tbuckley/cabot-search huggingface dataset:
Early Treatment Intensification in Advanced-Stage High-Risk Hodgkin Lymphoma (HL) Patients, with a Positive FDG-PET Scan After Two ABVD Courses – First Interim Analysis of the GITIL/FIL HD0607 Clinical Trial
Authors: Andrea Gallamini, Andrea Rossi, Caterina Patti, Marco Picardi, Francesco Di Raimondo, Maria Cantonetti, Giorgio La Nasa, Simonetta Viviani, Silvia Bolis, Livio Trentin, Attilio Olivieri, Valerio Zoli, Alberto Biggi, Stephane Chauvie, Francesca Fiore, Anna Cavallo, Giuseppe Prosperini, Roberto Marchioli, Guido Parvis, Roberta Zanotti, Paolo Gavarotti, Anna Dodero, Corrado Schiavotto, Fabio Ciceri, Abraham Avigdor, Antonino Mulè, Corrado Tarella, Alessandro M. Gianni, Alessandro Rambaldi
Journal: Blood (2012)
Membrane-organizing protein moesin controls Treg differentiation and antitumor immunity via TGF-β signaling
Authors: Ephraim A. Ansa-Addo, Yongliang Zhang, Yi Yang, George S. Hussey, Breege V. Howley, Mohammad Salem, Brian Riesenberg, Shaoli Sun, Don C. Rockey, Serhan Karvar, Philip H. Howe, Bei Liu, Zihai Li
Journal: Journal of Clinical Investigation (2017)

Moesin is a member of the ezrin-radixin-moesin (ERM) family of proteins that are important for organizing membrane domains and receptor signaling and regulating the migration of effector T cells. Whether moesin plays any role during the generation of TGF-β-induced Tregs (iTregs) is unknown. Here, we have discovered that moesin is translationally regulated by TGF-β and is also required for optimal TGF-β signaling that promotes efficient development of iTregs. Loss of moesin impaired the development and function of both peripherally derived iTregs and in vitro-induced Tregs. Mechanistically, we identified an interaction between moesin and TGF-β receptor II (TβRII) that allows moesin to control the surface abundance and stability of TβRI and TβRII. We also found that moesin is required for iTreg conversion in the tumor microenvironment, and the deletion of moesin from recipient mice supported the rapid expansion of adoptively transferred CD8+ T cells against melanoma. Our study establishes moesin as an important regulator of the surface abundance and stability of TβRII and identifies moesin's role in facilitating the efficient generation of iTregs. It also provides an advancement to our understanding about the role of the ERM proteins in regulating signal transduction pathways and suggests that modulation of moesin is a potential therapeutic target for Treg-related immune disorders.
Abstract P6-05-01: Low BRCA2 levels cause epigenetic activation of growth adaptive pathways without inducing recurrent genomic mutations
Authors: JJ Gruber, M Snyder
Journal: Cancer Research (2017)

Abstract The development of therapeutics to prevent cancer onset is hindered by a lack of robust cell systems to study the earliest steps of malignant transformation. Significant barriers to studying cancer-initiating events include intrinsic cellular pathways to prevent cell proliferation in the setting of activating oncogenes or genomic instability. To circumvent this limitation, we studied in vitro transient depletion of breast cancer tumor suppressor genes followed by selective growth conditions to enrich for de novo mutations or stable epigenetic alterations that can confer a growth advantage to non-transformed breast epithelial cells. We report that transient BRCA2 depletion, but not depletion of other breast cancer genes, leads to a selective growth advantage in EGF-free media. This is due to a failure of BRCA2 inactivated cells to enact a mesenchymal-to-epithelial transition upon withdrawal of EGF. Genomic profiling and biochemical approaches indicate that transient loss of BRCA2 induces chromatin remodeling in concert with NF-κB signaling and histone H2B deacetylation to repress genes associated with the epithelial state. Notably, this process did not appear to require recurrent driver mutations, nor DNA methylation changes, but was dependent on ATR signaling. Overall, our work suggests that transiently low BRCA2 levels are sufficient to induce aberrant cell proliferation under certain conditions and that targeting epigenetic modifiers may be an approach to prevent BRCA2-induced malignancy. Citation Format: Gruber JJ, Snyder M. Low BRCA2 levels cause epigenetic activation of growth adaptive pathways without inducing recurrent genomic mutations [abstract]. In: Proceedings of the 2016 San Antonio Breast Cancer Symposium; 2016 Dec 6-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2017;77(4 Suppl):Abstract nr P6-05-01.
Weekly Infusion of Bortezomib In Combination with Rituximab In Relapsed/Refractory Indolent Non-Follicular and Mantle Cell Lymphoma Is Safe and Effective: Two-Years Analysis of Phase II Trial BRIL06 of Intergruppo Italiano Linfomi (IIL)
Authors: Annalisa Chiappella, Patrizia Pregno, Pier Luigi Zinzani, Andrea Evangelista, Alberto Fabbri, Fabio Facchetti, Andres JM Ferreri, Silvia Franceschetti, Roberto Freilone, Livio Gargantini, Daniela Gioia, Anna Marina Liberati, Maura Nicolosi, Lorella Orsucci, Luigi Rigacci, Eleonora Russo, Vittorio Stefoni, Alessandra Tucci, Umberto Vitolo
Journal: Blood (2010)
Abstract A59: Glycosylation dynamically tunes the biophysical properties of the cancer cell glycocalyx
Authors: Carolyn Shurer, Matthew Paszek
Journal: Cancer Research (2017)

Abstract Muc1 is a large, heavily O-glycosylated membrane protein that is overexpressed in the majority of cancers and constitutes the major structural element of the cancer cell glycocalyx. While the biophysical properties of the glycocalyx directly regulate cell-ECM adhesion, cell-cell interactions, and receptor spatial organization, how these properties change dynamically during acquisition of a metastatic phenotype is largely unknown. To dissect the relationship among glycan biosynthesis, mucin rigidity, and the bulk properties of the cancer-specific glycocalyx, we isolated sub-populations of Muc1-expressing breast epithelial cells that present with distinct mucin glycophenotypes. Remarkably, alterations in glycosylation were associated with profound differences in glycocalyx structure, even in isogenic cell lines. In one stable glycophenotype, cellular mucins were highly rigid and mechanically disrupted integrin adhesion, resulting in complete dissociation of cells from the substrate. On the other extreme, we isolated a stable population of cells that expresses high levels of Muc1, but these mucins were apparently flexible and had no observable effect on cell adhesion or motility. Based on lectin profiling, we identified specific patterns of Muc1 O-glycosylation associated with the two extremes in glycocalyx structures. Of notable significance, we discovered that metabolic reprogramming by the H-Ras oncogene could induce a glycophenotype consistent with mechanically rigid mucins. Future studies will identify the specific glycosylation machinery associated with the different glycophenotypes, with the hope of identifying new avenues of therapeutic intervention based on normalizing the mechano-phenotype of the cancer cell glycocalyx. Citation Format: Carolyn Shurer, Matthew Paszek. Glycosylation dynamically tunes the biophysical properties of the cancer cell glycocalyx. [abstract]. In: Proceedings of the AACR Special Conference on Engineering and Physical Sciences in Oncology; 2016 Jun 25-28; Boston, MA. Philadelphia (PA): AACR; Cancer Res 2017;77(2 Suppl):Abstract nr A59.
Abstract P6-09-55: “Quality, not quantity”: 10X hot-spot (HS) analysis of lymphocyte markers (CD3, CD8, CD4, CD20) in tumor-infiltrating lymphocytes (TILs) is superior to whole tumor (WT) analysis in triple-negative breast cancer (TNBC)
Authors: X Cui, PJ McIntire, PS Ginter, L Irshaid, Z Chen, SJ Shin
Journal: Cancer Research (2017)

Abstract This abstract was withdrawn by the authors.
Gleevec Therapy in Advanced Phases of the Cml - Polish Study Report.
Authors: Bernadeta B. Ceglarek, Lech J. Konopka, Anna Sikorska, Kinga Kos, Jerzy Holowiecki, Malgorzata Kopera, Grazyna Bober, Tomasz Kruzel, Barbara Pienkowska-Grela, Renata Woroniecka, Joanna Rygier
Journal: Blood (2004)
Mutation Selective IDH Inhibitors Mediate Histone and DNA Methylation Changes
Authors: Katharine Yen, Fang Wang, Stefanie Schalm, Erica Hansen, Kimberly Straley, Andrew Kernytsky, Sung Choe, Wei Liu, Janeta Popovici-Muller, Jeremy Travins, Hua Yang, Lee Silverman, Julie Losman Aurore, William G. Kaelin, Stefan Gross, Lenny Dang, Frank Salituro, Jeffrey Saunders, Marion Dorsch, Samuel Agresta, David P. Schenkein, Michael Su, Scott Biller
Journal: Blood (2012)
Abstract P5-05-05: The role and regulation mechanism of HOXB5 in human breaset cancer cells
Authors: JM Kim, J-Y Lee, MH Kim
Journal: Cancer Research (2017)

Abstract HOX genes are transcription factors that play important roles in body patterning and cell fate specification during normal development. Among of these, HOXB5, is involved in a variety of developmental processes, particularly during the enteric nervous system (ENS) development, and thus, abnormalities in HOXB5 function during embryo stages lead to Hirschsprung's disease. Importantly, many HOX genes, including HOXB5, are expressed not only during embryogenesis but also in adults and are dysregulated in various cancers. In a previous study, we found aberrant overexpression of HOXB5 in breast cancer tissues and cell lines and demonstrated that HOXB5 is important in the regulation of cell proliferation in breast cancer cells. Also, HOXB5 induces invasive potential through epithelial-mesenchymal transition (EMT). The relationship between HOXB5 and phenotypic changes in MCF7 breast cancer cells has been studied, however, HOXB5 functions as a transcription factor and its involvement in signaling pathways remain unclear. In this study, we selected putative downstream target genes of HOXB5, such as interleukin (IL)-6, Snail2 and epidermal growth factor receptor (EGFR) by PCR array analysis. These genes have been reported to be involved in cacner progression, which is characterised by increased growth speed and invasiveness of the tumor cells. Here, we discovered that HOXB5 transcriptionally upregulates the promoter activity of these genes. Chromatin immunoprecipitation (ChIP) analysis to confirm direct binding of HOXB5 to the promoter region is now ongoing. Since we found that HOXB5 induces EGFR protein expression and SRC phosphorylation, we will further investigate signaling pathway components to understand the underlying molecular mechanisms of HOXB5 action in breast cancer. Citation Format: Kim JM, Lee J-Y, Kim MH. The role and regulation mechanism of HOXB5 in human breaset cancer cells [abstract]. In: Proceedings of the 2016 San Antonio Breast Cancer Symposium; 2016 Dec 6-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2017;77(4 Suppl):Abstract nr P5-05-05.
Robust detection and segmentation of cell nuclei in biomedical images based on a computational topology framework
Authors: Rodrigo Rojas-Moraleda, Wei Xiong, Niels Halama, Katja Breitkopf-Heinlein, Steven Dooley, Luis Salinas, Dieter W. Heermann, Nektarios A. Valous
Journal: Medical Image Analysis (2017)
Cellular Composition and Clonal Evolution of 295 Type III PNH Clones: An Italian Multi-Laboratory Study
Authors: Elisa Cannizzo, Domenico Susca, Anna Maria Triolo, Catia Lo Pardo, Francesco Buccisano, Elisabetta Tedone, Francesca Messana, Bianca Maria Oliva, Virginia Ottaviano, Giovanni Carulli, Franco Monti, Maria Stefania De Propris, Alessandra Stacchini, Laura Vanelli, Omar Perbellini, Mario Arpinati, Nadia Viola, Francesco Gervasi, Cinzia Armentano Conte, Donatella Tanca, Francesco Lanza, Massimo Geuna, Luigi Del Vecchio
Journal: Blood (2012)
Erlotinib + gemcitabine in patients with unresectable pancreatic carcinoma: Results from a phase IB trial
Authors: B. W. Porterfield, T. Dragovich, A. Patnaik, E. Rowinsky, M. Huberman, T. Clinebell, M. Hamilton, A. Zitelli, P. Nadler, D. Wood
Journal: Journal of Clinical Oncology (2004)

4110 Background: Erlotinib (Tarceva) is a reversible inhibitor of HER1/EGFR tyrosine kinase. It has demonstrated antitumor activity in various epithelial malignancies and additive antitumor effect when combined with chemotherapy drugs. The purpose of this trial was to evaluate the tolerability and preliminary activity of escalating doses of erlotinib given in combination with standard-dose gemcitabine (GEM 1000 mg/m2). Methods: Eligible patients included those with advanced pancreatic carcinoma or other malignancies potentially responsive to GEM. In the escalating phase of the trial patients with pancreatic and non-pancreatic carcinomas were enrolled in sequential cohorts using 100 mg or 150 mg oral daily dosing of erlotinib. GEM 1000 mg/m2 was given weekly for 7 weeks (1st cycle), then weekly x 3 every 4 weeks (subsequent cycles). Preliminary results from the dose-escalating phase of this trial were previously reported (ASCO 2003). After establishing tolerability, additional gemcitabine-naïve patients with pancreatic cancer were enrolled. Overall, we have enrolled 14 patients with unresectable pancreatic carcinoma: 2 patients at the 100 mg dose level of erlotinib and 12 patients at the 150 mg dose level. Characteristics: measurable or evaluable disease, gender M/F 7/7, median age 66 yrs (range 45–82), median PS 90 % KS (range 80–100%). Results: 1 partial response (PR, 7%), 3 minor responses and 6 with stable disease for an overall disease control rate of 70 % (PR+SD), and 4 patients progressed (PD, 30%). The median duration of study treatment was 4 months (range from 2 to 12+) with 4 patients remaining on study treatment. The most common toxicities included skin rash, neutropenia, fatigue, nausea and diarrhea. The full PK analysis is ongoing and will be updated at the time of meeting. Conclusion: The erlotinib + gemcitabine combination appears promising, with a high rate of disease stabilization and acceptable toxicity profile seen in patients with unresectable pancreatic carcinoma. This combination is currently being compared to standard GEM therapy in a phase III randomized trial conducted by the NCIC. Supported by grant from OSI Pharmaceuticals. No significant financial relationships to disclose.
Impact of Chromosomal Abnormalities in Acute and Lymphoma Types Adult T-Cell Leukemia-Lymphoma
Authors: Nobuaki Nakano, Hiroo Katsuya, Takahiro Itoyama, Mototsugu Shimokawa, Atae Utsunomiya, Shuichi Hanada, Tetsuya Eto, Yukiyoshi Moriuchi, Yoshio Saburi, Masaharu Miyahara, Eizaburo Sueoka, Naokuni Uike, Shinichiro Yoshida, Kiyoshi Yamashita, Kunihiro Tsukasaki, Hitoshi Suzushima, Yuji Ohno, Junji Suzumiya, Kazuo Tamura, Kenji Ishitsuka
Journal: Blood (2016)
Expression Profile of PIP Kinases During In Vitro Human Erythropoiesis
Authors: Tânia Regina Zaccariotto, Carolina Lanaro, Dulcinéia Martins Albuquerque, Magnun N N Santos, Marcos André Cavalcanti Bezerra, Aderson S Araujo, Fernando Ferreira Costa, Maria de Fátima Sonati
Journal: Blood (2010)
Prognostic Significance of SALL4 Expression Levels in Paediatric Acute Myeloid Leukaemia (AML).
Authors: Paola Ballerini, Pierre-Yves Boelle, Caroline Deswarte, Anne Auvrignon, Gabrielle Couchy, Judith Landman- Parker, Alain Robert, Brigitte Nelken, Mircea Adam, Helene Lapillonne, Eric Delabesse, Christine Perot, Jean Luc Lai, Nicole Dastugue, Claude Preudhomme, Jessica Zucman-Rossi, Guy Leverger
Journal: Blood (2008)
Combination therapy based on bortezomib for 102 patients with newly-diagnosed multiple myeloma: a Chinese experience
Authors: Jingsong He, Li Yang, Xiaoyan Han, Gaofeng Zheng, Xiaojian Meng, Guoqing Wei, Wenjun Wu, Weiyan Zheng, Xiujin Ye, Jimin Shi, Wanzhuo Xie, Jie Zhang, He Huang, Maofang Lin, Zhen Cai
Journal: Blood (2011)
Bloodstream Infections Caused By Klebsiella Pneumoniae in Onco-Hematological Patients: Incidence and Clinical Impact of Carbapenem Resistance in a Multicentre Prospective Survey
Authors: Enrico Maria Trecarichi, Mario Tumbarello, Roberta Di Blasi, Luana Fianchi, Simona Sica, Bruno Martino, Anna Candoni, Gianpaolo Nadali, Domenico Pastore, Vincenzo Perriello, Alessandro Busca, Franco Aversa, Rosa Fanci, Lorella Melillo, Federica Lessi, Maria Ilaria Del Principe, Chiara Cattaneo, Livio Pagano
Journal: Blood (2015)
Arsenic Trioxide with Ascorbic Acid and High-Dose Melphalan: A New Preparative Regimen for Autologous Hematopoietic Stem Cell Transplantation for Multiple Myeloma.
Authors: Muzaffar H. Qazilbash, Marilyn S. Davis, Aleman Ana, Linda Roden, Floralyn Libunao, Peter F. Thall, Xuemei Wang, Daniel Couriel, Marcos De Lima, Chitra Hosing, Partow Kebriaei, Donna Weber, Michael Wang, Roy B. Jones, Steven G. Matthes, Richard E. Champlin, Sergio A. Giralt
Journal: Blood (2005)
Astrocytes Control Circadian Timekeeping in the Suprachiasmatic Nucleus via Glutamatergic Signaling
Authors: Marco Brancaccio, Andrew P. Patton, Johanna E. Chesham, Elizabeth S. Maywood, Michael H. Hastings
Journal: Neuron (2017)

The suprachiasmatic nucleus (SCN) of the hypothalamus orchestrates daily rhythms of physiology and behavior in mammals. Its circadian (∼24 hr) oscillations of gene expression and electrical activity are generated intrinsically and can persist indefinitely in temporal isolation. This robust and resilient timekeeping is generally regarded as a product of the intrinsic connectivity of its neurons. Here we show that neurons constitute only one "half" of the SCN clock, the one metabolically active during circadian daytime. In contrast, SCN astrocytes are active during circadian nighttime, when they suppress the activity of SCN neurons by regulating extracellular glutamate levels. This glutamatergic gliotransmission is sensed by neurons of the dorsal SCN via specific pre-synaptic NMDA receptor assemblies containing NR2C subunits. Remarkably, somatic genetic re-programming of intracellular clocks in SCN astrocytes was capable of remodeling circadian behavioral rhythms in adult mice. Thus, SCN circuit-level timekeeping arises from interdependent and mutually supportive astrocytic-neuronal signaling.
Endoscopic and Histologic Healing in Children With Inflammatory Bowel Diseases Treated With Thalidomide
Authors: Marzia Lazzerini, Vincenzo Villanacci, Maria Chiara Pellegrin, Stefano Martelossi, Giuseppe Magazzù, Salvatore Pellegrino, Maria Cristina Lucanto, Arrigo Barabino, Angela Calvi, Serena Arrigo, Paolo Lionetti, Massimo Fontana, Giovanna Zuin, Giuseppe Maggiore, Matteo Bramuzzo, Massimo Maschio, Marianna Salemme, Stefania Manenti, Luisa Lorenzi, Giuliana Decorti, Marcella Montico, Alessandro Ventura
Journal: Clinical Gastroenterology and Hepatology (2017)
SPARC in pancreatic cancer: Results from the CONKO-001 study.
Authors: Marianne Sinn, Bruno Valentin Sinn, Jana Kaethe Striefler, Jens Stieler, Uwe Pelzer, Judith Prinzler, Peter Neuhaus, Manfred Dietel, Bernd Dörken, Helmut Oettle, Hanno Riess, Carsten Denkert
Journal: Journal of Clinical Oncology (2013)

4016 Background: Previous investigations in pancreatic cancer suggested an important prognostic role for SPARC (secreted protein acidic and rich in cysteine) expression in the peritumoral stroma but not for cancer-cell cytoplasmic SPARC expression. So far no data from prospective studies in patients after curatively intended surgery are available. Methods: CONKO-001, a prospective randomized phase III study, investigated the role of adjuvant gemcitabine as compared to observation. Tissue samples of 160 patients were collected and analysed by immunohistochemistry for the expression of SPARC in the peritumoral stroma (strong versus not strong [=moderate to negative]) and in the tumor cell cytoplasm (immunoreactive score IRS 0-12, 0-2 = negative, 3-12 = positive) by a pathologist blinded to clinical outcome. Kaplan-Meier analyses for disease-free survival (DFS) and overall survival (OS) were performed in dependence of SPARC expression. Results: Strong stromal SPARC expression was associated with worse DFS and OS in the overall study population (strong vs not-strong DFS 9.0 vs 12.6 months, p=0.005; OS 19.8 vs 26.6 months (p=0.033). It was highly prognostic in the subgroup treated with gemcitabine (strong vs not-strong DFS 12.1 vs. 18.4 months; p=0.007, OS 17.9 vs 30.2 months, p=0.006), but not in the observation group (strong vs not strong DFS 6.6 vs 7.3 months p=0.767; OS 21.5 vs 18.2 months, p=0.765). Cytoplasmic SPARC expression in the adenocarcinoma cells was also associated with worse patient outcome (positive vs negative DFS 7.4 vs 12.1 months, p=0.041; OS 14.1 vs 25.6 months, p=0.011), again the effect was restricted to patients treated with gemcitabine (positive vs negative DFS 8.3 vs 15.3 months, p=0.002; OS 11.0 vs 28.8 months, p= 0.003; control group DFS 5.8 vs 7.6 months, p=0.844; OS 14.9 vs 20.8 months, p=0.519). Conclusions: Our data confirm the prognostic significance of SPARC expression and demonstrate a significant prognostic factor of SPARC in patients with pancreatic cancer after curatively intended resection. The prognostic impact was restricted to patients who received adjuvant treatment with gemcitabine. In difference to former published data this was found for peritumoral SPARC as well as for SPARC expression in tumor cells.
Not All Middle Cerebral Artery M2 Segments Are the Same
Authors: Brian Silver
Journal: JAMA Neurology (2017)

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 Neurology 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 Neurology journal