PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 19587093-6 2009 In contrast to cord blood-derived CD34(+) and hESC-derived hematopoietic cells, exposure of undifferentiated hESCs to a single low dose of etoposide induced a pronounced cell death. Etoposide 139-148 CD34 molecule Homo sapiens 34-38 19899124-1 2009 The yield of CD34+ cells collected by apheresis for autologous peripheral blood stem cell (PBSC) transplantation was greatly increased when the appropriate timing was determined to begin using G-CSF after COAEP (Cytoxan, Vinblastine, Arabinosylcytosin, Etoposide and Prednisone) mobilization. Etoposide 253-262 CD34 molecule Homo sapiens 13-17 17618321-2 2007 Etoposide (VP) plus filgrastim (G) frequently mobilizes high numbers of CD34+ cells for autologous transplantation. Etoposide 0-9 CD34 molecule Homo sapiens 72-76 18510699-3 2008 Although etoposide treatment is sufficient to induce readily detectable MLL rearrangements in primary human CD34+ cells, the majority of cells that gain translocations do not proliferate in culture possibly due to reduced proliferative capacity of most CD34+ cells during normal differentiation [Blood 2005;105:2124]. Etoposide 9-18 CD34 molecule Homo sapiens 108-112 18510699-3 2008 Although etoposide treatment is sufficient to induce readily detectable MLL rearrangements in primary human CD34+ cells, the majority of cells that gain translocations do not proliferate in culture possibly due to reduced proliferative capacity of most CD34+ cells during normal differentiation [Blood 2005;105:2124]. Etoposide 9-18 CD34 molecule Homo sapiens 253-257 18510699-6 2008 Similar to results in CD34+ cells, a significant proportion of etoposide-treated HSC-derived clones harbored stable MLL rearrangements, including duplications, inversions and translocations. Etoposide 63-72 CD34 molecule Homo sapiens 22-26 17917963-6 2007 and total CD34+ cells harvested were higher in patients mobilized with intermediate dose etoposide (p = 0.003 and p = 0.004, respectively). Etoposide 89-98 CD34 molecule Homo sapiens 10-14 16503501-7 2006 The CD34 cell dose collected was greater in bolus etoposide patients (44 million per kilogram) than in continuous etoposide patients (10.9 million per kilogram; P<.0001). Etoposide 50-59 CD34 molecule Homo sapiens 4-8 16503501-7 2006 The CD34 cell dose collected was greater in bolus etoposide patients (44 million per kilogram) than in continuous etoposide patients (10.9 million per kilogram; P<.0001). Etoposide 114-123 CD34 molecule Homo sapiens 4-8 15815728-4 2005 Here we show that CML CD34(+) progenitors are sensitive to several apoptosis-inducing stimuli including the chemotherapeutic agents Ara-C and VP-16, radiation, arsenic trioxide, ceramide, growth factor withdrawal, and the death receptor activators TNFalpha and TRAIL. Etoposide 142-147 CD34 molecule Homo sapiens 22-26 14730338-6 2004 Pre-transplant cumulative doses of etoposide >750 mg/m(2) were associated with low CD34(+) cell collections on multivariate analysis. Etoposide 35-44 CD34 molecule Homo sapiens 86-90 14988151-6 2004 Furthermore, p53 gene silencing resulted in decreased p21 mRNA levels and reduced the sensitivity of CD34+ cells toward the cytotoxic drug etoposide. Etoposide 139-148 CD34 molecule Homo sapiens 101-105 15528316-0 2005 Therapy-related acute myeloid leukemia-like MLL rearrangements are induced by etoposide in primary human CD34+ cells and remain stable after clonal expansion. Etoposide 78-87 CD34 molecule Homo sapiens 105-109 15528316-4 2005 We used a culture system of primary human hematopoietic CD34+ cells and inverse polymerase chain reaction to characterize the spectrum of stable genomic rearrangements promoted by etoposide exposure originating within an MLL translocation hotspot in therapy-related leukemia. Etoposide 180-189 CD34 molecule Homo sapiens 56-60 12644023-0 2003 Profiling of differentially expressed apoptosis-related genes by cDNA arrays in human cord blood CD34+ cells treated with etoposide. Etoposide 122-131 CD34 molecule Homo sapiens 97-101 12644023-2 2003 Here we sought to systematically evaluate the basic molecular components and main pathways that govern and mediate cellular response initiated within human CD34(+) cells to etoposide-induced apoptosis. Etoposide 173-182 CD34 molecule Homo sapiens 156-160 12644023-5 2003 RESULTS: We identified a set of apoptosis-related genes expressed in highly purified normal human CB CD34(+) cells and determined how the expression of these genes changed in response to etoposide treatment. Etoposide 187-196 CD34 molecule Homo sapiens 101-105 12644023-8 2003 CONCLUSION: p53, c-Myc, and BAFF pathways are main pathways utilized by CD34(+) cells to arrest cell-cycle progression at multiple checkpoints, to halt proliferation, and to induce apoptosis as part of their cellular response to etoposide. Etoposide 229-238 CD34 molecule Homo sapiens 72-76 12644023-9 2003 Multiple known pro-survival and pro-apoptotic pathways are simultaneously activated in etoposide-treated CD34(+) cells. Etoposide 87-96 CD34 molecule Homo sapiens 105-109 11372740-5 2001 The mean number of CD34+ cells harvested per apheresis was larger in the group receiving high-dose cytosine arabinoside or high-dose etoposide plus granulocyte colony-stimulating factor (G-CSF) than in the group receiving conventional chemotherapy plus G-CSF. Etoposide 133-142 CD34 molecule Homo sapiens 19-23 11594568-4 2001 Mobilization of CD34+ stem cells was achieved with etoposide and G-CSF. Etoposide 51-60 CD34 molecule Homo sapiens 16-20 10414907-5 1999 The use of etoposide 500 mg/m2 (days 1-4) + G-CSF resulted in the successful collection of adequate numbers of PBSC with a median harvest of 3.6 x 10(6)/kg (range 2.2-12.6) CD34+ cells in all 16 patients. Etoposide 11-20 CD34 molecule Homo sapiens 173-177 10414907-8 1999 In addition, median peak values of circulating CD34+ cells were significantly higher after etoposide as compared to cyclophosphamide (49.2/microl vs 4.7/microl; P = 0.0004). Etoposide 91-100 CD34 molecule Homo sapiens 47-51 9516161-3 1998 After high-dose myeloablative chemotherapy (busulfan, cyclophosphamide, etoposide) CD34+) HPC were infused and lymphoid reconstitution was monitored using flow cytometry and reverse transcriptase-polymerase chain reaction (RT-PCR) amplification of VDJ T-cell receptor (TcR) sequences. Etoposide 72-81 CD34 molecule Homo sapiens 83-87 8794901-7 1996 CD34+ cells treated with etoposide (40 microM) or hydroquinone (50 microM) for 18 hr were stained and subjected to fluorescent microscopy as above. Etoposide 25-34 CD34 molecule Homo sapiens 0-4 9308634-10 1997 CONCLUSION: A regimen of cyclophosphamide, etoposide, and granulocyte-colony-stimulating factor led to the successful collection of adequate numbers of CD34+ cells in most patients without excessive toxicity. Etoposide 43-52 CD34 molecule Homo sapiens 152-156 29134688-11 2018 CONCLUSION: NF during etoposide priming is associated with lower likelihood of proceeding to transplant, lower CD34+ cell dose collection, more apheresis days required for collection and a higher 30-day readmission rate following transplant discharge. Etoposide 22-31 CD34 molecule Homo sapiens 111-115 7530135-0 1994 Idarubicin, intermediate-dose cytarabine, etoposide, and granulocyte-colony-stimulating factor are able to recruit CD34+/HLA-DR- cells during early hematopoietic recovery in accelerated and chronic phases of chronic myeloid leukemia. Etoposide 42-51 CD34 molecule Homo sapiens 115-119 7505211-4 1994 Comparative studies of CD34 cells showed that the percentage of CD34+ mononuclear cells was greatest in blood samples from patients following mobilization treatment with cyclophosphamide/etoposide/G-CSF averaging 2%. Etoposide 187-196 CD34 molecule Homo sapiens 64-68 33592119-10 2021 Patients treated with cytarabine had the highest yield of CD34+ cells (median 7.5 x 106 /kg vs 5.8 and 2.4 for etoposide and cyclophosphamide, P = .001). Etoposide 111-120 CD34 molecule Homo sapiens 58-62 32615949-5 2020 RESULTS: Retrospective analysis of the clinical data revealed that the etoposide with G-CSF mobilization group showed the highest yield of CD34+ cells and the lowest change in white blood cell counts during mobilization. Etoposide 71-80 CD34 molecule Homo sapiens 139-143 32216001-6 2020 To test this hypothesis, we detected gene rearrangements in etoposide-treated or non-treated CD34+ cells cultured with cytokines using inverse PCR. Etoposide 60-69 CD34 molecule Homo sapiens 93-97 27677634-4 2017 Treatment with Eto combined with IM markedly induced apoptosis in primitive CML CD34+ CD38- stem cells resistant to eradication by IM alone, but not in normal hematopoietic stem cells, CML and normal mature CD34- cells, and other leukemia and lymphoma cell lines. Etoposide 15-18 CD34 molecule Homo sapiens 80-84 27677634-4 2017 Treatment with Eto combined with IM markedly induced apoptosis in primitive CML CD34+ CD38- stem cells resistant to eradication by IM alone, but not in normal hematopoietic stem cells, CML and normal mature CD34- cells, and other leukemia and lymphoma cell lines. Etoposide 15-18 CD34 molecule Homo sapiens 207-211 24400988-4 2014 HD etoposide and G-CSF chemomobilization resulted in successful collection (>2 x 10(6) CD34+ cells/kg) in 82.3% of patients within a median 2 (1-6) apheresis days. Etoposide 3-12 CD34 molecule Homo sapiens 90-94 27334858-6 2016 A substantial high yield of CD34(+) cells was achieved when patients were treated with a dose-modified IVE regimen, compared with that during the previous regimen (two with the ifosfamide, carboplatin, and etoposide [ICE] regimen, one with high-dose cyclophosphamide and one with the original IVE regimen). Etoposide 206-215 CD34 molecule Homo sapiens 28-32 22019627-5 2012 Significant correlations were demonstrated between the peak number of CD34(+) cells and residual growth of colony-forming unit granulocyte-macrophage (CFU-GM) after maphosphamide (R = 0.550; p = 0.0003) and after etoposide (R = 0.793; p = 0.0003). Etoposide 213-222 CD34 molecule Homo sapiens 70-74 21097707-4 2011 We hypothesized, therefore, that one-electron oxidation of etoposide by MPO to its phenoxyl radical is important for converting this anticancer drug to genotoxic and carcinogenic species in human CD34(+) myeloid progenitor cells. Etoposide 59-68 CD34 molecule Homo sapiens 196-200 21135858-5 2011 In fact, chronic exposure of human embryonic stem cells (hESCs) to etoposide induces MLL rearrangements and makes hESC more prone to acquire subsequent chromosomal abnormalities than postnatal CD34(+) cells, linking embryonic exposure to topoisomerase II inhibitors to genomic instability and MLL rearrangements. Etoposide 67-76 CD34 molecule Homo sapiens 193-197 21097707-0 2011 Myeloperoxidase-dependent oxidation of etoposide in human myeloid progenitor CD34+ cells. Etoposide 39-48 CD34 molecule Homo sapiens 77-81 21097707-5 2011 In the present study, using electron paramagnetic resonance spectroscopy, we provide conclusive evidence for MPO-dependent formation of etoposide phenoxyl radicals in growth factor-mobilized CD34(+) cells isolated from human umbilical cord blood and demonstrate that MPO-induced oxidation of etoposide is amplified in the presence of phenol. Etoposide 136-145 CD34 molecule Homo sapiens 191-195 21097707-7 2011 In separate studies, etoposide-induced DNA damage and MLL gene rearrangements were demonstrated to be dependent in part on MPO activity in CD34(+) cells. Etoposide 21-30 CD34 molecule Homo sapiens 139-143 21097707-8 2011 Together, our results are consistent with the idea that MPO-dependent oxidation of etoposide in human hematopoietic CD34(+) cells makes these cells especially prone to the induction of etoposide-related acute myeloid leukemia. Etoposide 83-92 CD34 molecule Homo sapiens 116-120 21097707-8 2011 Together, our results are consistent with the idea that MPO-dependent oxidation of etoposide in human hematopoietic CD34(+) cells makes these cells especially prone to the induction of etoposide-related acute myeloid leukemia. Etoposide 185-194 CD34 molecule Homo sapiens 116-120 20642818-1 2010 BACKGROUND: According to the different sensitivity of their bone marrow CD34+ cells to in vitro treatment with Etoposide or Mafosfamide, Acute Myeloid Leukaemia (AML) patients in apparent complete remission (CR) after chemotherapy induction may be classified into three groups: (i) normally responsive; (ii) chemoresistant; (iii) highly chemosensitive. Etoposide 111-120 CD34 molecule Homo sapiens 72-76