Year-end Sale % OFF 
Abstract
Introduction: Gene mutation is an infrequent cause of tumor suppressor gene (TSG) defect in de novo AML patients. Instead, it seems that leukemic cells employ epigenetic tricks to attenuate the negative impacts of intact TSGs. Ordinarily, critical TSGs, such as p16INK4A, is hyper-methylated in AML blasts under the impact of master epigenetic regulators, such as UHRF1. In this study, we investigated the correlation between UHRF1 and p16INK4A gene expression levels in newly diagnosed AML patients.
 Methods: Bone marrow and peripheral blood samples were obtained from 50 newly diagnosed AML patients and 18 healthy normal control subjects. Gene expression levels of UHRF1 and P16INK4A were surveyed using SYBR Green Quantitative Real-time PCR. Statistical analyses were done using SPSS statistical software 21.0.
 Results: P16INK4A gene expression showed reduced levels in 80.64% of patients above 45 years of age, while only 32% of patients below 45 years had reduced expression levels. The Spearman correlation test also demonstrated a significant negative correlation between UHRF1 and p16INK4A gene expression levels in AML patients, which was not observed in the control group (r=0.343 and P= 0.015).
 Conclusion: Regarding the age-related patterns of UHRF1 and p16INK4A gene expression, and also the presence of negative correlation between them, we conclude that UHRF1 may potentially be involved in p16INK4A down-regulation in elderly AML patients, which may subsequently facilitate the progression of AML in older ages.
Highlights
Gene mutation is an infrequent cause of tumor suppressor gene (TSG) defect in de novo Acute myelogenous leukemia (AML) patients
We investigated the correlation between UHRF1 and p16INK4A gene expression levels in newly diagnosed AML patients
Regarding the age-related patterns of UHRF1 and p16INK4A gene expression, and the presence of negative correlation between them, we conclude that UHRF1 may potentially be involved in p16INK4A down-regulation in elderly AML patients, which may subsequently facilitate the progression of AML in older ages
Summary
Gene mutation is an infrequent cause of tumor suppressor gene (TSG) defect in de novo AML patients. New studies are necessary for the determination of appropriate prognostic markers and effective treatment protocols In this regard, recent studies have implicated that epigenetic modifications play a causal role in the initiation and progression of cancer at least as frequently as mutation [4,5]. The expression of some TSGs is an age-dependent process and increases with aging, probably to prevent clonal expansion of cells that have sufficient number of tumorigenic mutations [11,12] In this regard, we studied the expression of p16INK4A, a tumor preventive gene, as it has this pattern of gene expression 13. Sub-clinical studies have shown that some demethylase agents, such as cladribine and clofarabine, en-
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
