about
Identification of spectral modifications occurring during reprogramming of somatic cellsAHI-1 interacts with BCR-ABL and modulates BCR-ABL transforming activity and imatinib response of CML stem/progenitor cellsAmniotic fluid-derived mesenchymal stem cells prevent fibrosis and preserve renal function in a preclinical porcine model of kidney transplantation.Comprehensive characterization of a novel intronic pseudo-exon inserted within an e14/a2 BCR-ABL rearrangement in a patient with chronic myeloid leukemiaMicro-RNA response to imatinib mesylate in patients with chronic myeloid leukemiaProperties of CD34+ CML stem/progenitor cells that correlate with different clinical responses to imatinib mesylateThe HOXB4 homeoprotein promotes the ex vivo enrichment of functional human embryonic stem cell-derived NK cellsHodgkin's disease primarily involving the oropharynx: case report and review of the literature.Chronic myeloid leukemia stem cells in the era of targeted therapies: resistance, persistence and long-term dormancy.Tyrosine kinase inhibitor AG1024 exerts antileukaemic effects on STI571-resistant Bcr-Abl expressing cells and decreases AKT phosphorylation.Targeting primitive chronic myeloid leukemia cells by effective inhibition of a new AHI-1-BCR-ABL-JAK2 complex.Reversing clonality in leukemia.Non integrative strategy decreases chromosome instability and improves endogenous pluripotency genes reactivation in porcine induced pluripotent-like stem cellsMolecular analysis of clonality in Kaposi's sarcoma.Generation of an induced pluripotent stem cell line from a patient with chronic myeloid leukemia (CML) resistant to targeted therapies.Generation of an induced pluripotent stem cell line from a patient with hereditary multiple endocrine neoplasia 2A (MEN2A) syndrome with RET mutation.The downregulation of BAP1 expression by BCR-ABL reduces the stability of BRCA1 in chronic myeloid leukemia.Morphological analysis of human induced pluripotent stem cells during induced differentiation and reverse programming.Generation of multipotent early lymphoid progenitors from human embryonic stem cells.Biological effects of T315I-mutated BCR-ABL in an embryonic stem cell-derived hematopoiesis model.Toxicity and phototoxicity of Hypocrellin A on malignant human cell lines, evidence of a synergistic action of photodynamic therapy with Imatinib mesylate.Tyrosine phosphorylation of SHIP promotes its proteasomal degradation.A mesenchymal glioma stem cell profile is related to clinical outcome.Altered IFNgamma signaling and preserved susceptibility to activated natural killer cell-mediated lysis of BCR/ABL targets.p210BCR-ABL inhibits SDF-1 chemotactic response via alteration of CXCR4 signaling and down-regulation of CXCR4 expression.Mesenchymal cells generated from patients with myelodysplastic syndromes are devoid of chromosomal clonal markers and support short- and long-term hematopoiesis in vitro.Biological effects induced by variable levels of BCR-ABL protein in the pluripotent hematopoietic cell line UT-7.The leukaemic oncoproteins Bcr-Abl and Tel-Abl (ETV6/Abl) have altered substrate preferences and activate similar intracellular signalling pathways.BCR-ABL and constitutively active erythropoietin receptor (cEpoR) activate distinct mechanisms for growth factor-independence and inhibition of apoptosis in Ba/F3 cell line.BCR-ABL does not prevent apoptotic death induced by human natural killer or lymphokine-activated killer cells.Targeting BCR-ABL+ stem/progenitor cells and BCR-ABL-T315I mutant cells by effective inhibition of the BCR-ABL-Tyr177-GRB2 complex.Modeling the influence of stromal microenvironment in the selection of ENU-induced BCR-ABL1 mutants by tyrosine kinase inhibitors.Leukemic stem cell persistence in chronic myeloid leukemia patients in deep molecular response induced by tyrosine kinase inhibitors and the impact of therapy discontinuationGeneration of an induced pluripotent stem cell (iPSC) line from a patient with maturity-onset diabetes of the young type 13 (MODY13) with a the potassium inwardly-rectifying channel, subfamily J, member 11 (KCNJ11) mutation.Differential contributions of STAT5A and STAT5B to stress protection and tyrosine kinase inhibitor resistance of chronic myeloid leukemia stem/progenitor cells.Long-term follow-up of subtotal splenectomy for hereditary spherocytosis: a single-center study.Reversible lymph node follicular hyperplasia associated with dasatinib treatment of chronic myeloid leukemia in chronic phase.Constitutive and specific activation of STAT3 by BCR-ABL in embryonic stem cells.Loss of major molecular response as a trigger for restarting tyrosine kinase inhibitor therapy in patients with chronic-phase chronic myelogenous leukemia who have stopped imatinib after durable undetectable disease.[Imatinib mesylate: a major breakthrough in the treatment of chronic myelogenous leukemia].
P50
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P50
description
onderzoeker
@nl
researcher, ORCID id # 0000-0002-4861-0137
@en
name
Ali G Turhan
@ast
Ali G Turhan
@en
Ali G Turhan
@nl
type
label
Ali G Turhan
@ast
Ali G Turhan
@en
Ali G Turhan
@nl
prefLabel
Ali G Turhan
@ast
Ali G Turhan
@en
Ali G Turhan
@nl
P106
P31
P496
0000-0002-4861-0137