tbuckley/cabot-search huggingface dataset:
A large genome-wide association study of age-related macular degeneration highlights contributions of rare and common variants
Authors: Lars G Fritsche, Wilmar Igl, Jessica N Cooke Bailey, Felix Grassmann, Sebanti Sengupta, Jennifer L Bragg-Gresham, Kathryn P Burdon, Scott J Hebbring, Cindy Wen, Mathias Gorski, Ivana K Kim, David Cho, Donald Zack, Eric Souied, Hendrik P N Scholl, Elisa Bala, Kristine E Lee, David J Hunter, Rebecca J Sardell, Paul Mitchell, Joanna E Merriam, Valentina Cipriani, Joshua D Hoffman, Tina Schick, Yara T E Lechanteur, Robyn H Guymer, Matthew P Johnson, Yingda Jiang, Chloe M Stanton, Gabriëlle H S Buitendijk, Xiaowei Zhan, Alan M Kwong, Alexis Boleda, Matthew Brooks, Linn Gieser, Rinki Ratnapriya, Kari E Branham, Johanna R Foerster, John R Heckenlively, Mohammad I Othman, Brendan J Vote, Helena Hai Liang, Emmanuelle Souzeau, Ian L McAllister, Timothy Isaacs, Janette Hall, Stewart Lake, David A Mackey, Ian J Constable, Jamie E Craig, Terrie E Kitchner, Zhenglin Yang, Zhiguang Su, Hongrong Luo, Daniel Chen, Hong Ouyang, Ken Flagg, Danni Lin, Guanping Mao, Henry Ferreyra, Klaus Stark, Claudia N von Strachwitz, Armin Wolf, Caroline Brandl, Guenther Rudolph, Matthias Olden, Margaux A Morrison, Denise J Morgan, Matthew Schu, Jeeyun Ahn, Giuliana Silvestri, Evangelia E Tsironi, Kyu Hyung Park, Lindsay A Farrer, Anton Orlin, Alexander Brucker, Mingyao Li, Christine A Curcio, Saddek Mohand-Saïd, José-Alain Sahel, Isabelle Audo, Mustapha Benchaboune, Angela J Cree, Christina A Rennie, Srinivas V Goverdhan, Michelle Grunin, Shira Hagbi-Levi, Peter Campochiaro, Nicholas Katsanis, Frank G Holz, Frédéric Blond, Hélène Blanché, Jean-François Deleuze, Robert P Igo, Barbara Truitt, Neal S Peachey, Stacy M Meuer, Chelsea E Myers, Emily L Moore, Ronald Klein, Michael A Hauser, Eric A Postel, Monique D Courtenay, Stephen G Schwartz, Jaclyn L Kovach, William K Scott, Gerald Liew, Ava G Tan, Bamini Gopinath, John C Merriam, R Theodore Smith, Jane C Khan, Humma Shahid, Anthony T Moore, J Allie McGrath, Reneé Laux, Milam A Brantley, Anita Agarwal, Lebriz Ersoy, Albert Caramoy, Thomas Langmann, Nicole T M Saksens, Eiko K de Jong, Carel B Hoyng, Melinda S Cain, Andrea J Richardson, Tammy M Martin, John Blangero, Daniel E Weeks, Bal Dhillon, Cornelia M van Duijn, Kimberly F Doheny, Jane Romm, Caroline C W Klaver, Caroline Hayward, Michael B Gorin, Michael L Klein, Paul N Baird, Anneke I den Hollander, Sascha Fauser, John R W Yates, Rando Allikmets, Jie Jin Wang, Debra A Schaumberg, Barbara E K Klein, Stephanie A Hagstrom, Itay Chowers, Andrew J Lotery, Thierry Léveillard, Kang Zhang, Murray H Brilliant, Alex W Hewitt, Anand Swaroop, Emily Y Chew, Margaret A Pericak-Vance, Margaret DeAngelis, Dwight Stambolian, Jonathan L Haines, Sudha K Iyengar, Bernhard H F Weber, Gonçalo R Abecasis, Iris M Heid
Journal: Nature Genetics (2015)
A randomised trial of secondary prophylaxis using granulocyte colony-stimulating factor (‘SPROG’ trial) for maintaining dose intensity of standard adjuvant chemotherapy for breast cancer by the Anglo-Celtic Cooperative Group and NCRN
Authors: R.C.F. Leonard, J.L. Mansi, C. Keerie, A. Yellowlees, S. Crawford, K. Benstead, R. Matthew, D. Adamson, S. Chan, R. Grieve
Journal: Annals of Oncology (2015)
Prognostic Significance Of CRLF2 Over-Expression In Pediatric Acute Lymphoblastic Leukemia
Authors: Mio Yano, Toshihiko Imamura, Daisuke Asai, Akiko Moriya Saito, So-ichi Suenobu, Daiichiro Hasegawa, Takao Deguchi, Yoshiko Hashii, Hirohide Kawasaki, Hiroki Hori, Yoshiyuki Kosaka, Koji Kato, Keizo Horibe, Keiko Yagi, Junichi Hara, Kenji Matsumoto, Nobutaka Kiyokawa, Megumi Oda, Atsushi Sato
Journal: Blood (2013)
Prevalence, clinical characteristics, and prognosis of GATA2-related myelodysplastic syndromes in children and adolescents
Authors: Marcin W. Wlodarski, Shinsuke Hirabayashi, Victor Pastor, Jan Starý, Henrik Hasle, Riccardo Masetti, Michael Dworzak, Markus Schmugge, Marry van den Heuvel-Eibrink, Marek Ussowicz, Barbara De Moerloose, Albert Catala, Owen P. Smith, Petr Sedlacek, Arjan C. Lankester, Marco Zecca, Victoria Bordon, Susanne Matthes-Martin, Jonas Abrahamsson, Jörn Sven Kühl, Karl-Walter Sykora, Michael H. Albert, Bartlomiej Przychodzien, Jaroslaw P. Maciejewski, Stephan Schwarz, Gudrun Göhring, Brigitte Schlegelberger, Annámaria Cseh, Peter Noellke, Ayami Yoshimi, Franco Locatelli, Irith Baumann, Brigitte Strahm, Charlotte M. Niemeyer
Journal: Blood (2015)
Abstract 1443: BMP-2 induces motility and invasiveness of colon cancer through upregulation of cancer stem cell
Authors: Bo Ram Kim, Jung Lim Kim, Seong Hye Park, Yoon A Jeoung, Sun Il Lee, Byoung-Wook Min, Sang Cheul Oh
Journal: Cancer Research (2015)

Abstract The majority of deaths in cancer patients are will present with metastasis and relapses. One of the key steps in metastasis is the migration, and Cancer stem cells(CSCs) activate migration. So, targeting of CSC is an important strategy for cancers. Bone morphogenetic protein(BMP) signaling, member of the TGF-β superfamily, plays an important role in development of bone and in regulation of stem cell properties. In Previous study, Bone morphogenetic protein(BMP) signaling has been associated with various types of cancers. BMPs contributes through autocrine and paracrine mechanisms to tumor development, invasion and metastasis. However, their roles and mechanisms are unclear. In this study, we investigated the function of BMP-2 and relevance BMP-2 and CSCs in Colon cancer cells. First, We compared the endogenous protein level of parental and spheroid cells by western blotting. The spheroid cells showed higher level of EMT(Epithelial mesenchymal transition) markers N-Cadherin and Snail, CSC markers (EpCAM and CD133), and p Smad1/5 known BMP-2 downstream than the corresponding parental cells. Then expression of EpCAM and CD133 was confirmed by flow cytometry. We found that BMP-2 plays a key role in Cancer stem cell. To determine function of BMP-2 in Colon cancer cells, we stimulated the colon cancer cells with recombinant human BMP-2. Stimulation of BMP-2 increased EMT, CSC markers(EpCAM and CD133). In addition, BMP-2 enhanced cell motility, and invasiveness by wound healing and matrigel invasion assay. These results indicated BMP-2 signaling pathway enhance metastasis through increase of CSC portion. Blockade of BMP-2 pathway by Noggin(BMP2 antagonist) or Smad1/5 siRNA inhibited BMP2-induced EMT marker, MMP2, and CSC portion. The morphologic changes though the EMT process were monitored by immunofluorescence staining and Western blot for EMT markers. And Blockade of BMP-2 pathway inhibited cell motility and invasiveness. Our findings suggest that BMP-2 signaling regulates metastatic potential through regulation of CSCs in colon cancer cell. Citation Format: Bo Ram Kim, Jung Lim Kim, Seong Hye Park, Yoon A Jeoung, Sun Il Lee, Byoung-Wook Min, Sang Cheul Oh. BMP-2 induces motility and invasiveness of colon cancer through upregulation of cancer stem cell. [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 1443. doi:10.1158/1538-7445.AM2015-1443
Oral versus intravenous methotrexate: another opinion.
Authors: B A Kamen, N Winick, J S Holcenberg
Journal: Journal of Clinical Oncology (1998)

Article Tools Article Tools OPTIONS & TOOLS Export Citation Track Citation Add To Favorites Rights & Permissions COMPANION ARTICLES No companion articles ARTICLE CITATION DOI: 10.1200/JCO.1998.16.6.2283 Journal of Clinical Oncology - published online before print September 21, 2016 PMID: 9626235 Oral versus intravenous methotrexate: another opinion. B A KamenxB A KamenSearch for articles by this author , N WinickxN WinickSearch for articles by this author , J S HolcenbergxJ S HolcenbergSearch for articles by this author https://doi.org/10.1200/JCO.1998.16.6.2283 PDF "Oral versus intravenous methotrexate: another opinion.." Journal of Clinical Oncology, 16(6), pp. 2283–2285© 1998 by American Society of Clinical Oncology
Abstract 1672: Structural basis for inhibition of ligand-dependent and -independent ErbB3 activation by KTN3379
Authors: Diego Alvarado, Sangwon Lee, Etienne Greenlee, Gwenda F. Ligon, Jay S. Lillquist, Edward J. Natoli, Theresa M. LaVallee, Joseph Schlessinger
Journal: Cancer Research (2015)

Abstract ErbB3 signaling plays an important role in the progression of a number of solid tumor types, and is the target of several therapeutic monoclonal antibodies. In cancer, ErbB3 activation can be driven by its ligand Neuregulin, or in its absence, through high overexpression of its co-receptor ErbB2. Here, we report that the ErbB3 monoclonal antibody KTN3379, currently in phase 1 clinical development, robustly inhibits both mechanisms of ErbB3 activation in different tumor model settings. The crystal structure of a KTN3379 Fab in complex with the full ErbB3 extracellular domain reveals that the antibody binds with very high affinity to a novel and unique epitope in the boundary of domains 2 and 3, and locks the receptor in an inactive conformation. Thus, KTN3379 interferes with the first step of ErbB3 activation, which is required for both ligand-dependent and ligand-independent signaling. The mechanism of inhibition described here should be also applicable to EGFR and ErbB4. Citation Format: Diego Alvarado, Sangwon Lee, Etienne Greenlee, Gwenda F. Ligon, Jay S. Lillquist, Edward J. Natoli, Theresa M. LaVallee, Joseph Schlessinger. Structural basis for inhibition of ligand-dependent and -independent ErbB3 activation by KTN3379. [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 1672. doi:10.1158/1538-7445.AM2015-1672
Markers of a chronic inflammatory state and trial completion: Data from cancer cachexia trial
Authors: N. MacDonald, G. Kasymjanova, B. Gagnon, R. Sharma, V. Baracos, W. Droege, H. Kreisman
Journal: Journal of Clinical Oncology (2008)

9594 Background: Cancer cachexia trials are plagued by high drop out rates lessening the impact of such studies. We hypothesized that patients with a cancer-related chronic inflammatory state (CIS) as defined by a prognostic index (PI) are less likely to complete a cachexia clinical trial. Methods: A randomized trial comparing two protein supplements administered for 6 mo was done in pts with cachexia and either NSCLC or colon cancer. 77 pts with advanced NSCLC (58 pts) or colorectal cancer (20 pts), who were eligible for the trial and signed consent were included. All trial participants were assigned a prognostic index (PI) score as an indicator of CIS: 0 if CRP ≤10mg/L and WBC ≤ 11x109/L; 1 if one of the markers was elevated; or 2 if both were elevated (ASCO 2005, 17035). Results: 77 pts (M 55, F 22) aged 64 (31–87) years were studied. 28 pts completed the 6 month trial, 49 dropped out (20 died, 29 withdrew). Baseline CRP level was more than 3 fold higher in pts who dropped out compared to those who completed the study (80.1 mg/L vs 23.8 mg/L; p=0.002)). Baseline WBC was also higher in dropouts when compared to completers (10.4 vs 6.8; p=0.14). The PI distribution 0/1/2 of the 49 pts who dropped out was 12/25/12 pts compared to 14/12/2 respectively for the 28 who completed the study (p=0.03). Dropouts with higher PI had shorter length of stay on trial: 4.2 mo for pts with PI of 0, 3.4 mo for PI of 1 and 2.5 mo for PI of 2 (p=0.33). Death related dropouts increased from 11% in PI 0 to 43% in PI 2 (see the table). Weight loss at the time of enrolment was not associated either with PI or completion of the study. Conclusion: Patients with high PI are more likely to drop out of a cachexia-anorexia trial. Death-related dropouts seem to increase with increase in PI. A high CIS should be considered as a separate prospectively defined stratum. PI score Total 0 1 2 Number entered the trial 26 (100%) 37 (100%) 14 (100%) 77 Completed the trial 14 (54%) 12 (32%) 2 (14%) 28 Drop-outs: death-related 3 (11%) 11 (30%) 6 (43%) 20 Drop-outs: withdrawal 9 (35%) 14 (38%) 6 (43%) 29 Author Disclosure Employment or Leadership Consultant or Advisory Role Stock Ownership Honoraria Research Expert Testimony Other Remuneration Immunotec Inc Immunotec Inc Immunotec
Pigmented macules of bony prominences (PMBP): A distinct presentation in patients with red hair
Authors: Emilie Marmottant, Christine Chiaverini, Didier Bessis, Thomas Hubiche, Stéphanie Mallet, Annabel Maruani, Claire Abasq, Juliette Miquel, Nathalie Cardot-Leccia, Jean-Philippe Lacour, Thierry Passeron
Journal: Journal of the American Academy of Dermatology (2016)
Organ donation in adults: a critical care perspective
Authors: Giuseppe Citerio, Marcelo Cypel, Geoff J. Dobb, Beatriz Dominguez-Gil, Jennifer A. Frontera, David M. Greer, Alex R. Manara, Sam D. Shemie, Martin Smith, Franco Valenza, Eelco F. M. Wijdicks
Journal: Intensive Care Medicine (2016)
Prospective evaluation of the incidence of delayed nausea and vomiting in patients with colorectal cancer receiving oxaliplatin-based chemotherapy
Authors: P. J. Hesketh, P. Sanz-Altamira, J. Bushey, K. Malek, L. Insalaco, A. M. Hesketh
Journal: Journal of Clinical Oncology (2008)

9645 Background: Oxaliplatin (OX) is a platinum compound commonly used in colorectal cancer. The emetogenic potential of OX has not been well characterized despite reports of frequent nausea (N) and vomiting/retching (V) in phase I and II studies. Platinum compounds such as cisplatin and carboplatin have a well defined ability to cause delayed (> 24 hours post chemotherapy) NV in the absence of antiemetic prophylaxis. There is no information available on the potential for OX to produce delayed NV.This trial sought to prospectively determine the frequency of delayed N and V with OX-based chemotherapy following day 1 prophylaxis with a 5-HT3 antagonist (5-HT3A) and dexamethasone (DEX). Methods: Eligibility: Pts ≥ age 18 with colon cancer receiving OX (85–100mg/m2) as part of a standard FOLFOX (folinic acid, 5-fluorouracil, oxaliplatin) regimen for the first time. Performance status: 0–2. Antiemetic treatment: 5-HT3A (ondansetron, dolasetron, or granisetron but not palonosetron) at an approved dose and DEX 20mg PO/IV on day 1 prior to OX infusion. No routine prophylaxis for delayed N/V was given. Episodes of V, N, and use of rescue antiemetics were recorded in patient-completed diaries. Four point (none, mild, moderate, severe) categorical scales were used to assess N. Study period: 120 hours after OX administration. Definitions: complete response (CR) - no V and no use of rescue antiemetics (RA); complete control (CC) - no V, no N and no RA. Results: Pts: 36; evaluable 35; median age: 68 (48–85); M/F 46%/54%. History of moderate - heavy ethanol use: 8 pts (23%). Acute CR: 91% (32/35); Delayed CR: 51% (18/35); Delayed CC: 40% (14/35); Overall CR (0–120 hrs): 51% (18/35); Overall CC: 37% (13/35). Median time to first emesis/first rescue: 57 hrs/47 hrs. Conclusions: The use of a single dose of a 5-HT3A and DEX prior to OX results in excellent control of emesis (CR - 91%) during the 24 hours after chemotherapy. However, without further antiemetic treatment, complete response rate in the delayed period (hours 24 - 120) decreased to 51%. In addition, a majority of pts (57%) noted delayed N, with N of moderate to severe intensity in 9 (26%) pts. This study supports the need for routine antiemetic prophylaxis for delayed N and V following OX-based chemotherapy. Author Disclosure Employment or Leadership Consultant or Advisory Role Stock Ownership Honoraria Research Expert Testimony Other Remuneration sanofi-aventis sanofi-aventis
LRRK2 phosphorylates pre-synaptic N-ethylmaleimide sensitive fusion (NSF) protein enhancing its ATPase activity and SNARE complex disassembling rate
Authors: Elisa Belluzzi, Adriano Gonnelli, Maria-Daniela Cirnaru, Antonella Marte, Nicoletta Plotegher, Isabella Russo, Laura Civiero, Susanna Cogo, Maria Perèz Carrion, Cinzia Franchin, Giorgio Arrigoni, Mariano Beltramini, Luigi Bubacco, Franco Onofri, Giovanni Piccoli, Elisa Greggio
Journal: Molecular Neurodegeneration (2016)

Lrrk2, a gene linked to Parkinson's disease, encodes a large scaffolding protein with kinase and GTPase activities implicated in vesicle and cytoskeletal-related processes. At the presynaptic site, LRRK2 associates with synaptic vesicles through interaction with a panel of presynaptic proteins. Here, we show that LRRK2 kinase activity influences the dynamics of synaptic vesicle fusion. We therefore investigated whether LRRK2 phosphorylates component(s) of the exo/endocytosis machinery. We have previously observed that LRRK2 interacts with NSF, a hexameric AAA+ ATPase that couples ATP hydrolysis to the disassembling of SNARE proteins allowing them to enter another fusion cycle during synaptic exocytosis. Here, we demonstrate that NSF is a substrate of LRRK2 kinase activity. LRRK2 phosphorylates full-length NSF at threonine 645 in the ATP binding pocket of D2 domain. Functionally, NSF phosphorylated by LRRK2 displays enhanced ATPase activity and increased rate of SNARE complex disassembling. Substitution of threonine 645 with alanine abrogates LRRK2-mediated increased ATPase activity. Given that the most common Parkinson's disease LRRK2 G2019S mutation displays increased kinase activity, our results suggest that mutant LRRK2 may impair synaptic vesicle dynamics via aberrant phosphorylation of NSF.
Cyclin E1 (CCNE1) and E2 (CCNE2) as prognostic and predictive markers for endocrine therapy (ET) in early breast cancer
Authors: C. Sotiriou, M. Paesmans, A. Harris, M. A. Colozza, S. Fox, M. Taylor, A. Sorre, P. Martiat, F. Cardoso, M. Piccart
Journal: Journal of Clinical Oncology (2004)

9504 Background: CCNEs are important regulators of S phase entry in the cell cycle and are frequently deregulated in breast tumors. Recently, CCNE1 evaluated by western blot analysis was reported to be a very powerful prognostic factor in BC. To our knowledge no data have been reported for CCNE2. Methods: In this study we evaluated the prognostic and predictive value for ET of CCNE1 and CCNE2 by quantitative RT-PCR in 230 treated and untreated early BC patients. Median follow-up was 7.3 years for alive patients. Nineteen patients received adjuvant chemotherapy (CT), 151 ET and 71 no systemic treatment. Results: median expression values were 6.04 U and 1.56 U for CCNE1 and CCNE2 respectively. High levels (above the median) of CCNE1 and CCNE2 were associated with high grade (p<. 001) and ER- (p<. 001) tumors. Patient age <50 was correlated only with high levels of CCNE1 (p<. 008). In univariate analysis, high expression levels of both CCNEs were predictive of shorter relapse free survival (RFS) (HR=2.14, p= .001 for CCNE1 and HR=2.37, p< .001 for CCNE2), together with ER, grade, nodal status and T size. In a multivariate model, ER status (HR=0.39, p= .003), CCNE1 (HR=2.20, p=. 02) and nodal status (HR=2.90, p<0.001) were the three independent prognostic factors. CCNE2 became an independent prognostic marker with grade and tumor size when CCNE1 was omitted from the model. In the subgroup of node negative untreated patients (n=71), only CCNE2 was prognostic for RFS (HR=2.58, p= .04) while both markers appeared to be predictive factors for ET in the 112 ER+ patients (HR=2.79 for high CCNE1, p= .005 and .HR=1.97 for CCNE2, p= .05). Conclusions: Both CCNEs appear to have a predictive value for ET in ER+ BC patients. Interestingly, in the small subgroup of untreated node negative patients only CCNE2 was prognostic for RFS. Of note, CCNE2 was one of the genes found in common by several gene prognostic signatures identified through DNA microarray technology. Our results support a prospective study of these markers evaluating their potential clinical utility for treatment decision-making in early BC. No significant financial relationships to disclose.
Early radiation response between GnRH agonist versus antagonist combined with radiotherapy in high-risk prostate cancer.
Authors: Gilles Crehange, Alexandre Cochet, Adele Cueff, Etienne Martin, Philippe Maingon, Francois Brunotte, Paul M Walker
Journal: Journal of Clinical Oncology (2015)

97 Background: Degarelix, a GnRH antagonist, provides a very rapid and sustained testosterone suppression alongside with the VEGF pathway inhibition through the FSH receptors. This raises the question as to whether high risk localized prostate cancer (HRPCa) could respond differently to radiotherapy (RT) + Degarelix when compared with RT + GnRH agonist. Methods: 30 HRPCa patients were treated with exclusive RT combined with a GnRH agonist (n= 19) or Degarelix (n= 11). MRSI was performed before the start of hormones and 3 months after the end of RT. Choline (tumor metabolism) and citrate (healthy prostate metabolism) were quantified with MR spectroscopy and the slopes of gadolinium wash-in (SWI) and wash-out (SWO) were assessed in the peripheral zone (PZ), the central gland (CG) and the tumor with DCE-MRI. Results: At baseline, 14 patients had a T3 (46.7%) and 9 patients (30%) had a GS≥8. The median PSA values were 12.7 ng/mL [3.0-153.7] for agonists and 14.0 ng/mL [6.8-23.6] for Degarelix (p=ns). The mean prostate volumes (Pvol) were 32.0±15.5 mL for agonist and 33.0±10.0 mL for Degarelix (p=ns). The median dose of RT was 78Gy in each group, [72.0-80.0] with agonist and [70.2-80.0] with Degarelix. There were no significant differences in choline, citrate, SWI and SWO in the PZ, the CG and the tumor. At 3 months, Pvol were 20.8±8.0 mL for agonist and 21.4±6.2 mL for Degarelix (p=0.71) and the mean and median PSA values for agonist vs Degarelix were 0.5±0.8 ng/mL vs 0.1±0.1 ng/mL and 0.1 ng/mL [0.02-2.8] vs 0.1 ng/mL [0.005-0.3], respectively. Citrate was significantly decreased with Degarelix in the PZ (4.3±4.4 vs 1.1±0.8, p=0.0142), in the CG (4.0±4.0 vs 1.1±1.0, p=0.009) but not in the tumor (2.5±2.6 vs 1.7±1.9, p=0.23). Choline concentrations were similar between both groups in the PZ, the CG and the tumor. There was a trend towards a lower contrast uptake in the tumor with Degarelix (mean SWI and SWO: 134.6±56.2 s -1 vs 104.1±36.3 s -1 , p=0.13 and 259.6±103.1 s -1 vs 306.1±70.4 s -1 , p=0.15). Conclusions: Degarelix combined with RT offers a significant early, more profound metabolic atrophy in the prostate, but not in the tumor. There is a trend towards a lower tumor vascularization with Degarelix compared with GnRH agonists.
Cell-Freezing Devices Are Not Strictly Needed to Start an Autologous Hematopoietic Transplantation Program: Non-Cryopreserved Peripheral Blood Stem Cells Can be Used to Restore Hematopoiesis after High Dose Chemotherapy: A Multicenter Experience in 268 Autografts in Patients with Multiple Myeloma or Lymphoma. Study on Behalf of the Latin-American Bone Marrow Transplantation Group (LABMT)
Authors: Amado J Karduss-Urueta, Guillermo J. Ruiz-Arguelles, Rosendo Perez, Guillermo J Ruiz-Delgado, Angelica Maria Cardona, Nancy Labastida-Mercado, Luis R Gomez, Samantha Galindo-Becerra, Pedro Reyes, Juan Alejo Jimenez
Journal: Blood (2014)