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ONC213: a novel strategy to resensitize resistant AML cells to venetoclax through induction of mitochondrial stress.
J Exp Clin Cancer Res
January 2025
Cancer Biology Graduate Program, Wayne State University School of Medicine, Detroit, MI, 48201, USA.
Background: Venetoclax + azacitidine is a frontline treatment for older adult acute myeloid leukemia (AML) patients and a salvage therapy for relapsed/refractory patients who have been treated with intensive chemotherapy. While this is an important treatment option, many patients fail to achieve complete remission and of those that do, majority relapse. Leukemia stem cells (LSCs) are believed to be responsible for AML relapse and can be targeted through oxidative phosphorylation reduction.
View Article and Find Full Text PDFmiR-198 targets : implications for oral squamous cell carcinoma pathogenesis.
Front Oncol
December 2024
Department of Developmental Biology and Genetics, Indian Institute of Science, Bangalore, India.
Background: miRNAs play a critical role in the progression of various diseases, including oral squamous cell carcinoma (OSCC), which represents a major health concern and is one of the leading causes for new cancer cases worldwide. The miRNA dysregulation causes havoc and could be attributed to various factors, with epigenetic silencing of tumor suppressor genes being a major contributor to tumorigenesis. In this study, we have explored the tumor suppressive role of miR-198 in OSCC.
View Article and Find Full Text PDFMaternal high-fat diet orchestrates offspring hepatic cholesterol metabolism via MEF2A hypermethylation-mediated CYP7A1 suppression.
Cell Mol Biol Lett
December 2024
Department of Endocrinology, Peking University First Hospital, No. 8 Xishiku Ave, Xicheng, Beijing, 100034, People's Republic of China.
Background: Maternal overnutrition, prevalent among women of childbearing age, significantly impacts offspring health throughout their lifetime. While DNA methylation of metabolic-related genes mediates the transmission of detrimental effects from maternal high-fat diet (HFD), its role in programming hepatic cholesterol metabolism in offspring, particularly during weaning, remains elusive.
Methods: Female C57BL/6 J mice were administered a HFD or control diet, before and during, gestation and lactation.
Ascorbic Acid Ameliorates Molecular and Developmental Defects in Human-Induced Pluripotent Stem Cell and Cerebral Organoid Models of Fragile X Syndrome.
Int J Mol Sci
November 2024
Department of Biomedicine, University of Basel, Mattenstrasse 28, 4058 Basel, Switzerland.
Fragile X Syndrome (FX) is the most common form of inherited cognitive impairment and falls under the broader category of Autism Spectrum Disorders (ASD). FX is caused by a CGG trinucleotide repeat expansion in the non-coding region of the X-linked () gene, leading to its hypermethylation and epigenetic silencing. Animal models of FX rely on the deletion of the gene, which fails to replicate the epigenetic silencing mechanism of the gene observed in human patients.
View Article and Find Full Text PDFEffects of Hypomethylating Agents on Gene Modulation in the Leukemic Microenvironment and Disease Trajectory in a Mouse Model of AML.
bioRxiv
December 2024
Department of Immuno-Oncology, Beckman Research Institute of the City of Hope, Duarte, CA 91010, USA.
Hypomethylating agents (HMAs), such as decitabine and 5-azacytidine (AZA), are valuable treatment options for patients with acute myeloid leukemia that are ineligible for intensive chemotherapy. Despite providing significant extensions in survival when used alone or in combination, eventual relapse and resistance to HMAs are observed. The mechanisms leading to these outcomes are still not well defined and may, in part, be due to a focus on leukemic populations with limited information on the effects of HMAs on non-leukemic cells in the blood and other tissue compartments.
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