tbuckley/cabot-search huggingface dataset:
Docetaxel-estramustine in high-risk localized prostate cancer: First results of the French Genitourinary Tumor Group phase III trial (GETUG 12).
Authors: K. Fizazi, F. Lesaunier, R. Delva, G. Gravis, F. Rolland, F. Priou, J. Ferrero, N. Houede, L. Mourey, C. Theodore, I. Krakowski, J. F. Berdah, M. Baciuchka, P. Kerbrat, J. Davin, J. Berille, M. Habibian, J. Ichante, A. Laplanche, S. Culine
Journal: Journal of Clinical Oncology (2011)

4513 Background: Docetaxel improves survival in patients (pts) with castrate-resistant prostate cancer (CaP). This phase III trial assessed docetaxel-based chemotherapy in pts with high-risk localized CaP. Methods: Eligibility included non-pretreated high-risk localized CaP (defined as ≥1 of the following criteria: T3-T4, Gleason score (GS) ≥8, PSA ≥ 20 ng/mL, pN+). All pts had a staging pelvic lymph node dissection. This prospective, randomized trial was stratified on the four above-mentioned prognostic factors. Pts were randomly assigned to either goserelin 10.8 mg every 3 months for 3 years and 4 cycles of docetaxel 70 mg/m2 q3w + estramustine 10 mg/kg/d d1-5 (DE arm) or goserelin alone (H arm). Local therapy was administered at 3 months. The primary endpoint was progression-free survival (PFS). The hypothesis was based on an expected 70% 4-year PFS rate in the control arm. The planned number of pts was 400, to detect a 12% difference with a power of 80% and a type I error of 0.05 (two-sided Logrank Test). Results: 413 pts were accrued (207 DE arm, 206 H arm): T3-T4 (67%), GS ≥8 (42%), PSA > 20 ng/mL (59%), pN+ (29%). Local treatment consisted of radiotherapy in 358 pts (87%) (median dose 74 Gy). All characteristics were well balanced. 94% of the pts received the planned 4 cycles of docetaxel. Toxicity included grade 3-4 neutropenia (27%) with neutropenic fever in 2%. There was no toxicity-related death and no secondary leukemia. After 3 months of systemic treatment, the PSA response rate defined as a serum PSA ≤ 0.2 ng/mL was 34% in the DE arm vs 15% in the H arm (p< 0.0001). With a median follow-up of 4.6 years, the 4-year PFS rate is 85% [79–89] in the DE arm vs 81% [75–86] in the H arm. The adjusted hazard ratio for PFS between the two arms is 0.79 [0.53-1.18], (p=0.26). With a total of 44 deaths, the 4-year overall survival rate is 94% [91–96]. Conclusions: Docetaxel-estramustine can be safely combined with standard therapy in high-risk localized CaP and significantly improves the PSA response rate. With a lower than expected number of events in both arms, the observed difference in 4-year PFS did not reach significance. A longer follow-up is required.
Hematopoiesis of Human Induced Pluripotent Stem Cells Derived From Patients with Down Syndrome
Authors: Natsumi Nishihama, Yasuhiro Ebihara, Feng Ma, Wenyu Yang, Daisuke Tomizawa, Shinji Mochizuki, Kiyoshi Yamaguchi, Masaharu Hiratsuka, Yoichi Furukawa, Mitsuo Oshimura, Hiromitsu Nakauchi, Kohichiro Tsuji
Journal: Blood (2010)
Role for Interleukin-6 and Insulin like Growth Factor-I Via PI3-K/Akt Pathway in the Proliferation of CD56-Negative and Positive Multiple Myeloma Cells.
Authors: Naohi Sahara, Akihiro Takeshita, Miki Kobayashi, Kazuyuki Shigeno, Satoki Nakamura, Kaori Shinjo, Kensuke Naito, Takemi Otsuki, Kazunori Ohnishi, Ryuzo Ohno
Journal: Blood (2004)
Interim Analysis of the Mmrf Commpass Trial: Identification of Novel Rearrangements Potentially Associated with Disease Initiation and Progression
Authors: Sagar Lonial, Venkata D Yellapantula, Winnie Liang, Ahmet Kurdoglu, Jessica Aldrich, Christophe M. Legendre, Kristi Stephenson, Jonathan Adkins, Jackie McDonald, Adrienne Helland, Megan Russell, Austin Christofferson, Lori Cuyugan, Dan Rohrer, Alex Blanski, Meghan Hodges, Mmrf CoMMpass Network, Mary Derome, Daniel Auclair, Pamela G. Kidd, Scott Jewell, David Craig, John Carpten, Jonathan J. Keats
Journal: Blood (2014)
ZAP-70 Expression Assessed by Immunohistochemistry Correlates with Time to First Treatment in Patients with Chronic Lymphocytic Leukemia.
Authors: Peter Martin, Amy Chadburn, Wayne Tam, Lauren Tyrell, Rebecca Elstrom, Jia Ruan, Morton Coleman, Scott Ely, Daniel M. Knowles, John P. Leonard, Richard R Furman
Journal: Blood (2009)
Abstract 334: Glucose regulates chemoresistance and stemness via Wnt/β-catenin signaling in ovarian cancer cells
Authors: HyeRan Gwak, Soochi Kim, UnTek Jo, Yong Sang Song
Journal: Cancer Research (2015)

Abstract Glucose metabolic alteration is one of the hallmarks of ovarian cancer. Here, we first demonstrated the function of glucose as a signature molecule that regulated chemosensitivities in ovarian cancer cells. To verify the role of glucose on the chemoresistance in ovarian cancer cells, we used various concentrations of glucose containing media (0 mM to 20 mM). Glucose reduction inhibited proliferation of various ovarian cancer cell types; irrespective of p53 status and cisplatin (CDDP) sensitivities. Interestingly, CDDP (10 to 20 μM) induced apoptosis were increased and expressions of p-glycoprotein (multidrug resistance protein 1, MDR1) and ABCG2 (ATP-binding cassette sub-family G member 2) were decreased in both mRNA and protein levels by glucose free conditions. Moreover, sphere forming capacities and stemness related gene expressions, SOX2, OCT4, BMI1 and Nanog, were also decreased in ovarian cancer cells in response to glucose starvation. Suppression of CDDP resistance and stemness in ovarian cancer was found to be associated with the activation of GSK3β in response to limitation of glucose availabilities, as confirmed by the function of the GSK3β inhibitors (LiCl and SB SB216763) and also downstream molecules, β-catenin and cyclin D1. In contrast, high glucose (20 mM) environment enhanced CDDP resistance in ovarian cancer cells via elevation of p-glycoprotein and ABCG2 expressions, sphere forming capacities and stemness related gene expressions. Moreover, CDDP (10 to 20 μM) in high concentration of glucose media induced apoptotic cell death were significantly decreased. This study described the novel function of glucose in chemoresistance in ovarian cancer cells by deregulation of multidrug efflux pumps and stemness through Wnt/ β-catenin signaling cascades. Citation Format: HyeRan Gwak, Soochi Kim, UnTek Jo, Yong Sang Song. Glucose regulates chemoresistance and stemness via Wnt/β-catenin signaling in ovarian cancer cells. [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 334. doi:10.1158/1538-7445.AM2015-334
Granulocyte-Colony Stimulating Factor Use in Young Fit CLL Patients Receiving Fludarabine-Cyclophosphamide-Rituximab Frontline: Impact on Outcomes, Relative Dose Intensity and Toxicities
Authors: Emmanuelle Bouvet, Lucie Oberic, Christian Recher, Françoise Huguet, Xavier Carles, Guy Laurent, Loic Ysebaert
Journal: Blood (2011)
Molecular Characterization of the Idiopathic Hypereosinophilic Syndrome (HES) in 35 French Patients with Normal Conventional Cytogenetics.
Authors: Catherine Roche-Lestienne, Valerie Soenen-Cornu, Jean-Emmanuel Kahn, Jean-Luc Lai, Eric Hachulla, Francois Drupt, Anne-Laure Demarty, Martine Gardembas, Nathalie Philippe, Stephane Barette, Christian Libersa, Olivier Bletry, Christian Rose, Pierre Fenaux, Lionel Prin, Claude Preudhomme
Journal: Blood (2004)
Abstract 3766: Identifying rational combination therapies with rapamycin for the treatment of epithelial cancers
Authors: Moez Dawood, Yiling Lu, Gordon Mills
Journal: Cancer Research (2015)

Abstract Targeted therapies are designed to inhibit specific pathways driving the malignant phenotype while concurrently decreasing side effects on normal cells. However, very frequently, inhibition of the targeted pathway activates compensatory mechanisms designed to bring the pathway back into equilibrium allowing for cancer cell survival, a mechanism known as adaptive drug resistance. The purpose of this project is to identify and abrogate the adaptive drug resistance of epithelial cancers to rapamycin, an allosteric inhibitor of mTOR (mammalian target of rapamycin), and to rapamycin analogs in the PI3K (phosphoinositide-3-kinase) pathway, the most commonly dysregulated pathway in epithelial cancers. Using 3D- cultures, rapamycin-induced morphology changes and cell death were recorded. Changes in protein levels due to rapamycin-induced adaptive signaling were detected using reverse phase protein arrays (RPPA), verified by western blotting, and analyzed to determine potential adaptive mechanisms. Based on screening results from RPPA, rapamycin was combined with rationally selected drugs designed to thwart adaptive drug resistance to rapamycin. This co-extinction approach reinforced rapamycin into an effective inducer of cell death, ultimately bypassing drug resistance mechanisms and precluding the emergence of future therapeutic resistance. Successful combinations will be forwarded into animal studies to demonstrate in vivo efficacy for the treatment of epithelial cancers. Note: This abstract was not presented at the meeting. Citation Format: Moez Dawood, Yiling Lu, Gordon Mills. Identifying rational combination therapies with rapamycin for the treatment of epithelial cancers. [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 3766. doi:10.1158/1538-7445.AM2015-3766
Emerging Marrow Fibrosis Is an Early Indicator of Imatinib Failure and Shortened Survival Time in CML Independent of Hematologic, Cytogenetic and Molecular Response.
Authors: Guntram Buesche, Ruediger Hehlmann, Arnold Ganser, Hartmut Hecker, Mathias Freund, Hermann Heimpel, Barbara Heinze, Dorothea Gadzicki, Brigitte Schlegelberger, Christa Fonatsch, Bernd Frye, Andreas Tobler, Axel Georgii, Hans H. Kreipe
Journal: Blood (2005)
Manual of Emergencies: Medical. Surgical and Obstetric. Their Pathology, Diagnosis and Treatment (Based upon Lenzmann's "Emergencies in Medical Practice").
Journal: JAMA (1926)

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 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) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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
Pentraxins Coordinate Excitatory Synapse Maturation and Circuit Integration of Parvalbumin Interneurons
Authors: Kenneth A. Pelkey, Elizabeth Barksdale, Michael T. Craig, Xiaoqing Yuan, Madhav Sukumaran, Geoffrey A. Vargish, Robert M. Mitchell, Megan S. Wyeth, Ronald S. Petralia, Ramesh Chittajallu, Rose-Marie Karlsson, Heather A. Cameron, Yasunobu Murata, Matthew T. Colonnese, Paul F. Worley, Chris J. McBain
Journal: Neuron (2016)
Role of the type III TGF-β receptor in modulating antitumor immunity during breast cancer progression.
Authors: B. A. Hanks, O. M. Campbell, J. D. Lee, M. Morse, T. M. Clay, H. K. Lyerly, G. C. Blobe
Journal: Journal of Clinical Oncology (2011)

10540 Background: We have shown that breast cancers downregulate the expression of the type III TGF-β receptor (TβRIII) tumor suppressor during tumor progression. Previous work has shown TβRIII to undergo ectodomain shedding, enabling the sequestration of the soluble TGF-β ligand and the inhibition of the TGF-β signaling pathway. The TGF-β cytokine inhibits dendritic cell (DC)-dependent antigen presentation. We hypothesize that the downregulation of TβRIII during breast tumor development permits enhanced TGF-β signaling within the local DCs of the tumor microenvironment allowing the tumor to evade the host immune response. Methods: Our data suggest that the tumor suppressor properties of TβRIII in the 4T1 murine metastatic breast cancer model are diminished in immunosuppressed hosts. Indeed, loss of TβRIII allows for the progression of more immunogenic Her2/neu-expressing 4T1 tumors and suppresses Her2/neu-specific T cell responses. Flow cytometry and rt-PCR studies indicate that breast tumors which lack TβRIII expression exhibit reduced numbers of infiltrating CD8+ T cells and increased regulatoy T cells (Tregs), findings which are supported by human microarray data. In addition, DCs within TβRIIIlo tumors and their draining lymph nodes (TDLNs) express enhanced levels of the indoleamine 2,3-dioxygenase (IDO) enzyme as well as the CCL22 chemokine, which correlates with expanded local Treg populations. Studies have shown 4T1-RIII conditioned media to inhibit TGF-β signaling within DCs and to suppress the TGF-β-mediated inhibition of DC maturation. Our work is showing that DCs within the TDLNs of TβRIIIhi tumors exhibit a more mature phenotype. Results: The increased TGF-β signaling capacity of DCs residing in TβRIIIlo tumors may allow for increased local CCL22 expression; thereby promoting Treg recruitment and allowing for CTLA-4-mediated IDO upregulation by local DCs. Conclusions: This pathway represents a novel mechanism for evading the host anti-tumor immune response, supports the targeting of TGF-β as a strategy to enhance the efficacy of immunotherapeutic approaches for solid tumors, and suggests that serum levels of soluble TβRIII may represent a useful biomarker for immunotherapy.
The Comparison of In Vitro and In Vivo Anti-Host Responses as a Predictor of T Cell Reactivity after Allogeneic-BMT as Determined by TCR Vb Spectratype Analysis.
Authors: Thea M. Friedman, Olga Y. Azhipa, Joanne Filicko, Bijoyish Mookerjee, Neal Flomenberg, Michele L. Donato, Scott D. Rowley, Robert Korngold
Journal: Blood (2006)
PTH-026 Does reduction in midazolam concentration affect colonoscopy outcomes?: Abstract PTH-026
Authors: T Jackson, S Tran, T Sharp, S Singh, G R Lipscomb
Journal: Gut (2010)

<h3>Introduction</h3> Following BSG recommendations in 2006,1 we showed that replacement of 5 mg/ml with 2 mg/ml concentration of midazolam led to a decrease in the amount of midazolam used with no compromise in the quality of endoscopy.2 In December 2008 the National Patient Safety Agency issued a rapid response report on midazolam for conscious sedation.3 The recommendation was to replace all 5 mg/ml and 2 mg/ml vials of midazolam with the weaker 1 mg/ml strength. This was done in our unit in Feb 2009. We investigated the effects of this further reduction in midazolam concentration on total doses delivered during colonoscopy, adequacy of examinations and the incidence of over sedation. <h3>Methods</h3> We reviewed colonoscopy data from 2-month periods in 2006 (midazolam 5 mg/ml), 2008 (2 mg/ml) and 2009 (1 mg/ml). Mean doses of midazolam and pethidine were recorded. Outcome measures for colonoscopy were caecal intubation rate and detection of adenomas and carcinomas. We also determined the percentage of patients with a deterioration in their comfort scores collected prospectively for 2 weeks during each data collection period. Episodes of flumazenil use are also reported. <h3>Results</h3> Data from over 1250 cases are shown with mean±SD for drug doses. Mann–Whitney U test was used to compare drug doses between 2006 vs 2008 and 2008 vs 2009 (*p&lt;0.0001) (Abstract 026). <h3>Conclusion</h3> Reduction in midazolam concentration led to a reduction in the mean dose of midazolam given at colonoscopy without affecting the concomitant use of opiates. In addition, there were no adverse effects on colonoscopy outcomes. Although some of these finding may be attributable to better endoscopic skills, improved endoscopy equipment or closer adherence to recent guidelines, there is at least compelling evidence now that the drive towards safe sedation can be achieved without compromising quality during colonoscopic examination. We conclude that reduction in midazolam concentration to 1 mg/mL facilitates lower overall doses of sedation and subsequent improvements in patient safety while also providing adequate sedation with no detriment to procedural success.
De Novo ABL Kinase Domain Mutations in Murine Bone Marrow Cells Retrovirally Transduced with Wild-Type p210 BCR-ABL and Amplified in Culture with Imatinib Mesylate.
Authors: Stephane Flamant, Martine Guillier, Marie-Laure Bonnet, Jean-Pierre Lecouedic, William Vainchenker, Ali G. Turhan
Journal: Blood (2004)
A chikungunya fever vaccine utilizing an insect-specific virus platform
Authors: Jesse H Erasmus, Albert J Auguste, Jason T Kaelber, Huanle Luo, Shannan L Rossi, Karla Fenton, Grace Leal, Dal Y Kim, Wah Chiu, Tian Wang, Ilya Frolov, Farooq Nasar, Scott C Weaver
Journal: Nature Medicine (2016)
Colony Forming Unit (CFU) Assay with High Resolution Digital Imaging (HRDI): a Reliable, Standardized Technology for Evaluation of Cord Blood Potency Before and After Cryopreservation.
Authors: Maria S Albano, Ludy Dobrila, Anna Gora, Hazel Taik, Magdalena Mamczur-Madry, Rory Abrams, Andromachi Scaradavou, Pablo Rubinstein
Journal: Blood (2009)
Detection of Karyotype Evolution From Peripheral Blood by Sequential FISH Analyses of Circulating CD34+ Cells In MDS Patients: Results of the Ongoing German Multicenter Prospective Diagnostic Study
Authors: Friederike Braulke, Julie Schanz, Michael Metz, Sven Detken, Joerg Seraphin, Katharina Götze, Catharina Mueller-Thomas, Uwe Platzbecker, Tim Henrik Brümmendorf, Aristoteles A.N. Giagounidis, Ulrich Germing, Kathleen Jentsch-Ullrich, Angelika Boehme, Gesine Bug, Oliver G. Ottmann, Philippe Schafhausen, Lorenz Trümper, Detlef Haase
Journal: Blood (2010)
Specific activity of cyclin dependent kinase 1 as a novel predictor of recurrence risk in stage II colon cancer.
Authors: M. Maak, E. Zeestraten, M. Shibayama, T. Schuster, H. Friess, C. J. Van De Velde, H. Ishihara, R. Rosenberg, P. J. Kuppen, K. Janssen
Journal: Journal of Clinical Oncology (2011)

402 Background: Altered cell cycle dynamics and check points are typical features of solid tumors, and cyclin dependent kinases (CDKs) play pivotal roles in these processes. Previously we have demonstrated that CDK-based analysis, composed of CDK1 and CDK2, is useful in the prediction of outcomes in early breast cancer patients (Ann Oncol. 19(1):68-72, 2008, Br J Cancer. 100(3):494-500, 2009). Clinically, there is a need for risk stratification in patients with stage II colon cancer who have a recurrence risk of 20 to 30%. Therefore we investigated the use of CDK-based analysis for recurrence prediction of stage II colon cancer patients. Methods: Fresh frozen tissue samples of 254 patients with histologically confirmed adenocarcinoma of the colon, UICC stage II, who received primary tumor resection in Munich (217 cases), and Leiden (37 cases) were used. Protein expression and activity of CDK1 and CDK2 were determined by in vitro assays as previously described. Specific activity (SA) of CDKs was calculated as kinase activity in relation to its corresponding mass concentration. Results: Development of distant metastasis was observed in 27 patients (10.6%) after a median follow up of 86 months. We found that predictive performance of CDK1SA, but not CDK2SA, for the metastasis was substantial and almost constant for long-term event prediction (average area under the curve (AUC) = 0.69). Tumor recurrence risk analysis in association with CDK1SA identified a low- (41% of population) and high- risk group (59%). Cox proportional hazard model analysis retained the CDK-based patient classification as an independent prognostic factor for distant metastases-free survival (low vs. high-risk group: Hazard ratio = 6.2, 95% CI: 1.45 to 26.9, p=0.0049). Clinical parameters such as grading, T-categories, age, and sex were excluded as confounding factors for CDK1SA-risk. Conclusions: CDK1SA allows stratification of different risk subgroups of stage II colon cancer patients. CDK1SA-based analysis is useful for predicting patients with high risk of distant recurrence, who should be treated with chemotherapy. No significant financial relationships to disclose.
Severe Gut Acute Graft Versus host Disease (GVHD) Influence Thrombotic Microangiopathy in 86 Allogeneic Hematopoietic Stem Cell Recipients Who Received Tacrolimus-Based Regimen for GVHD Prophylaxis
Authors: Jorge Labrador, Oriana López-Godino, Lucía López-Corral, Estefanía Pérez-López, Mónica Cabrero-Calvo, Roberto Pérez-López, José María Bastida, Miriam López-Parra, Ignacio Alberca, José Ramón González-Porras, Dolores Caballero
Journal: Blood (2012)
Complete prevalence of malignant primary brain tumors registry data in the United States compared with other common cancers, 2010
Authors: Adah S. Zhang, Quinn T. Ostrom, Carol Kruchko, Lisa Rogers, David M. Peereboom, Jill S. Barnholtz-Sloan
Journal: Neuro-Oncology (2016)

Complete prevalence proportions illustrate the burden of disease in a population. This study estimates the 2010 complete prevalence of malignant primary brain tumors overall and by Central Brain Tumor Registry of the United States (CBTRUS) histology groups, and compares the brain tumor prevalence estimates to the complete prevalence of other common cancers as determined by the Surveillance, Epidemiology, and End Results Program (SEER) by age at prevalence (2010): children (0-14 y), adolescent and young adult (AYA) (15-39 y), and adult (40+ y).Complete prevalence proportions were estimated using a novel regression method extended from the Completeness Index Method, which combines survival and incidence data from multiple sources. In this study, two datasets, CBTRUS and SEER, were used to calculate complete prevalence estimates of interest.Complete prevalence for malignant primary brain tumors was 47.59/100000 population (22.31, 48.49, and 57.75/100000 for child, AYA, and adult populations). The most prevalent cancers by age were childhood leukemia (36.65/100000), AYA melanoma of the skin (66.21/100000), and adult female breast (1949.00/100000). The most prevalent CBTRUS histologies in children and AYA were pilocytic astrocytoma (6.82/100000, 5.92/100000), and glioblastoma (12.76/100000) in adults.The relative impact of malignant primary brain tumors is higher among children than any other age group; it emerges as the second most prevalent cancer among children. Complete prevalence estimates for primary malignant brain tumors fills a gap in overall cancer knowledge, which provides critical information toward public health and health care planning, including treatment, decision making, funding, and advocacy programs.