D.I.Y. Treatment of Cancer

The cancer cells are different from normal human body cells. The scientists advocating the Somatic Mutation Theory speculated that cancer is caused when mutations have caused the Human Genome of the human body-cells to be changed into the Cancer Genomes of the cancer cells. There is, however, no good reason to assume that mutations of the Human Genome would cause the cancer cells to grow and replicate out of control. There is, in fact, no good evidence indicating that there has ever been such mutations, or that cancer cells had been human body cells before they are changed by mutations into cancer cells. Perhaps cancer cells have always been cancer cells, but some cancer cells have not been inherited by the offsprings from their ancestors.Some of us believe that the difference between Human and cancer cells have resulted from the difference of their inherently different genomes, and have not resulted from changes, or mutations. The evolution of the eukaryote genomes and the evolution of the Cancer Genomes during the course of Earth’s history have followed parallel paths of evolution that indicate adaptations of the metabolic modes in response to the ever-increasing oxygenation of the Earth’s atmosphere during the past few billion years. Compared to that of the Human Genome of the human body cells, the cancer cells have genomes that indicate a retarded development in the evolution of the metabolisms. When the Human genome encodes a progressive mode of OXPHOS, the cancer genomes may still encode the anammox mode of metabolism.We cannot deny an assumption that cancer cells have inherited evolving cancer genomes that encode different metabolic modes, while their hallmark is the uncontrolled cell-growth and replications. |We have good evidence that cancer genomes have also evolved to encode progressively different metabolic modes. Chinese medical scientists have found, for example, a wealth of evidence that some forms of cancer may have been caused by the nitrite pollution of the public water supply. China’s Deep Standardized Well Water (DSWW) Program of substituting nitrite-free deep groundwaters as the source of public water supply was partially successful. Local cancer-mortality rates were reduced by half at places where there had been such substitutions. Nitrite, as a reducing agent, could be the indispensable chemical in our food or drink intakes that could render the interior of cancer cells anaerobic. Nitrite, as an oxidation agent, could then be the substrate of the metabolic reaction anaerobic ammonium oxidation (anammox). The source of oxygen would then be mineral-oxygen from the nitrite. PET scan studies have indicated an advanced stage of metabolism, when cancer cells have evolved to encode aerobic glycolysis under hypoxic conditions. We can postulate a hypothesis that predicts the starvation of cancer cells if there is no supply of nitrite in the food-take to the cancer cells as a substrate of anammox metabolism, or if there is no sufficient supply of glucose for glycolysis. We recommend thus to the UK’s National Health Services to look into this matter that nitrite in public water is a health hazard. Such an investigation serves as a clinical trial on the efficacy of diet-treatments to cure cancer

Sampling the proteome by emerging single-molecule and mass-spectrometry methods

Mammalian cells have about 30,000-fold more protein molecules than mRNA molecules. This larger number of molecules and the associated larger dynamic range have major implications in the development of proteomics technologies. We examine these implications for both liquid chromatography-tandem mass spectrometry (LC-MS/MS) and single-molecule counting and provide estimates on how many molecules are routinely measured in proteomics experiments by LC-MS/MS. We review strategies that have been helpful for counting billions of protein molecules by LC-MS/MS and suggest that these strategies can benefit single-molecule methods, especially in mitigating the challenges of the wide dynamic range of the proteome. We also examine the theoretical possibilities for scaling up single-molecule and mass spectrometry proteomics approaches to quantifying the billions of protein molecules that make up the proteomes of our cells.Comment: Recorded presentation: https://youtu.be/w0IOgJrrvN

Post-cure

The curative imaginary is a powerful driver of hope and investment in medicine, often displacing attention and resources given to other illness-related fields of practice. Whereas cure implies an end to the sick role and the possibility of an absolute state of health, in practice those fields that are touted as having high curative potential grapple with the ongoing nature and incompleteness of post-cure care. By capturing the public imagination and channelling research and funding in particular directions, the motif of cure risks drawing resources away from other, less seductive forms of treatment, and towards the technological at the expense of the social. Drawing on our research into precision medicine and deep brain stimulation, we track how cure operates as a concept in these fields, and compare this to how medical practitioners actually care for patients. We argue that a critical engagement with post-cure possibilities offers an opportunity to challenge and rethink what constitutes good medical care, as well as the social, political, and economic underpinnings of medical innovation

Phosphate steering by Flap Endonuclease 1 promotes 5´-flap specificity and incision to prevent genome instability

DNA replication and repair enzyme Flap Endonuclease 1 (FEN1) is vital for genome integrity, and FEN1 mutations arise in multiple cancers. FEN1 precisely cleaves single-stranded (ss) 50-flaps one nucleotide into duplex (ds) DNA. Yet, how FEN1 selects for but does not incise the ss 50-flap was enigmatic. Here we combine crystallographic, biochemical and genetic analyses to show that two dsDNA binding sites set the 50polarity and to reveal unexpected control of the DNA phosphodiester backbone by electrostatic interactions. Via ‘phosphate steering’, basic residues energetically steer an inverted ss 50-flap through a gateway over FEN1’s active site and shift dsDNA for catalysis. Mutations of these residues cause an 18,000-fold reduction in catalytic rate in vitro and large-scale trinucleotide (GAA)n repeat expansions in vivo, implying failed phosphate-steering promotes an unanticipated lagging-strand template-switch mechanism during replication. Thus, phosphate steering is an unappreciated FEN1 function that enforces 50-flap specificity and catalysis, preventing genomic instability

Phosphate steering by Flap Endonuclease 1 promotes 5´-flap specificity and incision to prevent genome instability

DNA replication and repair enzyme Flap Endonuclease 1 (FEN1) is vital for genome integrity, and FEN1 mutations arise in multiple cancers. FEN1 precisely cleaves single-stranded (ss) 50-flaps one nucleotide into duplex (ds) DNA. Yet, how FEN1 selects for but does not incise the ss 50-flap was enigmatic. Here we combine crystallographic, biochemical and genetic analyses to show that two dsDNA binding sites set the 50polarity and to reveal unexpected control of the DNA phosphodiester backbone by electrostatic interactions. Via ‘phosphate steering’, basic residues energetically steer an inverted ss 50-flap through a gateway over FEN1’s active site and shift dsDNA for catalysis. Mutations of these residues cause an 18,000-fold reduction in catalytic rate in vitro and large-scale trinucleotide (GAA)n repeat expansions in vivo, implying failed phosphate-steering promotes an unanticipated lagging-strand template-switch mechanism during replication. Thus, phosphate steering is an unappreciated FEN1 function that enforces 50-flap specificity and catalysis, preventing genomic instability

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