Cytogenetic and Molecular Biologic Alterations Associated with Anthracycline Resistance

1988 ◽  
pp. 259-276 ◽  
Author(s):  
JEFFREY M. TRENT ◽  
MARILYN L. SLOVAK ◽  
ANNA B. HILL ◽  
PAUL S. MELTZER ◽  
WILLIAM S. DALTON ◽  
...  
Keyword(s):  
Anthracycline Resistance

scholarly journals Chidamide increases the sensitivity of refractory or relapsed acute myeloid leukemia cells to anthracyclines via regulation of the HDAC3 -AKT-P21-CDK2 signaling pathway

2020 ◽  
Vol 39 (1) ◽  
Author(s):  
Hao Wang ◽  
Yu-chen Liu ◽  
Cheng-ying Zhu ◽  
Fei Yan ◽  
Meng-zhen Wang ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Signaling Pathway ◽  
Salvage Therapy ◽  
Myeloid Leukemia ◽  
Complete Response ◽  
Dependent Manner ◽  
Induce Cell Cycle Arrest ◽  
Anthracycline Resistance ◽  
Acute Myeloid ◽  
Resistant Cells

Abstract Background Induction therapy for acute myeloid leukemia (AML) is an anthracycline-based chemotherapy regimen. However, many patients experience a relapse or exhibit refractory disease (R/R). There is an urgent need for more effective regimens to reverse anthracycline resistance in these patients. Methods In this paper, Twenty-seven R/R AML patients with anthracycline resistance consecutively received chidamide in combination with anthracycline-based regimen as salvage therapy at the Chinese PLA General Hospital. Results Of the 27 patients who had received one course of salvage therapy, 13 achieved a complete response and 1 achieved a partial response. We found that the HDAC3-AKT-P21-CDK2 signaling pathway was significantly upregulated in anthracycline-resistant AML cells compared to non-resistant cells. AML patients with higher levels of HDAC3 had lower event-free survival (EFS) and overall survival (OS) rates. Moreover, anthracycline-resistant AML cells are susceptible to chidamide, a histone deacetylase inhibitor which can inhibit cell proliferation, increase cell apoptosis and induce cell-cycle arrest in a time- and dose-dependent manner. Chidamide increases the sensitivity of anthracycline-resistant cells to anthracycline drugs, and these effects are associated with the inhibition of the HDAC3-AKT-P21-CDK2 signaling pathway. Conclusion Chidamide can increase anthracycline drug sensitivity by inhibiting HDAC3-AKT-P21-CDK2 signaling pathway, thus demonstrating the potential for application.

Induction of 1C aldoketoreductases and other drug dose-dependent genes upon acquisition of anthracycline resistance

2009 ◽  
Vol 19 (6) ◽  
pp. 477-488 ◽  
Author(s):  
Zachary W. Veitch ◽  
Baoqing Guo ◽  
Stacey L. Hembruff ◽  
Adam J. Bewick ◽  
Allan D. Heibein ◽  
...  
Keyword(s):  
Drug Dose ◽  
Anthracycline Resistance ◽  
Dose Dependent

Anthracycline resistance mediated by reductive metabolism in cancer cells: The role of aldo-keto reductase 1C3

2014 ◽  
Vol 278 (3) ◽  
pp. 238-248 ◽  
Author(s):  
Jakub Hofman ◽  
Beata Malcekova ◽  
Adam Skarka ◽  
Eva Novotna ◽  
Vladimir Wsol
Keyword(s):  
Cancer Cells ◽  
Anthracycline Resistance ◽  
Reductive Metabolism

Lower Level of MAPK Expression Is Associated with Anthracycline Resistance and Decreased Survival in Patients with Hormone Receptor Negative Breast Cancer

2008 ◽  
Vol 26 (7) ◽  
pp. 671-679 ◽  
Author(s):  
Duygu Derin ◽  
Yesim Eralp ◽  
Yasemin Ozluk ◽  
Ekrem Yavuz ◽  
Nese Guney ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Hormone Receptor ◽  
Anthracycline Resistance
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