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Relevant bibliographies by topics / D 3.5 UL 2008 L115

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Journal articles

Academic literature on the topic 'D 3.5 UL 2008 L115'

Author: Grafiati

Published: 4 June 2021

Last updated: 14 February 2022

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Journal articles on the topic "D 3.5 UL 2008 L115"

1

Drullinsky, P., M. N. Fornier, S. Sugarman, et al. "Dose-dense (DD) cyclophosphamide, methotrexate, and fluorouracil (CMF) at 14-day intervals: A pilot study of every 14- and 10–11-day dosing intervals for women with early-stage breast cancer." Journal of Clinical Oncology 27, no. 15_suppl (2009): 590. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.590.

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590 Background: CMF (C 600 mg/m2, M 40 mg/m2, F 600 mg/m2) is an option for adjuvant therapy for patients with low risk early stage breast cancer. DD regimens as predicted by mathematical models of cancer growth and treatment response are superior. We previously demonstrated the safety of DD EC (epirubicin/cyclophosphamide) followed by paclitaxel at 10–11 day (d) intervals. We investigated the feasibility of administering DD adjuvant CMF every 14 d and then every 10–11 d in a 2-stage phase II trial. Methods: An initial cohort (A) was treated q 14 d with PEG-filgrastim (Neulasta) support. A sec

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2

Shastri, Aditi, Ira Braunschweig, Stefan Klaus Barta, et al. "Stimulation of Adrenergic Activity By Desipramine Enhances Hematopoietic Stem and Progenitor Cell Mobilization Along with G-CSF in Multiple Myeloma - a Pilot Study of Safety and Efficacy." Blood 126, no. 23 (2015): 3101. http://dx.doi.org/10.1182/blood.v126.23.3101.3101.

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Abstract Background: Hematopoietic stem cell release is regulated by the sympathetic nervous system through the β (3) adrenergic receptor [Mendez-Ferrer et al. Nature 2008]. Peripheral sympathetic nerve neurons express the G-CSF receptor and stimulation of peripheral sympathetic nerve neurons with G-CSF reduced norepinephrine (NE) reuptake significantly, suggesting that G-CSF potentiates the sympathetic tone by increasing NE availability [Lucas et al Blood 2012]. Based on preclinical data, we investigated the NE reuptake inhibitor desipramine in HSC mobilization. Despite augmentation with Pler

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3

Blum, William, Rebecca B. Klisovic, Alison Walker, et al. "Epigenetic Targeting Via Transcriptional Inhibition of DNA Methyltransferase: a Phase I Study of Bortezomib in Combination with 5-Azacytidine in Adults with Relapsed or Refractory Acute Myeloid Leukemia (AML)." Blood 114, no. 22 (2009): 2065. http://dx.doi.org/10.1182/blood.v114.22.2065.2065.

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Abstract Abstract 2065 Poster Board II-42 Background: Hypomethylating agents have significant clinical activity in myelodysplastic syndromes (MDS) and AML. In AML, we recently demonstrated a novel epigenetic mechanism of action for the proteasome inhibitor bortezomib (Liu, Blood 2008). Bortezomib induced hypomethylation of leukemic cells in vitro and in vivo via depletion of the Sp1/NF-kB transcriptional activation complex on the DNA methyltransferase 1 (DNMT1) gene promoter, which results in down-regulation of DNMT1 mRNA and enzyme, DNA hypomethylation and re-expression of otherwise hypermeth

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4

Chu, Yaya, Julie-An Talano, Lee Ann Baxter-Lowe, et al. "Sustained Donor Chimerism and Rapid Immune Cell Reconstitution Following Familial Haploidentical (FHI) CD34 Enriched Stem Cell Transplantation with Pbmnc Addback in Patients with High Risk Sickle Cell Disease (SCD) (IND 14359)." Blood 134, Supplement_1 (2019): 1990. http://dx.doi.org/10.1182/blood-2019-126757.

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Background: Allogeneic stem cell transplantation (AlloSCT) from an HLA-matched sibling donor is the only known curative therapy in patients with high-risk SCD (Talano/Cairo, EJH, 2015). Unfortunately only about 15% of high risk patients with SCD have an HLA-matched unaffected sibling donor. T cell depletion has been employed to reduce AGVHD e.g., CD3/CD19 cell depletion (Barfiled RC, et al, Cytotherapy, 2004), αβ T-cell/CD19 cell depletion (Locatelli F, et al, Blood, 2017), CD34+ positive selection (Aversa F, et al, NEJM, 1998). MUD transplantation in high-risk SCD recipients has shown unexpec

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5

Kim, Yeo-Kyeoung, Se Ryeon Lee, Yong Park, et al. "Efficacy Of Ruxolitinib In Korean Myelofibrosis Patients and Cases Complicated TB Lymphadenitis During The Treatment." Blood 122, no. 21 (2013): 1596. http://dx.doi.org/10.1182/blood.v122.21.1596.1596.

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Abstract Introduction Ruxolitinib is a selective JAK 1/2 inhibitor, which shows an excellent treatment outcome in myelofibrosis (MF) patients. Main side effect of JAK 1/2 inhibitors is an increased risk of infection. JAK1/2 inhibition may interfere with the differentiation of interferon-γ (IFN-γ) producing Th1 cells and IFN-γ is a key cytokine involved in protective immunity against Mycobacterium tuberculosis(TB). During COMPORT-II trial, a case of disseminated TB with ruxolitinib was reported. Here, we analyze the efficacy and safety of ruxolitinib in Korean MF patients and report cases of TB

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6

Medeiros, Larissa A., Samir K. Nabhan, Marco Antonio Bitencourt, et al. "Long-Term Clinical Outcome of Patients with Acquired Aplastic Anemia In Brazil Using Cyclosporine-A (CSA) and Prednisone (PRED): 20 Years Follow-up From a Single Institution." Blood 116, no. 21 (2010): 2234. http://dx.doi.org/10.1182/blood.v116.21.2234.2234.

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Abstract Abstract 2234 Introduction/Background: Immunosuppressive therapy is the best alternative for patients with severe aplastic anemia (SAA) without matched sibling donor or with age > 40 years. Since 1988, an alternative protocol was developed with cyclosporine (CSA) and prednisone (PRED) due to irregularity in distribution of anti-thymocyte globulin (ATG) in Brazil. This study aims to show the results of this treatment on the quality of response, overall survival and development of clonal evolution. Materials and methods: 384 patients diagnosed with SAA (Camitta and Bacigalupo criteri

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7

Blum, William, Rebecca B. Klisovic, Ramiro Garzon, et al. "Phase 1 Trial of Decitabine and Bortezomib in High Risk Acute Myeloid Leukemia (AML)." Blood 116, no. 21 (2010): 3293. http://dx.doi.org/10.1182/blood.v116.21.3293.3293.

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Abstract Abstract 3293 Background: The hypomethylating agent decitabine has significant activity in AML. We previously demonstrated a novel epigenetic mechanism of action for the proteasome inhibitor bortezomib in AML cells (Liu, Blood 2008). Bortezomib induced hypomethylation of leukemic cells in vitro and in vivo via disruption of the Sp1/NF-kB transcriptional activation complex on the DNA methyltransferase 1 (DNMT1) gene promoter, which resulted in down-regulation of DNMT1 mRNA and protein levels, DNA hypomethylation, and re-expression of otherwise hypermethylated target genes. Based on thi

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8

Rosenthal, Allison C., Amylou Constance Dueck, Katherine Gano, et al. "A Phase II Clinical Trial of Rituximab, Cyclophosphamide, Bortezomib, and Dexamethasone (R-CyBor-D) in Relapsed Low Grade and Mantle Cell Lymphoma." Blood 124, no. 21 (2014): 4410. http://dx.doi.org/10.1182/blood.v124.21.4410.4410.

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Abstract Introduction Non-Hodgkin lymphoma responds to single agents such as cyclophosphamide, combination therapy such as CVP and immunotherapy with monoclonal antibodies such as rituximab. There is no consensus on the optimal treatment for relapsed low grade or mantle cell lymphoma. Based on the success and tolerability of combining alkylating agents with proteasome inhibitors in multiple myeloma, a phase II clinical trial of rituximab, cyclophosphamide, bortezomib, and dexamethasone (R-CyBor-D) was designed to explore the efficacy and safety of this combination in relapsed low grade and man

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9

Awan, Farrukh, David Deremer, Elaine Mebel, Samith Thomas Kochuparambil, and Anand P. Jillella. "Utility of Plerixafor In Addition to Chemotherapy and G-CSF Mobilization Regimens." Blood 116, no. 21 (2010): 4443. http://dx.doi.org/10.1182/blood.v116.21.4443.4443.

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Abstract Abstract 4443 Introduction: Various chemotherapeutic agents particularly cyclophosphamide (CY) are utilized in combination with growth factors in an attempt to increase the number of stem cells available for collection in the peripheral blood. Plerixafor (P) is a reversible antagonist of CXCR4 and interrupts its interaction with SDF-1. This results in a rapid release of hematopoietic stem cells from the marrow to the circulation. Recent pivotal phase III trial data has established the efficacy of P in combination with G-CSF (G) in patients who had failed prior attempts at stem cell co

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10

Wang, Weiwei, Gabrielle Meyers, Haibo Li, Ying Wang, Lisong Shen, and Guang Fan. "Retrospect Reviews of PNH Tests with Long-Term Follow-up in a Single Institution." Blood 134, Supplement_1 (2019): 948. http://dx.doi.org/10.1182/blood-2019-124896.

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I ntroduction : Paroxysmal nocturnal hemoglobinuria (PNH) often presents as hemolysis and/or bone marrow failure. Flow cytometric testing can accurately detect PNH. However, the long term studies on PNH clone size and how it relates to clinical course are few. We sought to understand how PNH clone size correlates with clinical course over time and the impacts on clone size with different treatments. Here we report long term clone size monitoring and clinical data of 57 patients with PNH in a single intuition. Methods : High sensitivity PNH flow cytometry (0.01% limit of detection) was performe

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