Schlagwort: cell
Harnessing the organization of the cell surface
Magnetic resonance imaging (MRI) and artificial intelligence (AI) can detect early signs of tumor cell death after novel therapy
Discovery of a Stem-like T cell in type 1 diabetes holds potential for improving cancer immunotherapy
The prostate cancer cell that got away
Toward ‚off-the-shelf’ immune cell therapy for cancer
Using T cells to target malignant brain tumors
New technique may lead to safer stem cell transplants
CRISPR screen identifies new anti-inflammatory drug target
Landmark study points to source of rapid aging, chronic inflammation in people living with HIV
High cell membrane tension constrains the spread of cancer
It takes cellular teamwork to heal the intestine
Uncovering how injury to the pancreas impacts cancer formation
Researchers target tumors with intracellular precision
The human immune system is an early riser
Molecular atlas of small cell lung cancer reveals unusual cell type that could explain why it’s so aggressive
Mito warriors: Scientists discover how T cell assassins reload their weapons to kill and kill again
Solving mystery of rare cancers directly caused by HIV
Break through the tumor’s protective shield
New way to image whole organisms in 3D brings key skin color pigment into focus
How high-fat diets allow cancer cells to go unnoticed
Discovery of mechanics of drug targets for COVID-19
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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Mitochondria and the evolutionary roots of cancer
Cancer is a group of almost 200 diseases that involve variety of changes in cell structure, morphology, and physiology. Cancer phenotype is underlying several alterations in cellular dynamics with three most critical features, which includes self-sufficiency in growth signals and insensitivity to inhibitory signals, evasion of programmed cell death and limitless replicative potential with a potential for the invasion of other organs. Cancer disease is widespread among metazoans. Some properties of cancer cells such as uncontrolled cell proliferation, lack of apoptosis, hypoxia, fermentative metabolism and free cell motility, i.e. metastasis, resemble a prokaryotic lifestyle, which leads to the assumption of a reversal like evolution from eucariotic back to proteobacterial state. This phenotype matches the phenotype of the last universal common ancestor (LUCA) that resulted from the endosymbiosis between archaebacteria and α-proteobacteria, which later became the mitochondria.
About metabolism of a carcinoma cell
Most cancer cells utilize aerobic glycolysis irrespective of their tissue of origin. The alteration from oxidative phosphorylation to glycolysis – called the Warburg effect – is an universal phenomen and has now become a diagnostic tool for cancer detection.
Variation in cancer risk among tissues can be explained by the number of stem cell divisions
Tomasetti and Vogelstein show that the lifetime risk of cancers of many different types is strongly correlated with the total number of divisions of the normal self-renewing cells maintaining that tissue’s homeostasis. These results suggest that only a third of the variation in cancer risk among tissues is attributable to environmental factors or inherited predispositions. The majority is due to bad luck, that is, random mutations arising during DNA replication in normal, noncancerous stem cells.