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http://dx.doi.org/10.1093/hmg/ddaa207 | DOI Listing |
Int J Cancer
January 2025
Princess Margaret Cancer Centre, University Health Network, Toronto, Canada.
Prostate cancer is a common malignancy that in 5%-30% leads to treatment-resistant and highly aggressive disease. Metastasis-potential and treatment-resistance is thought to rely on increased plasticity of the cancer cells-a mechanism whereby cancer cells alter their identity to adapt to changing environments or therapeutic pressures to create cellular heterogeneity. To understand the molecular basis of this plasticity, genomic studies have uncovered genetic variants to capture clonal heterogeneity of primary tumors and metastases.
View Article and Find Full Text PDFHemasphere
January 2025
Université Paris Cité, Institut Cochin, INSERM U1016, CNRS UMR8104 Assistance Publique-Hôpitaux de Paris.Centre, Laboratory of Hematology, Hôpital Cochin Paris France.
Lower risk (LR) myelodysplastic syndromes (MDS) are heterogeneous hematopoietic stem and progenitor disorders caused by the accumulation of somatic mutations in various genes including epigenetic regulators that may produce convergent DNA methylation patterns driving specific gene expression profiles. The integration of genomic, epigenomic, and transcriptomic profiling has the potential to spotlight distinct LR-MDS categories on the basis of pathophysiological mechanisms. We performed a comprehensive study of somatic mutations and DNA methylation in a large and clinically well-annotated cohort of treatment-naive patients with LR-MDS at diagnosis from the EUMDS registry (ClinicalTrials.
View Article and Find Full Text PDFBMC Biol
January 2025
Division of Molecular Genome Analysis, German Cancer Research Center (DKFZ), Im Neuenheimer Feld 580, Heidelberg, 69120, Germany.
Background: Breast cancer is the leading cause of cancer-related mortality in women. Deregulation of miRNAs is frequently observed in breast cancer and affects tumor biology. A pre-miRNA, such as pre-miR-1307, gives rise to several mature miRNA molecules with distinct functions.
View Article and Find Full Text PDFBMC Cancer
January 2025
Department of Radiation Oncology, Xiamen Cancer Center, Xiamen Key Laboratory of Radiation Oncology, School of Medicine, The First Affiliated Hospital of Xiamen University, Xiamen University, Xiamen, China.
Background: Genome-wide association studies (GWAS) provide a powerful method for identifying the loci and genes that contribute to disease. However, in many cases, the specific cell types and states that confer disease risk through these genes remain unknown. Determining this relationship is crucial for identifying pathogenic processes and developing therapeutic strategies.
View Article and Find Full Text PDFJ Xenobiot
December 2024
Amity Institute of Biotechnology, Amity University Rajasthan, Jaipur 303002, India.
Addressing the consequences of exposure to endocrine-disrupting chemicals (EDCs) demands thorough research and elucidation of the mechanism by which EDCs negatively impact women and lead to breast cancer (BC). Endocrine disruptors can affect major pathways through various means, including histone modifications, the erroneous expression of microRNA (miRNA), DNA methylation, and epigenetic modifications. However, it is still uncertain if the epigenetic modifications triggered by EDCs can help predict negative outcomes.
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