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DOI . ORG {}

  1. Analyzed Page
  2. Matching Content Categories
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  4. Monthly Traffic Estimate
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  6. Keywords
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We began analyzing https://link.springer.com/article/10.1007/s00109-007-0221-2, but it redirected us to https://link.springer.com/article/10.1007/s00109-007-0221-2. The analysis below is for the second page.

Title[redir]:
Inhibition of tumor angiogenesis by p53: a new role for the guardian of the genome | Journal of Molecular Medicine
Description:
The p53 tumor suppressor protein has long been recognized as the central factor protecting humans from cancer. It has been famously dubbed “the guardian of the genome” due to its ability to respond to genotoxic stress, such as DNA damage and other stress signals, and to protect the genome by inducing a variety of biological responses including DNA repair, cell cycle arrest, and apoptosis. However, the tumor suppressive effects of p53 go far beyond its roles in mediating these three processes. There is growing evidence that p53 also exerts its effects on multiple aspects of tumor formation, including suppression of metastasis and, as summarized in this review, inhibition of new blood vessel development (angiogenesis). The p53 protein has been shown to limit angiogenesis by at least three mechanisms: (1) interfering with central regulators of hypoxia that mediate angiogenesis, (2) inhibiting production of proangiogenic factors, and (3) directly increasing the production of endogenous angiogenesis inhibitors. The combination of these effects allows p53 to efficiently shut down the angiogenic potential of cancer cells. Inactivation of p53, which occurs in approximately half of all tumors, reverses these effects; as a consequence, tumors carrying p53 mutations appear more vascularized and are often more aggressive and correlate with poor prognosis for treatment. Thus, the loss of functional p53 during tumorigenesis likely represents an essential step in the switch to an angiogenic phenotype that is displayed by aggressive tumors.

Matching Content Categories {📚}

  • Education
  • Science
  • Health & Fitness

Content Management System {📝}

What CMS is doi.org built with?

Custom-built

No common CMS systems were detected on Doi.org, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of doi.org audience?

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


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How Does Doi.org Make Money? {💸}

We can't see how the site brings in money.

Some websites aren't about earning revenue; they're built to connect communities or raise awareness. There are numerous motivations behind creating websites. This might be one of them. Doi.org might be earning cash quietly, but we haven't detected the monetization method.

Keywords {🔍}

pubmed, google, scholar, cas, article, cancer, angiogenesis, tumor, cell, growth, thrombospondin, res, factor, biol, cells, human, gene, endothelial, type, expression, protein, carcinoma, inhibition, hypoxia, vascular, nat, regulation, mol, bouck, role, suppressor, apoptosis, access, inhibitor, science, oncogene, collagen, genome, prolyl, cyclooxygenase, nature, rev, folkman, lawler, chem, usa, antiangiogenic, volpert, kalluri, privacy,

Topics {✒️}

transforming growth factor-beta-dependent brain-specific p53-target gene month download article/chapter node-negative breast carcinoma tumor suppressor-dependent inhibitor p53 tumour suppressor endothelium-specific tumor suppressors bfgf-binding protein expression p53-family proteins hypoxia-inducible factor 1alpha neck squamous-cell carcinoma cell cycle arrest ras-transformed epithelial cells tumor suppressor gene p53-mediated proteasomal degradation molecular biology full article pdf lewis lung carcinoma hypoxia-inducible factor 1 related subjects human collagen xv collagen prolyl hydroxylase o2-regulated prolyl hydroxylation privacy choices/manage cookies endogenous angiogenesis inhibitors epha2 tyrosine kinase hypoxia induces accumulation host–tumor interaction human prostatic carcinoma p53 protein expression tumour angiogenesis anti-angiogenic activity anti-angiogenic cues p53-dependent transactivation tgf-beta signaling increase tumor angiogenesis occult papillary carcinoma cyclooxygenase-2 gene expression medical foundation charles massachusetts medical school check access instant access hepatocellular carcinoma cells matrix protein thrombospondin-1 hypoxia-mediated selection viral myc oncoproteins myc oncoprotein leads caspase death pathway tumor microvessel density matrix-derived inhibitor

Schema {🗺️}

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         headline:Inhibition of tumor angiogenesis by p53: a new role for the guardian of the genome
         description:The p53 tumor suppressor protein has long been recognized as the central factor protecting humans from cancer. It has been famously dubbed “the guardian of the genome” due to its ability to respond to genotoxic stress, such as DNA damage and other stress signals, and to protect the genome by inducing a variety of biological responses including DNA repair, cell cycle arrest, and apoptosis. However, the tumor suppressive effects of p53 go far beyond its roles in mediating these three processes. There is growing evidence that p53 also exerts its effects on multiple aspects of tumor formation, including suppression of metastasis and, as summarized in this review, inhibition of new blood vessel development (angiogenesis). The p53 protein has been shown to limit angiogenesis by at least three mechanisms: (1) interfering with central regulators of hypoxia that mediate angiogenesis, (2) inhibiting production of proangiogenic factors, and (3) directly increasing the production of endogenous angiogenesis inhibitors. The combination of these effects allows p53 to efficiently shut down the angiogenic potential of cancer cells. Inactivation of p53, which occurs in approximately half of all tumors, reverses these effects; as a consequence, tumors carrying p53 mutations appear more vascularized and are often more aggressive and correlate with poor prognosis for treatment. Thus, the loss of functional p53 during tumorigenesis likely represents an essential step in the switch to an angiogenic phenotype that is displayed by aggressive tumors.
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      headline:Inhibition of tumor angiogenesis by p53: a new role for the guardian of the genome
      description:The p53 tumor suppressor protein has long been recognized as the central factor protecting humans from cancer. It has been famously dubbed “the guardian of the genome” due to its ability to respond to genotoxic stress, such as DNA damage and other stress signals, and to protect the genome by inducing a variety of biological responses including DNA repair, cell cycle arrest, and apoptosis. However, the tumor suppressive effects of p53 go far beyond its roles in mediating these three processes. There is growing evidence that p53 also exerts its effects on multiple aspects of tumor formation, including suppression of metastasis and, as summarized in this review, inhibition of new blood vessel development (angiogenesis). The p53 protein has been shown to limit angiogenesis by at least three mechanisms: (1) interfering with central regulators of hypoxia that mediate angiogenesis, (2) inhibiting production of proangiogenic factors, and (3) directly increasing the production of endogenous angiogenesis inhibitors. The combination of these effects allows p53 to efficiently shut down the angiogenic potential of cancer cells. Inactivation of p53, which occurs in approximately half of all tumors, reverses these effects; as a consequence, tumors carrying p53 mutations appear more vascularized and are often more aggressive and correlate with poor prognosis for treatment. Thus, the loss of functional p53 during tumorigenesis likely represents an essential step in the switch to an angiogenic phenotype that is displayed by aggressive tumors.
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External Links {🔗}(366)

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Mail Servers:

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