tbuckley/cabot-search huggingface dataset:
The Relationship between the Immunophenotypic Profile and Cytogenetic Abnormalities in Acute Myeloid Leukemia.
Authors: Monia Lunghi, Laura Vanelli, Paolo Bernasconi, Marina Boni, Monica Portolan, Cristiana Pascutto, Alessandra Algarotti, Vassiliky Griva, Carlo Castagnola, Mario Lazzarino
Journal: Blood (2005)
Abstract LB-095: Distribution and clearance of single-walled carbon nanotubes in mouse tissues: in situ detection, imaging and analysis
Authors: Afsar Barlas, Ke Xu, Yevgeniy Romin, Simone Alidori, Dmitry Yarilin, Ning Fan, Mesruh Turkekul, Sho Fujisawa, David A. Scheinberg, Michael R. McDevitt, Katia Manova-Todorova
Journal: Cancer Research (2015)

Abstract Single-walled carbon nanotubes (SWCNT) are the subject of expanding research in the fields of targeted drug delivery and biosensors for disease treatment and monitoring. Functionalization of the SWCNT has proven to enhance the efficiency of distribution in the organism. The goal of this project was to establish and standardize methods of detection and characterization of the local tissue distribution of functionalized SWCNT in mouse models. We investigated the distribution and clearance of SWCNT in several tissues at various times after injection, up to one month. We also try to standardize methods of tracking SWCNT in both live and fixed tissues and image analysis protocols to quantify the distribution of the SWCNT in tissues. Another aim is to evaluate local immune response to SWCNT. We have analyzed liver, kidney, spleen, lung, brain, ovary, colon and small intestine from mice sacrificed 24 hours, 3 days, 7 days and 30 days following the injection of SWCNT. Our evaluation revealed that some organs, like kidney and small intestine, retain SWCNTs for at least a month. Slow rates of SWCNT removal from these organs do not appear to affect the overall health of the animals. We have made multiple attempts to image anesthetized live animals and detect SWCNTs in situ, however, the fluorescent signal emitted from SWCNT is too low to be reliably detected. The tissues must be fixed and signals amplified through immunodetection. Detection of immune markers, especially in immunologically active tissues such as spleen is a challenge for histological experiments, but is extremely important and such experiments is underway. Our findings of SWCNT persistence in certain organs 30 days post-injection is surprising and should be studied further. This observation opens further questions about the effect of long-term presence of SWCNT in some tissues and shows that careful investigation into the advantages and disadvantages of SWCNT retention is necessary. Citation Format: Afsar Barlas, Ke Xu, Yevgeniy Romin, Simone Alidori, Dmitry Yarilin, Ning Fan, Mesruh Turkekul, Sho Fujisawa, David A. Scheinberg, Michael R. McDevitt, Katia Manova-Todorova. Distribution and clearance of single-walled carbon nanotubes in mouse tissues: in situ detection, imaging and analysis. [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 LB-095. doi:10.1158/1538-7445.AM2015-LB-095
Improved Engraftment of Human Hematopoietic Stem Cells in NOD/SCID Mice by the Antioxidant, N-Acetyl-L-Cysteine
Authors: Linping Hu, Yingdai Gao, Yanfeng Liu, Hui Cheng, Jing Xu, Ming Yang, Weiping Yuan, Tao Cheng
Journal: Blood (2012)
BMS-936564/MDX-1338: A Fully Human Anti-CXCR4 Antibody Induces Apoptosis In Vitro and Shows Anti Tumor Activity In Vivo
Authors: Michelle R. Kuhne, Tanya Mulvey, Sharline Chen, Chin Pan, Colin Chong, Wafa Niekro, Tom Kempe, Karla A. Henning, Lewis Cohen, Alan Korman, Pina M Cardarelli
Journal: Blood (2011)
Disease and Comorbidity Status Predict Outcome after Nonmyeloablative Allografting for Advanced Haematological Malignancies.
Authors: R. Sorasio, L. Giaccone, A.M. Carella, S. Guidi, B. Allione, E. Benedetti, F. Carnevale-Schianca, F.A. Peccatori, R. Raimomdi, F. Sorà, N. Mordini, J. Peccatori, F. Patriarca, F. Fiore, I. Baldi, I. Resta, M. Festuccia, A. Gallamini, S. Sica, M. Aglietta, A. Lewis, R. Fanin, A. Bosi, Mario Boccadoro, B. Bruno
Journal: Blood (2007)
The Impact of Obesity on the Presentation &amp; Outcome of Adult Acute Myeloid Leukemia (AML) - ECOG Studies E1900 &amp; E3999
Authors: James M. Foran, Zhuoxin Sun, Hugo F. Fernandez, Larry D Cripe, Rhett P Ketterling, Janis Racevskis, Selina M. Luger, Elisabeth Paietta, Hillard M. Lazarus, Mark R. Litzow, Martin S. Tallman
Journal: Blood (2011)
PO56EXPRESSION OF CD15 AND CD15S IS CORRELATED WITH GLIOMA CELL ARREST AT G1-PHASE
Authors: Samah A. Jassam, Zaynah Maherally, Paraskevi Chairta, Keyoumars Ashkan, Helen L. Fillmore, Geoffrey J. Pilkington
Journal: Neuro-Oncology (2015)

INTRODUCTION: CD15 and CD15s are cell surface epitopes, known for their ability to bind specific ligands. They are over-expressed on many non-central nervous system (CNS) cancers. Few reports show CD15 expression in CNS neoplasms and in fact, early studies reported the absence of CD15 expression. Recent published reports, however, have identified CD15 as a potential marker for cancer stem-like cells in glioblastomas (GBM). To obtain a better understanding, CD15 and CD15s expression were re-examined in glioma cell lines. METHOD: Extracellular expression of CD15 and CD15s were determined by Immunocytochemistry, Western blotting and flow cytometry in GBM cells (UP-007 and SNB-19). Non-neoplastic astrocytes (SC-1800) served as controls. Cells were synchronised at G1, S or G2/M phases via serum starvation, Hydroxyurea and Colcemid, respectively followed by validation using the fluorescence ubiqutination cell cycle indicator (FUCCI) system. RESULTS: In non-synchronised cultures, only 5-12% of GBM cells expressed CD15 and CD15s where respective cell cycle distributions averaged 55-59% for G1, 6-13% for S and 15-25% for G2/M. When GBM cells were synchronised in G1, a higher percentage of cells expressed CD15 (18-20%) and CD15s (35-50%) compared to SC-1800 cells CD15 (1.5%), CD15s (1.0%). Of GBM cells synchronised in S phase (G1, 25-34%; S, 56-64%; G2/M, 1-5%), 7-10% of GBM cells were CD15 positive. Of GBM cells synchronised to G1/M phase (G1, 20%; S, 6-18%; G2/M, 71-76%) 4.5-14% of cells were CD15 positive. CONCLUSION: CD15 and CD15s expression is cell cycle dependent in glioma cells and may account for the discrepancy of previous experimental data.
IKZF1 expression is a prognostic marker in newly diagnosed standard-risk multiple myeloma treated with lenalidomide and intensive chemotherapy: a study of the German Myeloma Study Group (DSMM)
Authors: J Krönke, F Kuchenbauer, M Kull, V Teleanu, L Bullinger, D Bunjes, A Greiner, S Kolmus, S Köpff, M Schreder, L-O Mügge, C Straka, M Engelhardt, H Döhner, H Einsele, F Bassermann, R Bargou, S Knop, C Langer
Journal: Leukemia (2016)
P256 Respiratory muscle strength measurements in primary school children
Authors: NTS Gharbawi, EA Gaillard, M Viskaduraki, CS Beardsmore
Journal: Thorax (2016)

<h3>Background</h3> Previous tests of respiratory muscle strength have rarely included measurements of inspiratory pressure. As part of a study looking at ethnic differences in respiratory muscle strength, we have measured maximum inspiratory and expiratory pressures in primary school children. <h3>Aim</h3> We sought to determine the success rate and within-test repeatability of respiratory muscle strength measurements. <h3>Methods</h3> We measured spirometry, height and weight and respiratory muscle strength by measuring maximal inspiratory and expiratory pressure (MIP and MEP) using Carefusion Vyntus in children aged 5–11 yr. Children breathed through a mouthpiece and pneumotachograph attached to a shutter, while wearing a noseclip. After a period of tidal breathing the child breathed in to total lung capacity and then tried to exhale forcibly against the shutter. We measured maximal (peak) expiratory pressure (MEP). For measurements of MIP, the child exhaled towards residual volume before making an inspiratory effort against the occlusion. Manoeuvres were excluded if the peak pressures were less than 3.50 kPa. We reported the largest pressures recorded, provided that the second-best was no more than 20% below the best. We calculated the percent difference between best and 2nd best manoeuvres and compared mean percentage differences in MIP and MEP. <h3>Results</h3> Two hundred and thirty-one children were studied. We obtained MEP on 199 and MIP on 216, and paired data for MIP and MEP on 165 (87 boys and 78 girls). Overall, MIP was higher than MEP (mean (SD) MIP = 7.26 (1.92) kPa, MEP = 6.64 (1.76) kPa, p = 0.002). However, MEP tended to be bigger than MIP when the values were smaller (in the younger, smaller children) (Figure). There was no significant difference between%difference MIP and%difference MEP (mean (SD) 5.50 ± 4.29 and 4.68 ± 3.96 kPa respectively, p = 0.07). <h3>Conclusion</h3> The success rates of MIP and MEP measurements were 94% and 86% respectively, suggesting that MIP was easier for the children to perform. The success rate for paired measurements was 71%. The repeatability of inspiratory and expiratory pressures was not different. We speculate that the change with age between which measurement was greatest (MIP or MEP) may reflect dysanaptic muscle development.
Abstract 2206: qPCR array of 84 cell cycle genes in oral squamous cell carcinoma reveals differently expressed genes in larger size tumors in relation to small tumors
Authors: Carolina C. Gomes, Marina G. Diniz, Fabricio T. de Souza, Jeane F. Correia-Silva, Ricardo S. Gomez
Journal: Cancer Research (2015)

Abstract The aim of the study is to investigate if larger oral squamous cell carcinoma (OSCC) tumors show a different transcriptional signature of cell cycle genes in relation to small OSCC tumor samples. To address this issue, 17 fresh OSCC tumor samples were included in the study, including T1(n = 5),T2 (n = 9),T3 (n = 2) and T4 (n = 1) samples. All tumors were either from the tongue or from the floor of the mouth and only two patients were non-smokers. Two samples were from female patients, while the other 15 were from men. Samples were categorized according to clinical tumor size in tumors ≤ 2cm (T1 n = 5) or tumors &amp;gt; 2cm (T2, T3 and T4, n = 12). The median age of both groups was similar (57 and 62, respectively). The group of tumors ≤ 2cm was considered the reference group in the qRT-PCR results interpretation, while the larger tumors were considered the test group. The RNA was extracted and the cDNA was synthesized. A commercially available 84 cell cycle genes PCR array kit was used (PAHS-020, Cell Cycle PCR Array - Human, Qiagen). The results were analyzed according to the formula 2^-deltaCT and differential expressions were considered statistically significant when p&amp;lt;0.05. The target genes expressions were normalized to two housekeeping endogenous genes B2M and HPRT1, considering both, the geometric and arithmetic CT means (that differed less than 1 CT between the reference and test groups). The following genes were downregulated in the test group (larger tumors) compared to the reference group (smaller tumors), showing a minimum fold change of 4: ANAPC4, E2F4, CUL1, PCNA, KNTC1, RPL13A, KPNA2, NBN, CCNG2 and SUMO1. These results need to be further confirmed in a larger cohort of samples. In conclusion, these findings suggest that the transcriptional activity of specific cell cycle genes changes according to the size of the OSCC tumor, which probably reflects tumor molecular evolution.Supported by: FAPEMIG (Fundação de Amparo à Pesquisa de Minas Gerais), CNPq (National Council for Scientific and Technological Development) and CAPES (Coordination for Improvement of Higher Education Personnel), Brazil Note: This abstract was not presented at the meeting. Citation Format: Carolina C. Gomes, Marina G. Diniz, Fabricio T. de Souza, Jeane F. Correia-Silva, Ricardo S. Gomez. qPCR array of 84 cell cycle genes in oral squamous cell carcinoma reveals differently expressed genes in larger size tumors in relation to small tumors. [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 2206. doi:10.1158/1538-7445.AM2015-2206
Excellent Outcomes at 3 Years with Nilotinib 800 Mg Daily In Early Chronic Phase, Ph+ Chronic Myeloid Leukemia (CML): Results of a Phase 2 GIMEMA CML WP Clinical Trial
Authors: Gianantonio Rosti, Fausto Castagnetti, Gabriele Gugliotta, Massimo Breccia, Luciano Levato, Adele Capucci, Mario Tiribelli, Alfonso Zaccaria, Monica Bocchia, Antonio Cuneo, Fabio Stagno, Giorgina Specchia, Ferdinando Porretto, Bruno Martino, Michele Cedrone, Tamara Intermesoli, Francesca Palandri, Marilina Amabile, Simona Soverini, Nicoletta Testoni, Giuliana Alimena, Fabrizio Pane, Giuseppe Saglio, Giovanni Martinelli, Michele Baccarani
Journal: Blood (2010)
Determination of the minimal erythema dose for ultraviolet A1 radiation
Authors: T. Gambichler, J. Majert, A. Pljakic, I. Rooms, P. Wolf
Journal: British Journal of Dermatology (2016)

There is limited knowledge of the potential of ultraviolet A1 (UVA1) radiation to induce erythema. To investigate the minimal erythema dose (MED) for UVA1 in a German and Austrian population and to determine UVA1 dose–response curves for erythema and pigmentation. We determined the UVA1‐MED in 59 participants using a geometric increase in the dose. Visual readings of erythema and pigmentation were performed at 10 min, 2 h and 24 h after the UVA1 irradiation. Colorimetric measurements were taken to determine erythema (a* value) and pigmentation (L* value) objectively. More than 30% (18 of 59) of the participants had a high‐dose UVA1‐MED (> 70–130 J cm−2); 56% (33) had no detectable UVA1‐MED after 24 h and eight (14%) had a medium‐dose UVA1‐MED (20–70 J cm−2). We observed a stepwise decrease of the a* value measured at the UVA1‐MED skin site from 10 min to 2 h and 24 h (P < 0·001). In contrast, there was a stepwise increase of the L* value measured at the UVA1‐MED skin site from 10 min to 2 h and 24 h (P < 0·001). Most participants had no measurable UVA1‐MED even after commencing high doses such as 130 J cm−2. Only a minority of participants (14%) may develop UVA1‐induced erythema in the low‐ and medium‐dose region. Hence, it appears to be safe to start UVA1 phototherapy with 20 J cm−2 of UVA1 and continue with subsequent daily dose increments of 10 J cm−2, up to the desired maximum dose.
Interdependence between Interleukin-1 and Tumor Necrosis Factor Regulates TNF-Dependent Control of Mycobacterium tuberculosis Infection
Authors: Nelson C. Di Paolo, Shahin Shafiani, Tracey Day, Thalia Papayannopoulou, David W. Russell, Yoichiro Iwakura, David Sherman, Kevin Urdahl, Dmitry M. Shayakhmetov
Journal: Immunity (2016)
The t(4;14) Is Present in Patients with Early Stage Plasma Cell Proliferative Disorders Including MGUS and Smoldering Multiple Myeloma (SMM).
Authors: Scott A. Van Wier, Gregory J. Ahmann, Kimberly J. Henderson, Philip R. Greipp, S. Vincent Rajkumar, Dirk M. Larson, Angela Dispenzieri, Morie A. Gertz, Robert A. Kyle, Rafael Fonseca
Journal: Blood (2005)
Arsenic Trioxide (ATO) Is Safe and Effective in Combination with Low-Dose Ara-C (LDAC) for the Treatment of IPSS-2 Myelodysplastic Syndrome (MDS) and Poor-Prognosis Acute Myeloid Leukemia (AML) in Elderly Patients.
Authors: Gail J. Roboz, Ellen K. Ritchie, Sandra Allen-Bard, Tania J. Curcio, Juliette L. Provenzano, Michael S. Samuel, Michael W. Schuster, Alison W. Bloch, Eric J. Feldman
Journal: Blood (2005)
Phase I study of TAK-285, an investigational HER2/EGFR inhibitor, in patients (pts) with advanced cancer: Updated results and assessment of human CSF distribution.
Authors: E. G. Chiorean, E. A. Sausville, E. I. Heath, A. Weise, J. Gomez-Navarro, K. Venkatakrishnan, S. Sankoh, J. Wu, M. Corvez, P. LoRusso
Journal: Journal of Clinical Oncology (2011)

2538 Background: TAK-285 is an investigational, orally active, dual HER2/EGFR inhibitor with antitumor activity in mouse xenograft models, including breast, gastric, lung, and colon cancer. TAK-285 is not a substrate for P-gp and BCRP, and has been shown to penetrate the blood–brain barrier in rats. This study assessed the safety, PK (including CSF distribution), and efficacy of TAK-285 in pts with advanced cancer. Methods: Adults with advanced refractory cancer and ECOG PS 0–2 were eligible; pts were not selected based on HER2/EGFR expression/amplification/mutation. Pts received oral TAK-285 50 mg QD or 50–500 mg BID in 28-day cycles. In cycle 1 of the recommended phase 2 dose (RP2D) expansion cohort, TAK-285 was dosed on Days 1–21 only to facilitate PK sampling for half-life estimation following multiple dosing. Toxicities were graded using NCI-CTCAE v3. Serial blood samples were taken post dose on Days 1 and 21, and trough samples on Days 8 and 15 for PK analysis. To determine the concentrations of unbound TAK-285 in CSF and plasma, pts treated at the RP2D underwent lumbar puncture 3–4 hours post morning dose on Day 15 of cycle 1 with concurrent blood sampling. Results: 43 pts were enrolled at 8 dose levels in the dose-escalation phase; median age was 60 years (range 43–76), 49% were male, and 86% white. Primary diagnoses included colon (26%), breast (14%), and pancreatic cancer (9%). MTD/RP2D was established as 400 mg BID. Most common AEs were fatigue (37%), diarrhea (37%), and nausea (28%); 47% had a grade 3/4 AE. Grade 1/2 rash was seen in 14%. PK analyses indicated that systemic exposures increased with increasing dose and steady-state was achieved by Day 8. In 7 pts treated at RP2D, absorption was fast (median Tmax: 2 hours), ~4-fold accumulation was noted, and the mean steady-state half-life was 10 hours. Mean CSF:plasma unbound concentration ratio was 0.66, indicating lack of a substantial barrier to human CNS penetration. Conclusions: TAK-285 400 mg BID appears to be well tolerated. Absorption was fast and exposure increased dose dependently. CSF distribution in humans was confirmed. Updated data will be presented, including safety and efficacy for the RP2D cohort.
322. Benign Herpes Simplex Virus Vector Design for Efficient Delivery of Large or Multiple Transgenes To a Diversity of Cells
Authors: Yoshitaka Miyagawa, Fang Han, Gianluca Verlengia, Hiroaki Uchida, Michele Simonato, Justus B. Cohen, Joseph C. Glorioso
Journal: Molecular Therapy (2015)

Viral vectors derived from herpes simplex virus (HSV) have the potential to revolutionize gene therapy due to their ability to accommodate large and multiple therapeutic transgenes. However, current HSV gene therapy vectors express toxic levels of an immediate-early (IE) protein, ICP0, whose function is required for robust and sustained transgene expression. Here we report the development of a new generation of HSV vectors that are IE-gene independent and non-toxic, yet capable of persistent transgene expression in a variety of human primary non-neuronal cell types. We identified a CTCF motif cluster upstream of the latency promoter and a known long-term regulatory region as key elements for the protection of transgene expression cassettes from global silencing of the viral genome in the absence of all viral IE gene products. Using this new HSV vector system, we have observed vigorous expression of full-length dystrophin cDNA (14 kb) for several weeks in a dystrophin-deficient muscle cell line. We further tested our vectors for transgene expression in rodent brain. While we detected variable persistence of gene expression from the latency locus, we were surprised to observe vigorous long-term reporter gene expression from one other locus despite the absence of gene expression from this locus in non-neuronal cells. These findings demonstrate that transgene expression in neurons is operatively different from that in non-neuronal cells and suggest that multiple loci can be used for expression of foreign genes in the nervous system. In addition, our data raise the prospect that our highly defective HSV vector system will be applicable as a safe delivery tool for large and multiple therapeutic genes to a wide range of non-neuronal tissues.
Immunization against HIF-1α Inhibits the Growth of Basal Mammary Tumors and Targets Mammary Stem Cells <i>In Vivo</i>
Authors: Denise L. Cecil, Meredith Slota, Megan M. O'Meara, Benjamin C. Curtis, Ekram Gad, Yushe Dang, Daniel Herendeen, Lauren Rastetter, Mary L. Disis
Journal: Clinical Cancer Research (2016)

Purpose: Triple-negative breast cancer (TNBC) represents a cancer stem cell-enriched phenotype. Hypoxia-inducible factor-1α (HIF-1α) induces the expression of proteins associated with stemness and is highly upregulated in TNBC. We questioned whether HIF-1α was immunogenic and whether vaccination targeting HIF-1α would impact the growth of basal-like mammary tumors in transgenic mice.Experimental Design: We evaluated HIF-1α-specific IgG in sera from controls and patients with breast cancer. Class II epitopes derived from the HIF-1α protein sequence were validated by ELISPOT. To assess therapeutic efficacy, we immunized Tg-MMTVneu and C3(1)Tag mice with HIF-1α Th1-inducing peptides. Stem cells were isolated via magnetic bead separation. Levels of HIF-1α and stem cells in the tumor were quantitated by Western blotting and flow cytometry.Results: The magnitude (P < 0.001) and incidence (P < 0.001) of HIF-1α-specific IgG were elevated in TNBC patients compared with controls. Both breast cancer patients and donors showed evidence of HIF-1α-specific Th1 and Th2 immunity. Three HIF-1α-specific Th1 class II restricted epitopes that were highly homologous between species elicited type I immunity in mice. After HIF-1α vaccination, mammary tumor growth was significantly inhibited in only C3(1)Tag (basal-like/stem cellhigh; P < 0.001) not TgMMTV-neu (luminal/neu/stem celllow; P = 0.859) murine models. Vaccination increased type I T cells in the tumor (P = 0.001) and decreased cells expressing the stem cell marker, Sca-1, compared with controls (P = 0.004).Conclusions: An HIF-1α vaccine may be uniquely effective in limiting tumor growth in TNBC. Inhibiting outgrowth of breast cancer stem cells via active immunization in the adjuvant setting may impact disease recurrence. Clin Cancer Res; 23(13); 3396-404. ©2016 AACR.