Decitabine in combination with low-dose cytarabine, aclarubicin and G-CSF tends to improve prognosis in elderly patients with high-risk AML.

Aging (Albany NY)

Department of Hematology, The First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital, Nanjing 210029, Jiangsu Province, China.

Published: April 2020

We evaluated the risk status and survival outcomes of 125 elderly acute myeloid leukemia (AML) patients treated with decitabine in combination with low-dose cytarabine, aclarubicin, and G-CSF (D-CAG). The risk status was evaluated by determining the frequency of recurring gene mutations using next-generation sequencing (NGS) analysis of 23 selected genes and cytogenetic profiling of bone marrow samples at diagnosis. After a median follow-up of 12 months (range: 2-82 months), 86 patients (68.8%) had achieved complete remission after one cycle of induction, and 94 patients (75.2%) had achieved it after two cycles. The median overall survival (OS) and disease-free survival (DFS) were 16 and 12 months, respectively. In 21 AML patients aged above 75 years, the median OS and DFS were longer in the low- and intermediate-risk group than the high-risk group, but the differences were not statistically significant. The median OS and DFS were similar in patients with or without , , and mutations. Multivariate analysis showed that patient age above 75 years, high-risk status, and genetic anomalies, like deletions in chromosomes 5 and/or 7, were significant variables in predicting OS. D-CAG regimen tends to improve the prognosis of a subgroup of elderly patients with high-risk AML.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7185116PMC
http://dx.doi.org/10.18632/aging.102973DOI Listing

Publication Analysis

Top Keywords

decitabine combination
8
combination low-dose
8
low-dose cytarabine
8
cytarabine aclarubicin
8
aclarubicin g-csf
8
improve prognosis
8
elderly patients
8
patients high-risk
8
high-risk aml
8
risk status
8

Similar Publications

Treating Hematological Malignancies With OR-2100, an Orally Bioavailable Prodrug of Decitabine.

Cancer Sci

January 2025

Department of Drug Discovery and Biomedical Sciences, Faculty of Medicine, Saga University, Saga, Japan.

DNA methylation is an enzyme-driven epigenetic modification that must be precisely regulated to maintain cellular homeostasis. Aberrant methylation status, especially hypermethylation of the promoter sites of tumor-suppressor genes, is observed in human malignancies and is a proven target for cancer therapy. The first-generation DNA demethylating agents, azacitidine and decitabine, are widely used for treating several hematological malignancies.

View Article and Find Full Text PDF

Triple-negative breast cancer (TNBC) is recognized as the most aggressive subtype of breast cancer. Epigenetic silencing, such as DNA methylation mediated by DNA methyltransferases (DNMTs) plays key roles in TNBC tumorigenesis. Hypomethylating agents (HMAs) such as azacitidine, decitabine, and guadecitabine are key inhibitors of DNMTs, and accumulating evidence has shown their immunogenicity properties.

View Article and Find Full Text PDF

Background: Poly (ADP-Ribose) polymerase inhibitors are approved for treatment of tumors with BRCA1/2 and other homologous recombination repair (HRR) mutations. However, clinical responses are often not durable and treatment may be detrimental in advanced cancer due to excessive toxicities. Thus we are seeking alternative therapeutics to enhance PARP-directed outcomes.

View Article and Find Full Text PDF

Cadmium (Cd) is a widely available metal that has been found to have a role in causing nonalcoholic fatty liver disease (NAFLD). However, the detailed toxicological targets and mechanisms by which Cd causes NAFLD are unknown. Therefore, the present work aims to reveal the main targets of action, cellular processes, and molecular pathways by which cadmium causes NAFLD.

View Article and Find Full Text PDF

Epigenetic dysregulation is a common feature of cancer. Promoter demethylation of tumor-promoting genes and global DNA hypomethylation may trigger tumor progression. Epigenetic changes are unstable; thus, research has focused on detecting remedies that target epigenetic regulators.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!