tbuckley/cabot-search huggingface dataset:
Melphalan, Thalidomide and Prednisone (MPT) Combined with Oral Panobinostat In Patients with Relapsed/Refractory MM: a Phase I-II Study
Authors: Massimo Offidani, Federica Cavallo, Claudia Polloni, Anna Marina Liberati, Stelvio Ballanti, Stefano Pulini, Massimo Catarini, Francesco Alesiani, Laura Corvatta, Silvia Gentili, Mario Boccadoro, Pietro Leoni, Antonio Palumbo
Journal: Blood (2010)
Expression of PIM kinases in Reed-Sternberg cells fosters immune privilege and tumor cell survival in Hodgkin lymphoma
Authors: Maciej Szydłowski, Monika Prochorec-Sobieszek, Anna Szumera-Ciećkiewicz, Edyta Derezińska, Grażyna Hoser, Danuta Wasilewska, Olga Szymańska-Giemza, Ewa Jabłońska, Emilia Białopiotrowicz, Tomasz Sewastianik, Anna Polak, Wojciech Czardybon, Michał Gałęzowski, Renata Windak, Jan Maciej Zaucha, Krzysztof Warzocha, Krzysztof Brzózka, Przemysław Juszczyński
Journal: Blood (2017)
The Impact of Bone Marrow Hematogones on Umbilical Cord Blood Transplant Outcomes in Acute Myeloid Leukemia Patients,
Authors: Theodore Honebrink, Vanessa J. Dayton, Karen Larsen, Qing Cao, Claudio Brunstein, Daniel J. Weisdorf, Jeffrey S. Miller, John E. Wagner, Michael R Verneris
Journal: Blood (2011)
Growth hormone deficiency and cardiovascular risk factors in childhood cancer survivors
Authors: K. Gujral, A. Petryk, L. Steffen, K. Baker, J. Perkins, A. S. Kelly, X. Zhou, A. Sinaiko, A. Moran, J. Steinberger
Journal: Journal of Clinical Oncology (2009)

6614 Background: Childhood cancer survivors (CCS) have a high frequency of growth hormone deficiency (GHD) and risk of early cardiovascular disease (CVD). This study examined the relations between GHD and risk factors for CVD in CCS. Methods: Anthropometrics, blood pressure, lipids, growth hormone (GH) stimulation test, dual-energy x-ray absorptiometry, abdominal CT, and insulin resistance (IR) (euglycemic, hyperinsulinemic clamp - low M/lbm signifies IR) were obtained in 174 CCS, mean age 15±2 years and 89 healthy sibling controls, mean age 13.5±3 years. Linear regression evaluated the relations between GHD and CVD risk factors, adjusted for sex, age, pubertal stage, and body mass index (BMI) or visceral fat. Results: 62 CCS (36%) had GHD. There were no significant measurement differences between non-GHD CCS and controls. Compared to controls, GHD CCS who never received GH (N = 34) had greater BMI (24.8 vs 20.8 kg/m2, p &lt; 0.0001), percent body fat (36.1% vs 25.8%, p &lt; 0.0001), visceral fat (34.8 vs 19.6 cm2, p &lt; 0.0001), and triglycerides (TG) (120.2 vs 83.8 mg/dL, p = 0.001) and were more IR (M/lbm 11.1 vs 14.2 mg/kg/min, p = 0.0006). Adjustment for BMI and visceral fat did not change the IR or TG results. GHD CCS currently on GH had lower BMI (21.9 kg/m2, p = 0.02), percent body fat (31.2%, p = 0.08), and visceral fat (26.5 cm2, p = 0.03) compared to those not treated. IR and TG were not different between treated and not treated GHD CCS. Conclusions: GHD is a common finding in CCS and is significantly associated with adiposity, IR, and elevated TG.There is a suggestion that GH treatment had a positive impact on adiposity, but not IR and TG levels. These study findings imply that CVD risk factors are present in CCS with GHD independent of body fatness, suggesting that the cancer diagnosis or treatments received may lead to early cardiovascular disease in childhood cancer survivors. No significant financial relationships to disclose.
Results of a Multi-Center Randomized Phase II Trial of Thalidomide and Prednisone Maintenance Therapy for Multiple Myeloma Following Autologous Stem Cell Transplant.
Authors: A. Keith Stewart, Christine Chen, Kang Howson-Jan, Darrell White, Jean Roy, Michael J. Kovacs, Chaim Shustik, Anna Sadura, Shepherd Lois, Keyue Ding, Ralph Melbourne Meyer, Andrew Belch
Journal: Blood (2004)
Palmitic acid mediates hypothalamic insulin resistance by altering PKC-θ subcellular localization in rodents
Authors: Stephen C. Benoit, Christopher J. Kemp, Carol F. Elias, William Abplanalp, James P. Herman, Stephanie Migrenne, Anne-Laure Lefevre, Céline Cruciani-Guglielmacci, Christophe Magnan, Fang Yu, Kevin Niswender, Boman G. Irani, William L. Holland, Deborah J. Clegg
Journal: Journal of Clinical Investigation (2010)
Hematopoietic Cell Kinase (HCK) Is Involved in Myelodysplastic Syndromes and Acute Leukemia Pathophysiology By Modulating PI3K Pathway and Enhancing Erythroid Differentiation
Authors: Fernanda Marconi Roversi, Fernando V Pericole, João Agostinho Machado-Neto, Ana Leda Longhini, Adriana Silva Santos Duarte, Bruna Palodetto, Flavia Adolfo Corrocher, Fabiola Traina, Sara T Olalla Saad
Journal: Blood (2014)
A Multi-Center, Open-Label Study To Evaluate the Safety and Efficacy of Pentostatin, Cytoxan, and Rituxan (PCR) in the Treatment of Previously Untreated or Treated, Stage III or IV, Low-Grade CLL.
Authors: Raul R. Mena, Robert Robles, David W. Nyman, Michael Auerbach, Lalita Pandit
Journal: Blood (2005)
Abstract 3086: From profiling to function: A role for microRNA miR-888 in promoting prostate cancer progression
Authors: Holly Lewis, Tsuyoshi Hasegawa, Garrison Glavich, Raymond Lance, O. John Semmes, Hind Beydoun, Richard Drake, Aurora Esquela-Kerscher
Journal: Cancer Research (2015)

Abstract Prostate cancer remains the second leading cause of cancer-related deaths among men in the United States despite the widespread use of prostate specific antigen (PSA) as a diagnostic marker for prostate cancer and as a predictor of treatment outcome. MicroRNAs (MiRNAs) belong to a growing class of small non-coding RNAs that are often abnormally expressed in fluid and tissue specimens from prostate cancer patients compared to non-cancer individuals. These miRNAs are hypothesized to play a direct role in promoting disease progression and metastasis in the prostate and are intensely studied for both their diagnostic and therapeutic potential for human cancer. Our laboratory profiled candidate prostate-cancer associated miRNAs in an innovative prostatic fluid biomarker source called expressed prostatic secretions in urine (EPS urine) to determine their utility as discriminating biomarkers for advanced forms of prostate cancer. 10 out of 50 miRNA tested showed statistically significant differences in expression between cancer and non-cancer patient groups within the supernatant but not pellet fractions of whole EPS urine. We are investigating if differential miRNA expression in EPS supernatant is due to exosomal populations and how miRNA-loaded exosomes modulate prostate tumorigenesis in mice. Our profiling studies identified miR-888 as a novel factor that correlates with advanced prostate cancer in human prostate cancer cell lines, EPS urine, and primary tumors. Functional assays revealed that miR-888 promotes proliferation, migration, and colony formation of hormone-refractory and androgen-sensitive human prostate cancer cells. Our working model is that miR-888 overexpression in the diseased prostate suppresses SMAD4, RBL1, and TIMP2 targets leading to tumor progression and metastasis. Human miR-888 belongs to a genomic cluster of seven miRNAs on human chromosome Xq27.3. We are currently testing how this miR-888 cluster interacts within a growing network of coding and non-coding genes to regulate prostate tumor progression. This research will provide a better understanding how prostate tumor cells progress to a more metastatic, aggressive state and facilitate the development of more effective diagnostic and therapeutic strategies for this prevalent and deadly disease. Citation Format: Holly Lewis, Tsuyoshi Hasegawa, Garrison Glavich, Raymond Lance, O. John Semmes, Hind Beydoun, Richard Drake, Aurora Esquela-Kerscher. From profiling to function: A role for microRNA miR-888 in promoting prostate cancer progression. [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 3086. doi:10.1158/1538-7445.AM2015-3086
Bullae and Atypical Target Lesions in a Young Woman
Authors: Natasha K. Klimas, Arturo R. Dominguez, Travis W. Vandergriff
Journal: JAMA Dermatology (2016)

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304. Deriving Useful Data from Next-Gen Sequencing of AAV Capsid Libraries
Authors: Damien Marsic, Sergei Zolotukhin
Journal: Molecular Therapy (2015)

The relatively short read lengths produced by the major Next-Gen sequencing platforms (up to 300 nt for Illumina, up to 200 nt for Ion Proton) are poorly suited for analyzing large combinatorial libraries of longer nucleotide sequences, such as those involving AAV capsid genes. Despite its much lower throughput and accuracy, the PacBio single-molecule real-time technology is currently the only option for long templates, with average read lengths of 10 to 15 kb. Using the Circular Consensus Sequencing (CCS) mode, in which template DNA fragments are circularized, allows a significant increase in accuracy due to the fact that each template is being sequenced multiple times. To interpret PacBio CCS data, we have previously reported a first version of the CapLib code, which was developed to identify variable regions in AAV combinatorial capsid libraries. DNA fragments, derived from purified DNA-containing AAV particles, 869 bp in length and including 27 variable nucleotide positions, were sequenced in CCS mode using the P6-C4 chemistry. A total of 26,897 reads were obtained, with a mean read length of 814 nt, a mean read quality of 0.9956 and a mean number of passes of 21.34. Only 5,456 reads had the correct size of 869 nt, and of these, only 1,638 had a sequence that matched the reference sequence, indicating that only 6% of reads were potentially error-free and that the vast majority had multiple insertions and deletions. In order to extract more useful information from the sequencing data, a new version of the CapLib software was developed. It is designed to correct sequencing reads in silico by assuming that constant nucleotide positions are wild-type and focusing on the detection of the variable positions. The premise was validated by Sanger sequencing of multiple clones, confirming that mutations were present only in the intended positions. Depending on the parameter values used, up to 14,000 reads could be recovered by CapLib 2. In addition to recovering PacBio CCS reads, CapLib 2 can also assemble Sanger sequencing data, translate recovered reads into protein sequences and perform detailed analyses of the dataset. It can also analyze clones resulting from directed evolution experiments and compare them with the original library.
Abstract 3606: Increase of MET gene copy number confers resistance to a monovalent MET antibody and establishes drug dependence
Authors: Valentina Martin, Simona Corso, Paolo Maria Comoglio, Silvia Giordano
Journal: Cancer Research (2015)

Abstract The tyrosine kinase receptor encoded by the MET oncogene is one of the most frequently altered oncogenes in human cancer. The relevant role played by the MET oncogene in cancer progression led to the development of specific inhibitors targeting MET, some of which are now in advanced phases of clinical trials. Previous experience has shown that the main limit to the efficacy of most targeted treatments is the advent of resistance. Mechanisms underlying resistance to MET-specific small tyrosine kinase inhibitors (TKIs) have been already described, while nothing is known about resistance to MET monoclonal antibodies, nor about bypassing resistance to chemical TKIs by antibodies or vice-versa. A monovalent form of an anti-MET monoclonal antibody (MV-DN30) was previously generated to target MET by promoting receptor “shedding”, inactivation and by inhibiting the MET-mediated invasive growth program both in vitro and in vivo cancer models. In our study EBC1 lung cancer cells that are MET-addicted as a consequence of gene amplification and thus sensitive to MET inhibitors, including the MV-DN30 were used as cell model. Upon prolonged treatment of these cells with the MV-DN30 we generated EBC1 cells resistant to this antibody and found that resistance was due to a further increase of MET gene copy number and a dramatic over-expression of the MET receptor. Such an excess of expression saturated the ‘shedding’ activity of MV-DN30, and prevented both the efficient down-regulation of the MET receptor from the surface and the inhibition of the ensuing constitutive activation. Notably, antibody-resistant cells became ‘drug-dependent’, since the removal of MV-DN30 led them to death due to an excess of MET signal and a concomitant p38MAPK activation. Moreover, antibody-resistant cells remained MET-’addicted’ and were still sensitive to MET TKIs. Finally, cells made resistant to MET specific TKIs were still sensitive to treatment with the antibody MV-DN30. These findings suggest that a discontinuous or combined treatment by antibodies and chemical kinase inhibitors may increase the clinical response and bypass resistance to anti-MET targeted therapies. Citation Format: Valentina Martin, Simona Corso, Paolo Maria Comoglio, Silvia Giordano. Increase of MET gene copy number confers resistance to a monovalent MET antibody and establishes drug dependence. [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 3606. doi:10.1158/1538-7445.AM2015-3606
CD49d Expression Identifies a Chronic Lymphocytic Leukemia (CLL) Subset with High Levels of Circulating CD34 +Cells Co-Expressing Endothelial Cell Markers.
Authors: Francesca Maria Rossi, Davide Rossi, Antonella Zucchetto, Riccardo Bomben, Michele Dal Bo, Dania Benedetti, Claudio Tripodo, Gabriele Pozzato, Gianluca Gaidano, Giovanni Del Poeta, Valter Gattei
Journal: Blood (2009)
Abstract 4180: TGF-beta promotes angiogenesis in an RB-deficient, Kras-driven mouse model of pancreatic cancer
Authors: Jesse Gore, Kelly E. Craven, Julie L. Wilson, Murray Korc
Journal: Cancer Research (2015)

Abstract Pancreatic ductal adenocarcinoma (PDAC) is a deadly disease that is projected to become the 2nd leading cause of cancer deaths by 2030. PDACs are associated with a high frequency of KRAS mutations (95%) and overexpression of many pro-angiogenic cytokines and growth factors. Using a genetically engineered mouse model (GEMM) that we established in which oncogenic Kras is combined with loss of RB (KRC), we have determined that PDACs arising in these mice (mPDACs) harbor many endothelial cells (ECs) and sinusoidal-like vessels that have blood flow, as determined by intravital confocal microscopy. Array analysis of pancreatic cancer cells (PCCs) derived from KRC tumors revealed gene expression profiles that correlate with active TGF-β signaling pathways, as determined by gene set enrichment analysis (GSEA), and include increased expression of multiple pro-angiogenic genes. In silico analysis indicated that many of these pro-angiogenic genes were TGF-β targets, and inhibition of the type I TGF-β receptor (TβRI) with SB505124 confirmed that TGF-βs drive pro-angiogenic gene expression in KRC PCCs. Moreover, TGF-β increased the levels of pro-angiogenic cytokines in conditioned media (CM) prepared from KRC PCCs, which when added to ECs, activated canonical TGF-β signaling pathways and stimulated EC proliferation and migration. Although SB505124 blocked TGF-β pathway activation in ECs, it failed to suppress CM-enhanced EC proliferation and migration. By contrast, SB505124 attenuated tumor angiogenesis, growth and metastasis in a syngeneic orthotopic mouse model using KRC PCCs. Taken together, these results suggest that TGF-β promotes angiogenesis in an indirect manner, by up-regulating pro-angiogenic factors in PCCs that act on ECs in a paracrine manner. Therefore, targeting TGF-β in PDAC could be a beneficial anti-angiogenic strategy. Citation Format: Jesse Gore, Kelly E. Craven, Julie L. Wilson, Murray Korc. TGF-beta promotes angiogenesis in an RB-deficient, Kras-driven mouse model of pancreatic cancer. [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 4180. doi:10.1158/1538-7445.AM2015-4180
FDG-PET/CT as a predictor of pathological complete response (pCR) in breast cancer (BC) patients (pts) treated with neoadjuvant chemotherapy (NAC): a single center retrospective study
Authors: A. Inno, G. Lunardi, M. Turazza, S. Pasetto, F. Severi, G. Gorgoni, G. Bogina, L. Bortesi, A. Russo, F. Alongi, A. Fiorentino, S. Duranti, A. Massocco, F. Marchetti, M. Valerio, M. Salgarello, S. Gori
Journal: Annals of Oncology (2015)
Abstract 61: Dendritic Cell Regulates Monocyte/Macrophage Polarization and Inflammatory Response After Myocardial Infarction in Mice
Authors: Atsushi Anzai, Toshihisa Anzai, Keiichi Fukuda
Journal: Circulation Research (2012)

Inflammation and immune responses are integral components in the healing process after MI. We previously reported dendritic cell (DC) infiltration in the infarcted heart. However, the precise contribution of DC in postinfarction healing is unclear. Bone-marrow (BM) cells from CD11c-diphtheria toxin receptor/GFP transgenic mice were transplanted into lethally irradiated WT recipient mice. After reconstitution of BM-derived cells, the recipient mice were treated with either diphtheria toxin (DC ablation) or vehicle (control), and MI was created by left coronary ligation. CD11c + GFP + DCs expressing CD11b and MHC class II were recruited into the heart, peaking on day 7 after MI in control group. Mice with DC ablation for 7 days showed deteriorated left ventricular function and remodeling. DC-ablated group demonstrated enhanced and sustained expression of inflammatory cytokines such as IL-1β, IL-18 and tumor necrosis factor-α, prolonged extracellular matrix degradation associated with a high level of MMP9 activity, and diminished expression level of IL-10 and endothelial cell proliferation following MI compared with control group. In vivo and in vitro analyses revealed that DC-ablated infarcts had an enhanced capacity of monocytes/macrophages recruitment. Among these cells, augmented infiltration of proinflammatory Ly6C high monocytes and F4/80 + CD206 - M1 macrophages, and conversely impaired recruitment of anti-inflammatory Ly6C low monocytes and F4/80 + CD206 + M2 macrophages in the infarcted myocardium were identified in DC-ablated group than in control group. To confirm these results, adoptive transfer experiment was performed. BM cells from WT mice were cultured with recombinant mouse GM-CSF for 6 days and CD11c + BMDCs were then positively collected by magnetic sorting. We confirmed that intravenously injected CFSE-labeled BMDCs reached infarcted zone. Adoptive transfer of BMDCs into DC-depleted mice restored LV function and negated the increases of inflammatory Ly6C high monocytes and myocardial MMP-9 activity following MI. In conclusion, dendritic cell is a potent immunoprotective regulator during the postinfarction healing process, via controlling monocyte/macrophage homeostasis.
Allogeneic Stem Cell Transplantation with Peripheral Blood Stem Cells Mobilized by Pegylated-G-CSF.
Authors: Geoff Hill, Edward S. Morris, Maddona Fuery, Cheryl Hutchins, Jason Butler, Andrew Grigg, Andrew Roberts, Ken Bradstock, Jeffrey Szer, Glen Kennedy, James Morton, Simon Durrant
Journal: Blood (2005)
556. Analytical Ultracentrifugation as an Approach to Characterize Recombinant AAV Vectors
Authors: Brenda Burnham, Shelley Nass, Elton Kong, MaryEllen Mattingly, Denise Woodcock, Tony Song, Seng Cheng, Abraham Scaria, Catherine O'Riordan
Journal: Molecular Therapy (2015)

Appropriately engineered recombinant adeno-associated viral (rAAV) vectors represent a novel class of biopharmaceutical drugs. The production of clinical-grade rAAV vectors for gene therapy would benefit from analytical methods that are able to monitor drug product quality with regard to homogeneity, purity and manufacturing consistency. Here, we demonstrate the novel application of analytical ultracentrifugation (AUC) to characterize the homogeneity of preparations of rAAV vectors. We show that a single sedimentation velocity run of rAAV vectors detected and quantified a number of different viral species, such as vectors harboring an intact genome, lacking a vector genome (empty particles) and containing fragmented or incomplete vector genomes. This information is obtained by direct boundary modeling of the AUC data generated from refractometric or UV detection systems using the computer program SEDFIT. Using AUC, we show that multiple parameters contributed to vector quality, including the AAV genome form (i.e., self-complementary vs single-stranded), vector genome size, and the production and purification methods. Hence, AUC is a critical tool for identifying optimal production and purification processes and for monitoring the physical attributes of rAAV vectors to ensure their quality.
Azacitidine Is Effective in Patients with Myelodysplastic Syndrome Managed in Community-Based Practice: Preliminary Data From the Spanish Azacitidine Compassionate Use Registry.
Authors: Regina Garcia, Dunia de Miguel, Alicia Bailen, Jose Ramon Gonzalez, Rafael Andreu, Mar Tormo, Jose F Falantes, Guillermo Sanz, Rafael F Duarte, Antonio Figueredo
Journal: Blood (2009)