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Showing 1 to 9 of 9 for “"AML1/ETO"”.

  1. AML1/ETO Downregulates the Transcription Factor PU.1 in Acute Myeloid Leukemia

    AML1-ETO is a fusion protein encoded by the translocation t(8;21) and found in 15% of acute myeloid leukemia patients. Here, we report a negative functional impact of AML1-ETO on the transcriptional activity of PU.1, an important transcription factor for normal myeloid differentiation. We have …

    lmu-germany Repository record for AML1/ETO Downregulates the Transcription Factor PU.1 in Acute Myeloid Leukemia (opens in a new tab)

  2. Proto-oncogene c-jun expression is induced by AML1-ETO in a JNK dependent manner:possible role in the pathogenesis of acute myeloid leukemia

    … AML-associated translocation and results in the AML1-ETO fusion protein. Overexpression of AML1-ETO in NIH3T3 cells leads to increased phosphorylation of Ser63 in c-Jun, which is generally JNK dependent. The role of the JNK signaling pathway for the functional properties of AML1-ETO is, however, …

    lmu-germany Repository record for Proto-oncogene c-jun expression is induced by AML1-ETO in a JNK dependent manner:possible role in the pathogenesis of acute myeloid leukemia (opens in a new tab)

  3. Characterisation of the leukaemia-associated ETO homologues

    … in the expression of the chimeric protein AML1-ETO. AML1 is a transcription factor of crucial importance during hematopoiesis. The function of the fusion partner eight-twenty-one (ETO) is much less understood. The aim of this thesis was to characterise ETO and its two homologues, myeloid …

    lund Repository record for Characterisation of the leukaemia-associated ETO homologues (opens in a new tab)

  4. The role of the leukemia-associated ETO homologue repressors in hematopoiesis

    The fusion protein AML1-ETO is observed in acute myeloid patients with the chromosomal translocation t(8;21). Cells with this chimeric protein have impaired granulocytic and erythroid differentiation with accumulation of myeloblasts. The transcriptional co-repressor ETO (Eight Twenty One) was …

    lund Repository record for The role of the leukemia-associated ETO homologue repressors in hematopoiesis (opens in a new tab)

  5. Characterization of chromosomal abnormalities in acute myeloid leukaemia patients at the university teaching hospital, Lusaka, Zambia

    … 4 genetic abnormalities, PML/RARα for t(15;17), AML1/ETO for t(8;21), CBFβ/MYH11 for inv(16)/t(16;16) and rearrangements of the MLL gene for 11q23 abnormalities. AML was classified using the new World Health Organization (WHO) classification for haematologic malignancies. The techniques used were …

    zimbabwe Repository record for Characterization of chromosomal abnormalities in acute myeloid leukaemia patients at the university teaching hospital, Lusaka, Zambia (opens in a new tab)

  6. Characterization of chromosomal abnormalities in acute myeloid leukaemia patients at the university teaching hospital, Lusaka, Zambia

    … 4 genetic abnormalities, PML/RARα for t(15;17), AML1/ETO for t(8;21), CBFβ/MYH11 for inv(16)/t(16;16) and rearrangements of the MLL gene for 11q23 abnormalities. AML was classified using the new World Health Organization (WHO) classification for haematologic malignancies. The techniques used were …

    zambia Repository record for Characterization of chromosomal abnormalities in acute myeloid leukaemia patients at the university teaching hospital, Lusaka, Zambia (opens in a new tab)

  7. Nachweis zytogenetischer Aberrationen nach Chemotherapie zur diagnostischen Früherkennung therapieassoziierter hämatologischer Neoplasien

    … bzw. ihrer jeweiligen Fusionstranskripte t(8;21)/AML1/ETO, inv(16)/CBFB-MYH11, t(15;17)/PML-RARα und t(9;22)/BCR-ABL in 42 Leukapheresaten (33 Patienten mit NHL und 9 gesunde Spender) mittels konventioneller und Real-Time-PCR untersucht. Weder die Translokationen t(8;21), inv(16) noch t(9;22) …

    goettingen Repository record for Nachweis zytogenetischer Aberrationen nach Chemotherapie zur diagnostischen Früherkennung therapieassoziierter hämatologischer Neoplasien (opens in a new tab)

  8. Analysis of senescence-like growth arrest induced by RUNX1 and its fusion derived oncoproteins

    … in the truncated C-terminal fusion protein RUNX1-ETO (AML1-ETO). The potential to drive senescence is retained by the deletion mutant RUNX1-ETO[]469 which lacks critical corepressor binding sites suggesting that the repression of target genes may be a primary mechanism implicated in RUNX1-ETO

    glasgow Repository record for Analysis of senescence-like growth arrest induced by RUNX1 and its fusion derived oncoproteins (opens in a new tab)