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We are analyzing https://link.springer.com/article/10.1007/s11357-024-01113-3.

Title:
Somatic mutations in aging and disease | GeroScience
Description:
Time always leaves its mark, and our genome is no exception. Mutations in the genome of somatic cells were first hypothesized to be the cause of aging in the 1950s, shortly after the molecular structure of DNA had been described. Somatic mutation theories of aging are based on the fact that mutations in DNA as the ultimate template for all cellular functions are irreversible. However, it took until the 1990s to develop the methods to test if DNA mutations accumulate with age in different organs and tissues and estimate the severity of the problem. By now, numerous studies have documented the accumulation of somatic mutations with age in normal cells and tissues of mice, humans, and other animals, showing clock-like mutational signatures that provide information on the underlying causes of the mutations. In this review, we will first briefly discuss the recent advances in next-generation sequencing that now allow quantitative analysis of somatic mutations. Second, we will provide evidence that the mutation rate differs between cell types, with a focus on differences between germline and somatic mutation rate. Third, we will discuss somatic mutational signatures as measures of aging, environmental exposure, and activities of DNA repair processes. Fourth, we will explain the concept of clonally amplified somatic mutations, with a focus on clonal hematopoiesis. Fifth, we will briefly discuss somatic mutations in the transcriptome and in our other genome, i.e., the genome of mitochondria. We will end with a brief discussion of a possible causal contribution of somatic mutations to the aging process.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {πŸ“š}

  • Education
  • Science
  • Business & Finance

Content Management System {πŸ“}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {πŸ“ˆ}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 7,626,182 visitors per month in the current month.

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How Does Link.springer.com Make Money? {πŸ’Έ}

We can't figure out the monetization strategy.

While profit motivates many websites, others exist to inspire, entertain, or provide valuable resources. Websites have a variety of goals. And this might be one of them. Link.springer.com might be plotting its profit, but the way they're doing it isn't detectable yet.

Keywords {πŸ”}

pubmed, article, google, scholar, cas, central, somatic, human, mutations, mutation, aging, httpsdoiorgs, cell, nature, mutational, cancer, cells, nat, sequencing, genome, dna, sci, vijg, clonal, science, genet, singlecell, analysis, disease, zhang, signatures, natl, acad, single, normal, httpsdoiorgpnas, sun, lee, agerelated, tissues, proc, dong, maslov, huang, kim, ren, hematopoiesis, landscapes, landscape, ageing,

Topics {βœ’οΈ}

month download article/chapter high-sensitivity c-reactive protein single-cell dna-sequencing data neoplastic ibd-affected colon age-related telomere attrition low-input dna sequencing single-cell analysis reveals alexandrov lb copy-number variations sequencing error profiles single-cell genome sequencing short-lived rodent species article geroscience aims low-abundance somatic mutations single-molecule resolution age-related somatic mutations primary template-directed amplification dna double-strand breaks full article pdf genome-amplified single cells age-related clonal hematopoiesis tissue-specific mutation accumulation mitochondria-specific mutational signature article ren genome sequencing reveals peijun ren somatic mutation burden diaz la jr human somatic variation privacy choices/manage cookies mech ageing dev ageing mouse heart somatic mutation landscapes genome-wide analysis high-throughput sequencing nucleotide sequence analysis somatic gene mutation luquette lj volkova nv impair tumor growth genome dna sequencing sequencing coverage depth illumina sequencing instruments massively parallel sequencing genome sequence integrity unique mutation signature single human neurons age-related remodelling tumor cell populations shorten cellular lifespan

Questions {❓}

  • Mitochondrial DNA mutations and aging: devils in the details?
  • Premature ovarian aging in BRCA carriers: a prototype of systemic precocious aging?

Schema {πŸ—ΊοΈ}

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         headline:Somatic mutations in aging and disease
         description:Time always leaves its mark, and our genome is no exception. Mutations in the genome of somatic cells were first hypothesized to be the cause of aging in the 1950s, shortly after the molecular structure of DNA had been described. Somatic mutation theories of aging are based on the fact that mutations in DNA as the ultimate template for all cellular functions are irreversible. However, it took until the 1990s to develop the methods to test if DNA mutations accumulate with age in different organs and tissues and estimate the severity of the problem. By now, numerous studies have documented the accumulation of somatic mutations with age in normal cells and tissues of mice, humans, and other animals, showing clock-like mutational signatures that provide information on the underlying causes of the mutations. In this review, we will first briefly discuss the recent advances in next-generation sequencing that now allow quantitative analysis of somatic mutations. Second, we will provide evidence that the mutation rate differs between cell types, with a focus on differences between germline and somatic mutation rate. Third, we will discuss somatic mutational signatures as measures of aging, environmental exposure, and activities of DNA repair processes. Fourth, we will explain the concept of clonally amplified somatic mutations, with a focus on clonal hematopoiesis. Fifth, we will briefly discuss somatic mutations in the transcriptome and in our other genome, i.e., the genome of mitochondria. We will end with a brief discussion of a possible causal contribution of somatic mutations to the aging process.
         datePublished:2024-03-15T00:00:00Z
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      headline:Somatic mutations in aging and disease
      description:Time always leaves its mark, and our genome is no exception. Mutations in the genome of somatic cells were first hypothesized to be the cause of aging in the 1950s, shortly after the molecular structure of DNA had been described. Somatic mutation theories of aging are based on the fact that mutations in DNA as the ultimate template for all cellular functions are irreversible. However, it took until the 1990s to develop the methods to test if DNA mutations accumulate with age in different organs and tissues and estimate the severity of the problem. By now, numerous studies have documented the accumulation of somatic mutations with age in normal cells and tissues of mice, humans, and other animals, showing clock-like mutational signatures that provide information on the underlying causes of the mutations. In this review, we will first briefly discuss the recent advances in next-generation sequencing that now allow quantitative analysis of somatic mutations. Second, we will provide evidence that the mutation rate differs between cell types, with a focus on differences between germline and somatic mutation rate. Third, we will discuss somatic mutational signatures as measures of aging, environmental exposure, and activities of DNA repair processes. Fourth, we will explain the concept of clonally amplified somatic mutations, with a focus on clonal hematopoiesis. Fifth, we will briefly discuss somatic mutations in the transcriptome and in our other genome, i.e., the genome of mitochondria. We will end with a brief discussion of a possible causal contribution of somatic mutations to the aging process.
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         Cancer
         Mutational signatures
         Cell Biology
         Geriatrics/Gerontology
         Molecular Medicine
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