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Discovering cancers of epigenetic origin without DNA mutation

Science Daily: Pharmacology News

A research team has discovered that cancer, one of the leading causes of death worldwide, can be caused entirely by epigenetic changes, in other words, changes that contribute to how gene expression is regulated, and partly explain why, despite an identical genome, an individual develops very different cells (neurons, skin cells, etc.).

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Scientists discover new code governing gene activity

Science Daily: Pharmacology News

A newly discovered code within DNA -- coined 'spatial grammar' -- holds a key to understanding how gene activity is encoded in the human genome. This breakthrough finding revealed a long-postulated hidden spatial grammar embedded in DNA.

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The physics of fat droplets reveal DNA danger

Science Daily: Pharmacology News

The stakes of their findings are high: a ruptured nucleus can lead to elevated DNA damage that is characteristic of many diseases, including cancer.

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Formaldehyde regulates S-adenosylmethionine biosynthesis and one-carbon metabolism

Covalent Modifiers

We deciphered a compensatory biochemical feedback cycle where FA-dependent SAM deficiency led to an increase in MAT1A expression through genetic and epigenetic mechanisms regulated by FA-dependent transcription factors and DNA promoter hypomethylation, respectively.

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Nuclear DNA influences variation in mitochondrial DNA

Broad Institute

Nuclear DNA influences variation in mitochondrial DNA By Allessandra DiCorato August 16, 2023 Breadcrumb Home Nuclear DNA influences variation in mitochondrial DNA Whole genomes from hundreds of thousands of people reveal new complexity in how the nuclear and mitochondrial genomes interact, which may influence how cells produce energy.

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How MMR-deficient colorectal cancers regulate their growth

Drug Target Review

For the first time, scientists at UCL and University Medical Center Utrecht have observed bowel cancer cells’ ability to regulate their growth using a genetic on-off switch to increase their likelihood of survival. While this unrestrained mutation rate kills many cancer cells, it also produces a few ‘winners’ that fuel tumour development.”

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Irreversible inhibition of TRF2TRFH recruiting functions by a covalent cyclic peptide induces telomeric replication stress in cancer cells

Covalent Modifiers

2023.11.008 The TRF2 shelterin component is an essential regulator of telomere homeostasis and genomic stability. Mutations in the TRF2TRFH domain physically impair t-loop formation and prevent the recruitment of several factors that promote efficient telomere replication, causing telomeric DNA damage.

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