.5 years for phase I trials, 4 years for phase II trials, 5 years for phase III trials and an average of 5 phase I trials, 7 phase II trials, and 4 phase III trials per approved drug. All funding costs are in US dollars (USD). Results: 2,407 clinical trials met search criteria. 676 trials and 199 unique compounds met our inclusion criteria. The likelihood, or cumulative clinical trial success rate, that a new drug would pass all phases of clinical testing and be approved was found to be 11%, which is less than the expected industry aggregate rates (16.5%). The success of phase III trials was found to be the biggest obstacle for drug approval with a success rate of only 28%. Biomarker-guided targeted therapies (with a success rate of 62%) and receptor targeted therapies (with a success rate of 31%) were found to have the highest likelihood of success in clinical trials. The risk-adjusted cost for NSCLC clinical drug development was calculated to be 1.89 billion US dollars. Use of biomarkers decreased drug development cost by 26% to 1.4 billion US dollars. Potential savings may be even higher if fewer clinical trials are required for successful development. Conclusions: Physicians that enroll patients in NSCLC trials should prioritize their participation in clinical trial programs that involve either a biomarker or receptor targeted therapy, which appear to carry the best chances for a successful treatment response. Given the high adjusted cost of clinical testing alone in NSCLC, efforts to mitigate the risk of trial failure need to explore these factors more fully.
Assessment of the role of Fanconi Anemia (FA) genes in colorectal cancer: A new pathogenetic pathway?
Authors: G. Palmieri, M. Colombino, M. G. Camboni, A. Manca, P. Baldinu, F. Izzo, F. Tatangelo, R. Calemma, A. Cossu, F. Galimi
Journal: Journal of Clinical Oncology (2006)

3629 Background: Fanconi Anemia (FA) is an autosomal recessive disease marked by congenital defects, bone marrow failure, and high incidence of leukemia and solid tumors. Eight FA associated genes have been cloned, and their products are thought to function in an integrated pathway which includes BRCA genes and maintains genomic stability. A molecular mechanism involved in the development and progression of some human malignancies, including colorectal cancer, is represented by a defective replication fidelity. Here we tested the role of the main FA genes in colorectal cancer (CRC). Methods: One hundred consecutively-collected patients with histologically-proven diagnosis of CRC and no mutation in the main mismatch repair genes (MLH1 and MSH2) were included into the study. Genomics DNA was screened using DHPLC for FANC-C/G/E/F genes and using MPLA for FANC-A/D2 genes. All PCR products with abnormal DHPLC profiles were sequenced on an automated sequencer. For 28 cases, tumor tissue samples were also analyzed. To date, total RNA was isolated from paired normal and tumor samples of 12 CRC patients. Gene expression was quantified by real-time RT-PCR using the Taqman approach. Results: At germline level, 2 cases presented FANC-C sequence variations (Asp267Ser, Val449Ser) and 5 cases showed a exon 26 deletion in FANC-A as detected by MLPA analysis. Among the 28 tumor samples available from patients negative for mutations in germline DNA, 2 (7%) cases presented a FANC-E mutation (Ala552Thr). Moreover, one of such somatic samples presented a BRCA2–8765delAG mutation (BRCA2 is also recognized as FANC-D1 gene). Assuming as significant difference in gene expression the presence of a variation of more than 50% in mRNA levels between normal and corresponding tumor samples, all tested FA genes (FANC-C/G/E/F) were found overexpressed in 5/12 (42%) tumor samples. Conclusions: Although preliminary, our findings seem to identify a subset of CRC patients with alterations in the FA/BRCA pathway which is required for the activation of DNA repair. Ongoing molecular analyses will better clarify the real frequency of each alteration in FA genes and their relationship with the histological and/or clinical features in colorectal cancer. No significant financial relationships to disclose.