Results 91 to 100 of about 509,494 (205)

Therapy of Acute Myeloid Leukemia

open access: yesCancer Control, 2001
The Eastern Cooperative Oncology Group (ECOG) has recently reviewed the outcome for more than 1,400 patients with previously untreated AML entered on five successive clinical trials.5,6 Each trial included daunorubicin and cytarabine for induction.
openaire   +2 more sources

Chidamide and cytarabine synergistically treat acute myeloid leukemia: inhibiting ribosome biogenesis via the MYC-RRP9 pathway

open access: yesCell Death and Disease
This study explores innovative therapeutic approaches for acute myeloid leukemia by examining the synergistic effects of the histone deacetylase inhibitor chidamide in combination with cytarabine. In both in vitro and in vivo models, the drug combination
Qing Li   +13 more
doaj   +1 more source

MicroRNA let-7a-3 gene methylation is associated with karyotyping, CEBPA promoter methylation, and survival in acute myeloid leukemia

open access: yes, 2017
Let-7a-3 transcribes the miRNA let-7a, of which the expression is dysregulated in cancer. We evaluated the significance of let-7a-3 gene methylation in patients with de novo acute myeloid leukemia (AML).
Ko, Ya-Chen;Fang, Woei-Horng;Lin, Tsung-Chin;Hou, Hsin-An;Chen, Chien-Yuan;Tien, Hwei-Fang;Lin, Liang-In   +1 more
core   +1 more source

Epigenetic remodeling via HDAC6 inhibition amplifies anti-tumoral immune responses in myeloid leukemia cells

open access: yesCell Death and Disease
Histone deacetylase 6 (HDAC6) has emerged as a promising therapeutic target in cancer due to its immunomodulatory effects. While its prognostic significance remains debated, we demonstrate that HDAC6 loss significantly impairs myeloid leukemia ...
Julian Schliehe-Diecks   +19 more
doaj   +1 more source

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

open access: yes, 2003
Overexpression of proto-oncogene c-jun and constitutive activation of the Jun NH2-terminal kinase (JNK) signaling pathway have been implicated in the leukemic transformation process.
Elsaesser, Annika
core  

Detection of BCR-ABL kinase domain mutations in CD34+ cells from newly diagnosed chronic phase CML patients and their association with imatinib resistance [PDF]

open access: yes, 2011
BCR-ABL kinase domain (KD) mutations, the most common cause of imatinib resistance, are infrequently detected in newly diagnosed chronic-phase chronic myeloid leukemia (CP-CML) patients.
Riaz ul-Haq   +19 more
core  

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