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LINK . SPRINGER . COM {}

  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Link.springer.com Make Money
  6. Keywords
  7. Topics
  8. Questions
  9. Schema
  10. External Links
  11. Analytics And Tracking
  12. Libraries
  13. CDN Services

We are analyzing https://link.springer.com/article/10.1007/s00204-008-0280-3.

Title:
Chromosomal instability in bladder cancer | Archives of Toxicology
Description:
Chromosomal instability (CIN) distinguishes invasive urothelial carcinomas from less malignant papillary subtypes. Recent results implicate checkpoint dysfunction as a crucial factor underlying the emergence of aneuploidy in urothelial carcinogenesis. It may moreover contribute to DNA repair defects. Therefore, defects in cell cycle regulation, p53 function, and checkpoint signaling initially caused by carcinogens in the urothelium could ultimately elicit CIN. Among several mechanisms contributing to aneuploidy, breakage-fusion-bridge (BFB) cycles initiated by defective telomeres may be particularly relevant. The mechanism generating large interstitial deletions, prominently at 9p21, appears to be distinct. New experimental approaches are required to address important unresolved questions such as the precise relationship between telomere erosion and telomerase activation, the influence of checkpoint defects on DNA double-strand repair by non-homologous and homomologous recombination repair systems, and the mechanism responsible for megabase-sized interstitial deletions.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Education
  • Health & Fitness
  • Telecommunications

Content Management System {📝}

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 {📈}

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 5,000,019 visitors per month in the current month.
However, some sources were not loaded, we suggest to reload the page to get complete results.

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How Does Link.springer.com Make Money? {💸}

The income method remains a mystery to us.

Not all websites are made for profit; some exist to inform or educate users. Or any other reason why people make websites. And this might be the case. Link.springer.com might be making money, but it's not detectable how they're doing it.

Keywords {🔍}

google, scholar, article, pubmed, cas, cancer, dna, bladder, repair, human, urothelial, res, instability, cell, deletions, florl, schulz, chromosome, carcinoma, chromosomal, access, natl, genetic, pathway, risk, carcinogenesis, doublestrand, usa, nature, privacy, cookies, content, mechanisms, oncogene, gene, proc, acad, sci, break, biol, fragile, cells, genes, molecular, site, publish, search, checkpoint, factor, defects,

Topics {✒️}

double-strand break repair month download article/chapter dna double-strand repair dna double-strand breaks dna damage checkpoints megabase-sized interstitial deletions fanconi anemia-brca pathway cancer-specific chromosome alterations cyclin-dependent kinase control p53-p21waf1/cip1 pathway candidate anti-cancer barrier cisplatin-sensitive ovarian tumors heinrich-heine-university duesseldorf dna damage response p16ink4a/cdkn2a tumor suppressor cell-cycle-control genes common fragile site full article pdf dna repair defects optimizing dna repair human dna repair genomic instability privacy choices/manage cookies fa/brca pathway chromosome 9p21 deletions dna substrate dependence van gils ch van der kwast constitutional chromosomal rearrangements chromosome arm 9p bladder cancer predisposition heinrich-heine-universität dna end joining renal cell carcinomas bladder cancer genotoxicity chromosomal aberrations induced article florl bladder cancer risk checkpoint defects telomeric chromatin alterations knowles ma iarc cancer base inverted growth pattern elevated microsatellite instability article archives telomere dysfunction human bladder cancer transitional cell carcinoma cell cycle regulation urothelial cell carcinoma

Questions {❓}

  • Gisselsson D (2003) Chromosome instability in cancer: how, when, and why?
  • Knowles MA (2006) Molecular subtypes of bladder cancer: Jekyll and Hyde or chalk and cheese?
  • Mohrenweiser HW, Jones IM (1998) Variation in DNA repair is a factor in cancer susceptibility: a paradigm for the promises and perils of individual and population risk estimation?

Schema {🗺️}

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         headline:Chromosomal instability in bladder cancer
         description:Chromosomal instability (CIN) distinguishes invasive urothelial carcinomas from less malignant papillary subtypes. Recent results implicate checkpoint dysfunction as a crucial factor underlying the emergence of aneuploidy in urothelial carcinogenesis. It may moreover contribute to DNA repair defects. Therefore, defects in cell cycle regulation, p53 function, and checkpoint signaling initially caused by carcinogens in the urothelium could ultimately elicit CIN. Among several mechanisms contributing to aneuploidy, breakage-fusion-bridge (BFB) cycles initiated by defective telomeres may be particularly relevant. The mechanism generating large interstitial deletions, prominently at 9p21, appears to be distinct. New experimental approaches are required to address important unresolved questions such as the precise relationship between telomere erosion and telomerase activation, the influence of checkpoint defects on DNA double-strand repair by non-homologous and homomologous recombination repair systems, and the mechanism responsible for megabase-sized interstitial deletions.
         datePublished:2008-02-06T00:00:00Z
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            Occupational Medicine/Industrial Medicine
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      headline:Chromosomal instability in bladder cancer
      description:Chromosomal instability (CIN) distinguishes invasive urothelial carcinomas from less malignant papillary subtypes. Recent results implicate checkpoint dysfunction as a crucial factor underlying the emergence of aneuploidy in urothelial carcinogenesis. It may moreover contribute to DNA repair defects. Therefore, defects in cell cycle regulation, p53 function, and checkpoint signaling initially caused by carcinogens in the urothelium could ultimately elicit CIN. Among several mechanisms contributing to aneuploidy, breakage-fusion-bridge (BFB) cycles initiated by defective telomeres may be particularly relevant. The mechanism generating large interstitial deletions, prominently at 9p21, appears to be distinct. New experimental approaches are required to address important unresolved questions such as the precise relationship between telomere erosion and telomerase activation, the influence of checkpoint defects on DNA double-strand repair by non-homologous and homomologous recombination repair systems, and the mechanism responsible for megabase-sized interstitial deletions.
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         Interstitial deletion
         Telomere
         DNA double-strand break
         DNA repair
         Checkpoint signaling
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         Occupational Medicine/Industrial Medicine
         Environmental Health
         Biomedicine
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External Links {🔗}(210)

Analytics and Tracking {📊}

  • Google Tag Manager

Libraries {📚}

  • Clipboard.js
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CDN Services {📦}

  • Crossref

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