tbuckley/cabot-search huggingface dataset:
Scavenger Receptor Type B1 Is Essential for High Density Lipoprotein Nanoparticle Induced B-Cell Lymphoma Cell Death
Authors: Jonathan Scott Rink, Shuo Yang, Osman Cen, Fei Ying, Young Kwang Chae, Denise Scholtens, Jonathan Moreira, Amy Chadburn, Leo I. Gordon, Colby Shad Thaxton
Journal: Blood (2015)
IMST-24. COMBINATION OF VEGF-A AND PD-1 BLOCKADE MAY ENHANCE ANTITUMOR EFFICACY IN GBM
Authors: Yu Long, Changlin Yang, Linchun Jin, Haitao Ge, Hongbo Bao, Catherine Flores, Zhiguo Lin, Duane Mitchell, Jianping Huang
Journal: Neuro-Oncology (2016)
Next Generation XPO1 Inhibitor Shows Improved Efficacy and In Vivo Tolerability in Hematologic Malignancies
Authors: Zachary A. Hing, Ho Yee Joyce Fung, Parvathi Ranganathan, Shaneice Mitchell, Dalia El-Gamal, Jennifer A. Woyach, Katie Williams, Virginia M. Goettl, Jordan L. Smith, Xueyan Yu, Xiaomei Meng, Qingxiang Sun, Tolga Cagatay, John B. MacMillan, Amy M. Lehman, David M. Lucas, Erkan Baloglu, Sharon Shacham, Michael Kauffman, John C. Byrd, Yuh Min Chook, Ramiro Garzon, Rosa Lapalombella
Journal: Blood (2015)
NIMG-41. ENHANCING TUMOR VOLUME AT RECURRENCE AS A PREDICTOR OF GLIOBLASTOMA GROWTH
Authors: Roberto Jose Diaz, Macarena Ines De La Fuente
Journal: Neuro-Oncology (2016)

In glioblastoma, greater resection of enhancing tumor is associated with improved progression free survival. However, the basis of this phenomenon has not been elucidated. Since glioblastoma demonstrates an exponential growth rate in xenograft models, we hypothesized that volumetric growth rate of enhancing recurrent tumor correlates with recurrent tumor volume in humans. We retrospectively identified patients with recurrent glioblastoma treated at the University of Miami Sylvester Comprehensive Cancer Centre from 2014 to 2015. The RANO criteria were used to define recurrence more than 3 months after maximal safe resection followed by RT/TMZ. Serial MRIs done from the time of recurrence until surgery were used for volumetric measurement of enhancing tumor. Results in 14 patients with a median age of 60 (Range 28-85) years show a median tumor volume at recurrence of 4.20 cm3 (Range 0.50-132 cm3). The median time from surgery to recurrence was 229 days (Range 96-356 days). A total of 21 measuring intervals were available for growth rate analysis giving a median growth rate of 0.77 cm3/day (Range 0.02-22.9 cm3/day). The growth rate was not normally distributed (Kolmogorov-Smirnov, P<0.001). The median doubling time was 27 days (Range 5-38 days) and did not correlate with volume of enhancing tumor at recurrence. When tumor growth is plotted against tumor volume at recurrence an increase in growth rate is observed for increasing volume of recurrent tumor. The relationship is best fit with a quadratic function [Growth Rate (cm3/day) = 0.0012 x Volumet=02 + 0.003 x Volumet=0, R2=0.94, N=21]. The presence of residual tumor after first resection was not associated with a difference in growth rate at the time of recurrence (P>0.05). These findings suggest that glioblastoma growth rate at recurrence is correlated with volume of enhancing tumor at recurrence. Expansion of the discovery data set will refine the growth-rate prediction model.
STMC-07. PRMT5-PTEN MOLECULAR PATHWAY REGULATES SENESCENCE AND SELF-RENEWAL OF GLIOBLASTOMA NEUROSPHERES
Authors: Yeshavanth Kumar Banasavadi-Siddegowda, Luke Russell, Emma Frair, Vrajesh Karkhanis, Theresa Relation, Ji Young Yoo, Jianying Zhang, Said Sif, Jaime Imitola, Robert Baiocchi, Balveen Kaur
Journal: Neuro-Oncology (2016)

Glioblastoma (GBM) represents the most common and aggressive histologic subtype among malignant astrocytoma and is associated with poor outcomes because of heterogeneous tumor cell population including mature non-stem like cell and immature stem-like cells within the tumor. Thus, it is critical to find new target-specific therapeutic modalities. Protein arginine methyltransferase enzyme 5 (PRMT5) regulates many cellular processes through its methylation activity and its overexpression in GBM is associated with more aggressive disease. Previously, we have shown that silencing of PRMT5 expression in differentiated GBM cell lines results in apoptosis and reduced tumor growth in mice. Here we report the critical role of PRMT5 in GBM differentiated cells (GBMDC) grown in serum and GBM neurospheres (GBMNS) grown as neurospheres in vitro. Our results uncover a very significant role for PRMT5 in GBMNS self-renewal capacity and proliferation. PRMT5 knockdown in GBMDC led to apoptosis, knockdown in GBMNS led to G1 cell cycle arrest through upregulation of p27 and hypophoshorylation of Rb protein, leading to senescence. Comparison of impact of PRMT5 on cellular signaling by Human Phospho-Kinase Array and ChIP-PCR revealed that unlike GBMDC, PRMT5 controls both AKT and ERK activity by direct repression of PTEN in GBMNS. In vivo transient depletion of PRMT5 decreased intracranial tumor size and growth rate in mice implanted with both primary tumor derived GBMNS and GBMDC. This is the first study to identify PTEN as a potential downstream target of PRMT5 and vital to support both mature and immature GBM tumor cell populations.
Final Results of a Multicenter Phase II Trial Assessing the Activity and Efficacy of Helicobacter Pylori-Eradicating Antibiotic Therapy As Exclusive Treatment for Patients with Stage I-II1 Diffuse Large B-Cell Lymphoma of the Stomach (the HGL-1 Trial)
Authors: Silvia Govi, Caterina Patti, Markus Raderer, Alessandro Andriani, Daniele Caracciolo, Anna Guidetti, Fiorella Ilariucci, Stefano Luminari, Antonino Mulè, Edi Viale, Paolo Giorgio Arcidiacono, Maurilio Ponzoni, Andrés J.M. Ferreri
Journal: Blood (2011)
First Isolated Extramedullary Relapse in Children with B-Cell Acute Lymphoblastic Leukemia: Results of the Coprall-97 Study.
Authors: Carine Domenech, Mariette Mercier, Emmanuel Plouvier, Marc Puraveau, Pierre Bordigoni, Yves Benoit, Guy Leverger, Andre Baruchel, Yves Bertrand
Journal: Blood (2007)
Influence of diabetes and congestive heart failure (CHF) on selection of first-line (1L) treatment for metastatic renal cell carcinoma (mRCC)
Authors: J. Gong, D. George, S. Mhatre, S.-W. Lin, A. Surinach, H. Wallen, R. Vohra, J. Simpson, S. Ogale, S.K. Pal
Journal: Annals of Oncology (2016)
ATIM-30. PHASE 1B OPEN-LABEL RANDOMIZED STUDY OF THE ONCOLYTIC VIRUS DNX-2401 ADMINISTERED WITH OR WITHOUT INTERFERON GAMMA FOR RECURRENT GLIOBLASTOMA
Authors: Frank Tufaro, Joanna Peterkin
Journal: Neuro-Oncology (2016)

DNX-2401 is a conditionally replicative oncolytic adenovirus that causes durable tumor destruction by killing tumor cells and eliciting antitumor immunity for a period of weeks to months. OBJECTIVES. To investigate the safety, overall response rate, overall survival (OS) and quality of life of intratumoral DNX-2401 alone versus DNX-2401 with gamma IFN. A total of 36 evaluable (i.e., remain on-study 4+ weeks) patients with glioblastoma at first or second relapse are planned to receive a single intratumoral injection of 3e10vp DNX-2401. All patients were subsequently randomized at a 2:1 ratio to receive 50 mcg/m2of subcutaneous interferon gamma (gIFN [Actimmune]) x3/week 14 days after DNX-2401 and followed at regular intervals for adverse events, quality of life, tumor response and survival. Twenty-five (25) evaluable patients were treated with 3e10vp DNX-2401 (16 patients DNX-2401/gIFN:9 patients DNX-2401), in addition to a monotherapy subset (8 patients to date) who received 5e10vp of intratumoral DNX-2401 by a proprietary cannula designed to optimize delivery of virus to brain tumors. The most frequent grade 3-4 AEs across treatment groups were fatigue, headache, and seizures, all consistent and expected according to pre-existing symptoms and underlying disease, surgical procedure, and concomitant use of steroids and anticonvulsants. The cannula device has been well tolerated, and imaging evidence demonstrates efficient and targeted intratumoral delivery. Preliminary OS-12 for all patients is 39%. The evaluation of safety, quality of life, efficacy, and brain delivery is ongoing. Early results are promising and support a similar design of a Phase II study of DNX-2401 with asequential pembrolizumab (Keytruda) in recurrent glioblastoma.
MGMT methylated (Met) patients (p) with glioblastoma (GBM) have a better prognosis with an earlier response (ER) than those who have a late response or pseudoprogression (LR/PsP). Results of the Gliocat study
Authors: A. Estival, E. Pineda, M. Martinez-Garcia, J. Marruecos, C. Mesía, A. Lucas, M. Macia, M. Gil, O. Gallego, E. Verger, S. Del Barco, R. Fuentes, J. Craven, N. García, S. Villà, J.M. Velarde, C. Carrato, T. Ribalta, O. Arpi, C. Balana
Journal: Annals of Oncology (2016)
TMIC-24. THE CONTRIBUTION OF VASCULAR CO-OPTION AND TUMOR-DERIVED ENDOTHELIAL CELLS TO GBM RECURRENCE
Authors: Brenda Auffinger, Tanwir Hasan, Gina Lee, Alex Tobias, Marc Deheeger, Yu Han, Donna Guo, Maciej Lesniak, C. David James, Atique Ahmed
Journal: Neuro-Oncology (2016)

Despite aggressive treatment, the prognosis for glioblastoma (GBM) is very poor. The rate of recurrence is nearly 100%, and the recurrent tumor is usually more aggressive and resistant to treatment. The presence of a small population of tumor-initiating cells, the glioma stem cells (GSCs), has been associated with tumor recurrence and resistance to further therapy. To understand the role of GSCs on recurrence, we performed gene expression analysis on human-derived GBM xenografts (PDX) in both primary and recurrent models in vivo. The analysis indicated 3 angiogenesis-associated genes in recurrent GBM samples: CD34, CD105, and SERPINB2. These markers are directly related to neo angiogenesis and migration of GBM cells. The use of an in vivo cranial window model allowed us to identify fluorescently labeled GBM cells in proximity to newly formed blood vessels in the recurrent model. Further analysis indicated that the labeled GBM cells expressed markers of progenitor and mature endothelial cells (ECs), both in vivo and in vitro. The GSC-specific reporter system showed that GSC populations also increase in the EC population after primary chemotherapy. The functionality of these newly formed ECs was demonstrated through tube formation assay and Dio-Ac-LDL uptake. In vivo and in vitro analysis of untreated PDX models did not show such increase in the GSC or EC population over time. Our results strongly suggest increased conversion of GSCs into ECs in the recurrent GBM model following primary chemotherapy, and these newly formed ECs are functional and contribute to tumor neovascularization in recurrent tumor. This knowledge will allow for a better understanding of therapeutic resistance and malignant recurrence after initial therapy.
BCR-ABL Lacking the Pleckstrin Homology (PH) Domain of BCR Induces a More Aggressive Leukemia Than P210BCR-ABL in a Murine Model of CML.
Authors: Shadmehr Demehri, Thomas O’Hare, Lisa J. Wood, Marc Loriaux, Brian J. Druker, Michael W. Deininger
Journal: Blood (2004)
Lurbinectedin (PM01183) plus paclitaxel (P), recommended dose (RD) expansion results with or without the addition of bevacizumab (Bev) in patients (pts) with selected solid tumors
Authors: A. Drilon, E. Garralda, A. Stathis, S. Szyldergemajn, D. Hyman, V. Boni, G. Griguolo, E. Jimenez Martinez, V. Makker, L. Canziani, C. Fernandez Teruel, A. Soto-Matos, C. Sessa, E. Calvo
Journal: Annals of Oncology (2016)
STMC-31. STIMULATION OF MICROGLIA AND MACROPHAGES AND GROWTH ATTENUATION OF BRAIN TUMOR-INITIATING CELLS WITH TUMOR NECROSIS FACTOR-ALPHA
Authors: Candice C. Poon, Susobhan Sarkar, Michael Blough, J. Gregory Cairncross, V. Wee Yong, John Kelly
Journal: Neuro-Oncology (2016)

Microglia and macrophages (M/Ms) are functionally plastic entities that are compelled by glioblastoma (GBM) to adopt anti-inflammatory phenotypes and become major players in GBM progression. Understanding how to reverse this compulsion and maintain a pro-inflammatory tumor microenvironment is critical to developing effective therapeutics for GBM. Our studies have uncovered that GBM-associated M/Ms (GAM/Ms) can be pharmacologically compelled to shed the influence of GBM and secrete inhibitory factors that decrease the proliferation of GBM stem cell (GSC) lines and xenografts (Nature Neurosci 17:46-55, 2014). GSCs are a cellular reservoir that support GBM treatment resistance so it is important to development therapeutics that target this population. Our recent studies show that the most potent M/M-secreted factor behind GSC inhibition is tumor necrosis factor-alpha (TNF). We found that TNF decreases GSC proliferation and self-renewal through cytotoxic effects as well as G1 cell cycle arrest. TNF also induces differentiation in molecularly diverse GSCs. Additionally, we found that TNF can compel freshly-isolated human GAM/Ms to adopt a pro-inflammatory phenotype and inhibit GSCs in co-culture. The TNF receptors, TNFR1/2, are differentially expressed on GSCs and M/Ms. TNFR1, associated with apoptosis, is expressed by GSCs, while TNFR2, associated with survival mechanisms, is expressed on GAM/Ms. Moreover, TNFR1 on GSCs co-labels with OLIG2, one of the most specific markers of stemness in GBM, supporting the notion that TNF can target GSCs. Normal brain expresses low to non-existent levels of TNFR1, lending further support to this notion. Given the lack of studies investigating the effect of TNF on GSCs and the immunomodulatory effects TNF can exert on GAM/Ms, we feel it is a promising strategy to harness the effects of this powerful pro-inflammatory cytokine against GBM.
B Cells Are Primed for Survival by BAFF-Driven Bim Degradation In Chronic Graft Versus Host Disease (cGVHD) Patients
Authors: Jenna Wooten, Bhuiya S. Nazmim, Kristy Richards, Andrew Sharf, Joseph H. Antin, Robert J. Soiffer, Jerome Ritz, Thomas C. Shea, Jonathan Serody, Albert S. Baldwin, Stefanie Sarantopoulos
Journal: Blood (2010)
Effector CD4+CD45RA−CD25brightFoxp3bright Regulatory T Cell (eTreg) Distribution Is Significantly Impaired in Chronic Myelomonocytic Leukemia (CMML) and Correlates with TET 2 Mutational Status.
Authors: Thorsten Braun, Makoto Miyara, Raphael Itzykson, Aline Renneville, Olivier Kosmider, Claude Gardin, Eric Solary, Guy Gorochov, Pierre Fenaux, Lionel Ades
Journal: Blood (2012)
Mismatch repair protein expression and inflammation in human pancreatic cancer
Authors: A. Bittoni, A. Lanese, C. Pellei, A. Mandolesi, R. Giampieri, M.G. Baleani, T. Meletani, L. Cantini, M. Del Prete, M. Scarpelli, R. Berardi, S. Cascinu
Journal: Annals of Oncology (2016)
Switch to Subsequent Line of Treatment in Children and Adolescents with Chronic Myeloid Leukemia (CML) Treated with Imatinib: Experience of the International Registry for Chronic Myeloid Leukemia in Children and Adolescents (I-CML-Ped Study)
Authors: Frédéric Millot, Joelle Guilhot, Meinolf Suttorp, Anne Sophie Meunier, Gunes Adalet Meral, Petr Sedlacek, Eveline de Bont, Chi Kong Li, Krzysztof Kalwak, Birgitte Lausen, Srdjana Culic, Barbara De Moerloose, Andrea Biondi, Andre Baruchel
Journal: Blood (2015)
Psychosocial factors in hypertension.: Psychosocial factors in hypertension
Authors: D. S. Krantz, V. DeQuattro, H. W. Blackburn, E. Eaker, S. Haynes, S. A. James, S. B. Manuck, H. Myers, R. B. Shekelle, S. L. Syme
Journal: Circulation (1987)
Novel Chromosomal Rearrangements and Sequence Mutations in High-Risk Ph-Like Acute Lymphoblastic Leukemia
Authors: Kathryn G. Roberts, Ryan D Morin, Jinghui Zhang, Martin Hirst, Richard C. Harvey, Corynn Kasap, Xiang Chen, Michael Edmonson, I-Ming Chen, Neil Shah, Meenakshi Devidas, Gregory H. Reaman, Malcolm A. Smith, Ching-Hon Pui, James R. Downing, Daniela S Gerhard, Cheryl L Willman, Mignon L Loh, Stephen P Hunger, Marco A. Marra, Charles G Mullighan
Journal: Blood (2011)
Mesenchymal Stem Cells from Bone Marrow of Children with Malignant and Non Malignant Hematological Disorders Are Not Quantitatively and Qualitatively Affected.
Authors: Helen Dimitriou, Emmanouela Linardakis, Georgia Martimianaki, Eftichia Stiakaki, Anthi Fillipidi, Maria Kaparou, Maria Kalmanti
Journal: Blood (2005)
PALL-04. RACE AND GENDER DIFFERENCES IN HOSPICE ENROLLMENT OF MEDICARE BENEFICIARIES WITH PRIMARY BRAIN TUMORS
Authors: Caleb Dulaney, Laura Dover
Journal: Neuro-Oncology (2016)

Primary malignant brain tumors (PMBTs) most commonly occur in older patients resulting in devastating effects on quality of life and functional status and often require significant care at the end of life. Earlier integration of hospice care in various cancers is associated with improved quality of life for patients and caregivers and lower healthcare utilization and costs. The purpose of this study was to evaluate hospice enrollment patterns in a regional database of Medicare beneficiaries with PMBTs. Administrative claims were obtained for deceased Medicare beneficiaries with PMBT (ICD-9 191.X) in the UAB Health System Cancer Community Network (AL, GA, FL, MS, TN) from 2012-2015 and reviewed for enrollment in hospice before death. Logistic regression analysis was performed to determine if race or gender was associated with hospice enrollment. 383 patients with PMBTs died between 2012-2015 (51.4% male, 87% white). 81.5% were enrolled in hospice prior to death (median duration 21 days, inter-quartile range: 8-57.5 days) compared to 76.8% of patients with brain metastases from another primary cancer and 68% of all cancer patients within the same network. Among those enrolled in hospice, 60.6% were enrolled >2 weeks, 32.7% between 2 weeks and 2 days, and 6.7% less than 2 days prior to death. In adjusted analysis, race was an independent predictor of hospice enrollment with non-whites substantially less likely to enroll prior to death (OR=0.43; 95%CI: 0.22-0.85). Gender was an independent predictor of timing of hospice enrollment with women less likely to enroll late (<2 days prior to death) (OR=0.37; 95%CI: 0.14-0.98). The majority of Medicare beneficiaries with PMBTs are enrolled in hospice care for a meaningful duration prior to death and more frequently than those with brain metastases or other cancers. However, significant racial and gender differences in enrollment patterns exist.
Bisphosphonate‐Functionalized Imaging Agents, Anti‐Tumor Agents and Nanocarriers for Treatment of Bone Cancer
Authors: Robin A. Nadar, Nicola Margiotta, Michele Iafisco, Jeroen J. J. P. van den Beucken, Otto C. Boerman, Sander C. G. Leeuwenburgh
Journal: Advanced Healthcare Materials (2017)

Bone metastases result from the invasion of primary tumors to bone. Current treatment modalities include local treatments such as surgery and radiotherapy, while systemic treatments include chemotherapy and (palliative) treatment of skeletal metastases. Nevertheless, once bone metastases have been established they remain incurable leading to morbidity and mortality. Bisphosphonates are a well‐established class of drugs, which are increasingly applied in the treatment of bone cancers owing to their effective inhibition of tumor cells and suppression of bone metastases. The increased understanding of the mechanism of action of bisphosphonates on bone and tumor cells has prompted the development of novel bisphosphonate‐functionalized imaging and therapeutic agents. This review provides an update on the preclinical efficacy of bisphosphonate‐functionalized fluorophore, anti‐tumor agents and nanocarriers for the treatment of bone metastases. After an overview of the general characteristics of bisphosphonates and their mechanisms of action, an outline is provided on the various conjugation strategies that have become available to functionalize imaging agents, anti‐tumor agents and nanocarriers with bisphosphonates. Finally, the efficacy of these bisphosphonate‐modified agents and carriers in preclinical studies is evaluated by reviewing their potential to target tumors and inhibit tumor growth in clinically relevant animal models for the treatment of bone cancer.
Abnormal Electrocardiogram in a Woman With Atrial Fibrillation and Recent Care Transition
Authors: Katie E. Raffel, Nora Goldschlager
Journal: JAMA Internal Medicine (2017)

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Surface Adhesion and Growth of Microaggregates under Flow Condition (II): Clinical Findings in Patients with Thrombosis and Thrombocytopenia.
Authors: Loreta Bidot, Wenche Jy, Lawrence L. Horstman, Carlos Jr. Bidot, Vincenzo Fontana, Joaquin J. Jimenez, Carlos J. Bidot, Yeon-Soong Ahn
Journal: Blood (2007)
GENT-15. INTEGRATED MOLECULAR PROFILING OF HUMAN BRAIN TUMORS THROUGH MULTIOMIC ANALYSIS OF SERIAL SECTIONS (MASS)
Authors: Samuel J. Shelton, Brett E. Johnson, Tali Mazor, Matthew B. Potts, Michael F. McDermott, Eric J. Huang, Dan Lim, Russel O. Pieper, Mitchel S. Berger, Joanna J. Phillips, Joseph F. Costello, Michael C. Oldham
Journal: Neuro-Oncology (2016)

Brain tumors can be classified by highly recurrent somatic alterations that have predictable molecular consequences and promote malignancy. By correlating mutant allele frequencies with molecular features such as DNA methylation and gene expression over many tumor specimens, it should be possible to identify and prioritize molecular features of malignant cells that are sensitive, specific, and druggable. However, this task is complicated by the variability that characterizes tumors from different individuals, which arise from unique genetic backgrounds, exist in variable environments, exhibit clonal heterogeneity, and may originate in different cell types. These factors, along with technical variation introduced during the collection and processing of tumor specimens from different individuals, obscure the molecular consequences of oncogenic mutations. We describe a novel strategy that controls for these factors by generating an arbitrary number of standardized biological replicates from a single tumor through serial sectioning for personalized multiomic analysis. We apply this strategy to low-grade glioma by analyzing mutant allele frequencies, copy number variation, DNA methylation, and gene expression in serial sections of individual tumor specimens. We identify genetic, epigenetic, and transcriptional signatures of clonal malignant populations and chart their distributions. More specifically, we observe DNA methylation and gene expression signatures that are almost perfectly associated with the distribution of IDH1MUT / TP53MUT cells within astrocytoma, including MGMT, whose methylation status correlates inversely with expression. Comparison of molecular signatures associated with IDH1 mutant allele frequencies using MASS or TCGA data reveals significant overlap, but with far stronger associations in serial sections vs. single biopsy specimens. In summary, MASS offers an unbiased, personalized, and generalizable approach for determining the molecular consequences of driver mutations in solid tumors while abrogating the need for large cohorts of samples sharing common genomic aberrations.