PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 8289478-1 1994 BCR-ABL antisense oligonucleotides can specifically reduce colony formation of early hematopoietic progenitor cells from chronic myeloid leukemia (CML) patients. Oligonucleotides 18-34 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 0-7 8289478-7 1994 We detected a decrease in bcr-abl mRNA after 3 days of treatment with antisense oligonucleotides, but much less in controls. Oligonucleotides 80-96 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 26-33 8500581-7 1993 Experiments are underway to use this in vivo model to assess the antileukemic activity of BCR/ABL antisense oligonucleotides. Oligonucleotides 108-124 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 90-97 8329715-2 1993 Inhibition of bcr-abl gene expression may have profound effects on the cell biology of Ph1+ cells, as recent experiments with antisense oligonucleotides have shown. Oligonucleotides 136-152 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 14-21 23721517-3 2013 This QDs modified electrode has been utilized to serve as a transducer surface for covalent immobilization of chronic myelogenous leukemia (CML) specific probe oligonucleotide, designed from the BCR-ABL fusion gene. Oligonucleotides 160-175 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 195-202 8479075-12 1993 Lastly, the use of antisense oligonucleotides for the BCR-ABL junctions should result in the inhibition of growth of CML clone. Oligonucleotides 29-45 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 54-61 27457438-0 1990 Inhibition of P210BCR/ABL Expression in K562 Cells by Electroporation with an Antisense Oligonucleotide. Oligonucleotides 88-103 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 22-25 27457438-1 1990 We designed experiments to study the effects on P210BCR/ABL expression of introducing antisense oligonucleotides into K562 cells. Oligonucleotides 96-112 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 56-59 22772337-7 2012 Validating the hybridization-mediated multiplexed kinase assay, when three peptide substrate-oligonucleotide conjugates were mixed with the tyrosine kinase c-Abl and ATP, we readily observed their differential phosphorylation yet measured a common IC(50) for the Abl kinase inhibitor imatinib. Oligonucleotides 93-108 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 156-161 22647531-3 2012 This novel composite platform has been explored to fabricate an electrochemical DNA biosensor for detection of chronic myelogenous leukemia (CML) by immobilizing amine terminated oligonucleotide probe sequence containing 22 base pairs, identified from BCR-ABL fusion gene. Oligonucleotides 179-194 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 252-259 15631652-0 2004 [Identification bcr-abl fusion gene in leukemia cells with oligonucleotide microarray]. Oligonucleotides 59-74 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 16-23 17160016-2 2007 By oligonucleotide microarray hybridization of polysomal RNA of untreated and STI571-treated 32D-BCR/ABL cells, we identified the beta-chemokine CCL9 as a gene regulated by BCR/ABL in a tyrosine kinase-dependent manner. Oligonucleotides 3-18 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 173-180 17488685-0 2007 Characterization of ABL1 expression in adult T-cell acute lymphoblastic leukemia by oligonucleotide array analysis. Oligonucleotides 84-99 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 20-24 16891454-4 2006 In this work, we used locked nucleic acid (LNA)-modified oligonucleotides to silence BCR/ABL and reduce CML cell proliferation, as these oligonucleotides are resistant to nucleases and exhibit an exceptional affinity for cognate RNA. Oligonucleotides 57-73 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 85-92 15592617-0 2004 Synthesis of N3- and 2-NH2-substituted 6,7-diphenylpterins and their use as intermediates for the preparation of oligonucleotide conjugates designed to target photooxidative damage on single-stranded DNA representing the bcr-abl chimeric gene. Oligonucleotides 113-128 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 221-228 12661602-0 2002 Targeting of photooxidative damage on single-stranded DNA representing the bcr-abl chimeric gene using oligonucleotide-conjugates containing [Ru(phen)3](2+)-like photosensitiser groups. Oligonucleotides 103-118 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 75-82 10390076-5 1999 In oncohematology, a number of trials have been initiated with antisense oligonucleotides directed against molecular targets, including the bcl-2, c-myc, bcr-abl, c-myb or p53 oncogenes and tumor suppressor genes. Oligonucleotides 73-89 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 154-161 10583226-13 1999 Transfection of K-562 cells with antisense oligonucleotides directed against bcr-abl caused a specific suppression of K-562 clonogenicity. Oligonucleotides 43-59 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 77-84 10583226-17 1999 Transfection with bcr-abl directed antisense oligonucleotides reduces the clonogenicity of K-562 cells. Oligonucleotides 45-61 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 18-25 10419896-7 1999 BCR-ABL peptide-specific T-cell clones did respond to autologous EBV cells transfected with invariant chain (li) cDNA in which the HLA class II-associated invariant chain peptide (CLIP) was replaced by a BCR-ABL b2a2 fusion oligonucleotide sequence, illustrating the potential of these T cells to recognize an endogenous BCR-ABL(b2a2) ligand. Oligonucleotides 224-239 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 0-7 10099134-2 1999 Various attempts to design antisense oligonucleotides that specifically cleave abnormal L6 BCR-ABL fusion mRNA have not been successful. Oligonucleotides 37-53 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 91-98 8649049-4 1996 The role and contribution of apoptosis in the progression of CML and the possible role of antisense oligonucleotides to the bcr-abl gene as therapeutic agents is discussed. Oligonucleotides 100-116 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 124-131 9639422-1 1998 Downregulation of bcr-abl expression in the chronic myelogenous leukemia cell line K562 using antisense oligonucleotides has been shown to enhance the sensitivity of the cells to apoptotic stimuli, suggesting that p210 bcr-abl, like bcl-2 functions as an anti-apoptosis factor (McGahon A et al, Blood 1994, 83: 1179). Oligonucleotides 104-120 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 18-25 8709619-3 1996 We have studied the mechanism of action of bcr-abl in chronic myeloid leukemia (CML) by inhibiting its expression using antisense oligonucleotides. Oligonucleotides 130-146 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 43-50 9558345-6 1998 The c-Abl DNA-binding domain recognizes specific sequences and interacts with deformed DNA structures such as four-way junctions and bubble DNA containing a large single-stranded loop, as determined by electromobility shift assay, melting temperature studies, and binding to specific oligonucleotides covalently linked to beads. Oligonucleotides 284-300 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 4-9 9525737-5 1998 Treatment with antisense oligonucleotides directed to bcr decreased the expression of the ectopic bcr - abl and restored susceptibility to apoptosis. Oligonucleotides 25-41 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 98-107 9029029-1 1997 The specificity of antisense oligonucleotides targeted to the mRNA breakpoint region of the Bcr-Abl oncogene, found in leukaemic cells from patients with chronic myeloid leukaemia, remains controversial due to non-specific effects. Oligonucleotides 29-45 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 92-99 9029029-3 1997 Growth of chronic myeloid leukaemia (CML) cell lines BV173, KCL-22 and cells of CML patients tested was inhibited by the b2a2 type antisense Bcr-Abl oligonucleotide and not with controls. Oligonucleotides 149-164 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 141-148 9029029-5 1997 Bcr-Abl protein studies in combination with growth-determination experiments indicated that the antisense methylphosphonate Bcr-Abl oligonucleotide tested is a potent inhibitor of the growth of CML cells but works in a non-antisense manner. Oligonucleotides 132-147 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 0-7 9029029-5 1997 Bcr-Abl protein studies in combination with growth-determination experiments indicated that the antisense methylphosphonate Bcr-Abl oligonucleotide tested is a potent inhibitor of the growth of CML cells but works in a non-antisense manner. Oligonucleotides 132-147 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 124-131 8798460-3 1996 Instead, oligonucleotides with runs of A/T sequences were isolated, and purified c-Abl was shown to bind A/T-containing oligonucleotides better than those without A/T sequences. Oligonucleotides 9-25 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 81-86 8798460-3 1996 Instead, oligonucleotides with runs of A/T sequences were isolated, and purified c-Abl was shown to bind A/T-containing oligonucleotides better than those without A/T sequences. Oligonucleotides 120-136 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 81-86 8798460-4 1996 DNA binding of c-Abl was dependent on three high mobility group 1-like boxes (HLBs), which bound cooperatively to the A/T-rich oligonucleotides. Oligonucleotides 127-143 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 15-20 8798460-9 1996 Interestingly, the HLBs of c-Abl bound better to the oligonucleotide containing the bubble, suggesting a higher affinity for bent DNA rather than A/T sequences per se. Oligonucleotides 53-68 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 27-32 7579442-8 1995 Exposure to antisense oligonucleotides specifically inhibited the accumulation of c-abl mRNA in CD34+ cells. Oligonucleotides 22-38 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 82-87 8590842-1 1995 Antisense oligonucleotides were used to determine the role of the BCR-ABL gene in the proliferation of chronic myeloid leukaemia (CML) clonogenic cells. Oligonucleotides 10-26 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 66-73 7545682-7 1995 However, down-regulation of Bcr-Abl protein levels in K562.Fas cells using antisense oligonucleotides targeted to bcr-abl mRNA rendered these cells highly susceptible to Fas-induced death. Oligonucleotides 85-101 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 28-35 7545682-7 1995 However, down-regulation of Bcr-Abl protein levels in K562.Fas cells using antisense oligonucleotides targeted to bcr-abl mRNA rendered these cells highly susceptible to Fas-induced death. Oligonucleotides 85-101 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 114-121 7524739-11 1994 The direct implication of BCR-ABL was further documented (1) by studies of alpha-interferon-treated patients with a chimerism in which the abnormal growth correlates with the presence of the malignant clone and (2) by the use of antisense oligonucleotide against BCR-ABL transcript, which abrogated this abnormal growth. Oligonucleotides 239-254 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 26-33 8161775-5 1994 We found that BCR-ABL expression inappropriately prolongs the growth factor-independent survival of CML myeloid progenitors and granulocytes by inhibiting apoptosis, a genetically programmed process of active cell death; inhibition of BCR-ABL expression by antisense oligonucleotides reversed the suppression of apoptosis as well as the enhancement of survival. Oligonucleotides 267-283 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 14-21 8118022-4 1994 Expression of a temperature sensitive v-Abl protein reverses the effects of the antisense oligonucleotides, such that the cells remain resistant to apoptosis at the permissive temperature. Oligonucleotides 90-106 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 38-43 8063271-9 1994 Selective inhibition of this proto-oncogene and of the abl-bcr oncogene have been achieved by using of c-abl sequence specific antisense oligonucleotides; this approach sheds new light on the function of this gene in CML. Oligonucleotides 137-153 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 55-58 8063271-9 1994 Selective inhibition of this proto-oncogene and of the abl-bcr oncogene have been achieved by using of c-abl sequence specific antisense oligonucleotides; this approach sheds new light on the function of this gene in CML. Oligonucleotides 137-153 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 103-108 8542954-0 1995 Inhibition of chronic myelogenous leukemia cells harboring a BCR-ABL B3A2 junction by antisense oligonucleotides targeted at the B2A2 junction. Oligonucleotides 96-112 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 61-68 8542954-3 1995 As the BCR-ABL rearrangement is specific to leukemic cells, selective inhibition of leukemic cell growth by BCR-ABL antisense oligonucleotides (ASO) has been reported in vitro for CML patients and cell lines. Oligonucleotides 126-142 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 7-14 8542954-3 1995 As the BCR-ABL rearrangement is specific to leukemic cells, selective inhibition of leukemic cell growth by BCR-ABL antisense oligonucleotides (ASO) has been reported in vitro for CML patients and cell lines. Oligonucleotides 126-142 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 108-115 8535187-5 1995 This resistance can be overcome with the use of appropriate antisense oligonucleotides to the bcr-abl gene. Oligonucleotides 70-86 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 94-101 7812014-0 1995 Specificity of BCR-ABL antisense oligonucleotides. Oligonucleotides 33-49 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 15-22 7845006-0 1995 Phosphorothioate BCR-ABL antisense oligonucleotides induce cell death, but fail to reduce cellular bcr-abl protein levels. Oligonucleotides 35-51 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 17-24 8207957-0 1994 Capping of bcr-abl antisense oligonucleotides enhances antiproliferative activity against chronic myeloid leukemia cell lines. Oligonucleotides 29-45 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 11-18 8207957-3 1994 We have found antisense phosphodiester oligonucleotides directed at the bcr-abl junction to be ineffective in inhibiting the growth of CML cell lines. Oligonucleotides 39-55 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 72-79