Schlagwort: cancer cells
Novel hydrogel carriers for anti-cancer drugs offer new hope for cancer treatment
Bespoke neuroblastoma therapy weaponizes cell metabolism
Protein rewires metabolism to block cancer cell death, may allow cancer spread
A clue to how some fast-growing tumors hide in plain sight
New strategy for fighting brain cancer
Image analysis based on machine learning reliably identifies haematological malignancies
Pancreatic cancer tumors use multiple mechanisms to avoid starvation: new target for treatment?
Cancer cells may evade chemotherapy by going dormant
RNA editing protein ADAR1 protects telomeres and supports proliferation in cancer cells
New inhibitor found to combat drug-resistant cancer cells
Switching Off the „Survival Protein“ for Cancer Cells
Retracing the history of the mutation that gave rise to cancer decades later
Single cell sequencing opens new avenues for eradicating leukemia at its source
Sulfur metabolism may have paved the way for evolution of multicellularity
Proton therapy induces biologic response to attack treatment-resistant cancers
It takes two to tango: When cells interact
Ionic liquid uniformly delivers chemotherapy to tumors while destroying cancerous tissue
Stirring up Conflicts in Tumour Cells
How cells recycle the machinery that drives their motility?
Injection to treat skin cancer developed
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.
Implications of quantum metabolism and natural selection for the origin of cancer cells and tumor progression
Energy transfer in material solids is driven primarily by differences in intensive thermodynamic quantities such as pressure and temperature. The crucial observation in quantum-theoretical models was the consideration of the heat capacity as associated with the vibrations of atoms in a crystalline solid. However, living organisms are essentially isothermal. Because of very little differences in temperature between different parts of a cell it is assumed that energy flow in living organisms is mediated by differences in the turnover time of various metabolic processes in the cell, which occur in cyclical fashion. It has been shown that the cycle time of these metabolic processes is related to the metabolic rate, that is the rate at which the organism transforms the free energy of whatever source into metabolic work, maintenance of constant temperature and structuraland functional organization of the cells. Quantum Metabolism exploits the methodology of the quantum theory of solids to provide a molecular level which derives new rules relating metabolic rate and body size.
Einstein A (1920), Schallausbreitung in teilweise dissozieirten Gasen
Einstein A (1924) Quantentheorie des einatomigen, idealen Gases