Schlagwort: DNA
MCM-Moleküle begrenzen die Bildung von DNA-Schleifen
MCM molecules impede the formation of DNA loops
Gene deletion behind anomaly in blood cancer cells
Gene deletion behind anomaly in blood cancer cells
DNA discovery reveals a critical ‚accordion effect‘ for switching off genes
DNA discovery reveals a critical ‚accordion effect‘ for switching off genes
New pathway for DNA transfer discovered in tumor microenvironment
Chronologically young, biologically old: DNA linked to cancer survivors premature aging
Research advances understanding of DNA repair
Visualizing the invisible: New fluorescent DNA label reveals nanoscopic cancer features
RNA molecules control repair of human DNA in cancer cells
RNA ‘heroes’ can disarm bad-actor proteins in leukemia
Researchers identify key regulator of blood stem cell development
Ground-breaking study reveals dynamics of DNA replication ‘licensing’
Newly discovered DNA repair mechanisms point to potential therapy targets for cancer and neurodegenerative diseases
Research team identifies new mechanism for protecting DNA
Lymphoma: Key signaling pathway involved in tumor formation identified
Microorganism sheds new light on cancer resistance
New findings on the link between CRISPR gene-editing and mutated cancer cells
Cell-free DNA identifies early signs of relapse in pediatric medulloblastoma
Super-enhancers: The villain fueling certain cancers
Looking beyond DNA to see cancer with new clarity
Insights from our genome and epigenome will help prevent, diagnose and treat cancer
A global assessment of cancer genomic alterations in epigenetic mechanisms
Muhammad A Shah, Emily L Denton, Cheryl H Arrowsmith, Mathieu Lupien and Matthieu Schapira
Abstract
Background
The notion that epigenetic mechanisms may be central to cancer initiation and progression is supported by recent next-generation sequencing efforts revealing that genes involved in chromatin-mediated signaling are recurrently mutated in cancer patients.
Results
Here, we analyze mutational and transcriptional profiles from TCGA and the ICGC across a collection 441 chromatin factors and histones. Chromatin factors essential for rapid replication are frequently overexpressed, and those that maintain genome stability frequently mutated. We identify novel mutation hotspots such as K36M in histone H3.1, and uncover a general trend in which transcriptional profiles and somatic mutations in tumor samples favor increased transcriptionally repressive histone methylation, and defective chromatin remodeling.
Conclusions
This unbiased approach confirms previously published data, uncovers novel cancer-associated aberrations targeting epigenetic mechanisms, and justifies continued monitoring of chromatin-related alterations as a class, as more cancer types and distinct cancer stages are represented in cancer genomics data repositories.
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A Mitochondrial Paradigm of Metabolic and Degenerative Diseases, Aging, and Cancer: A Dawn for Evolutionary Medicine
Progressive increase in mtDNA 3243A>G heteroplasmy causes abrupt transcriptional reprogramming
Wallace hypothesized mitochondrial dysfunction as a central role in a wide range of age-related disorders and various forms of cancer. Steadily rising increases in mitochondrial DNA mutations cause abrupt shifts in diseases. Discrete changes in nuclear gene expression in response to small increases in DNA mutant level are analogous to the phase shifts that is well known in physics: As heat is added, the ice abruptly turns to water or with more heat abruptly to steam. Therefore, a quantitative change that is an increasing proportion of mitochondrial DNA mutation results in a qualitative change which coordinate changes in nuclear gene expression together with discrete changes in clinical symptoms.