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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
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We are analyzing https://link.springer.com/article/10.1007/s10014-013-0174-9.

Title:
The mechanism of chemoresistance against tyrosine kinase inhibitors in malignant glioma | Brain Tumor Pathology
Description:
Glioblastoma (GBM) is one of the most lethal malignancies in humans, and novel therapeutic strategies are urgently required for its treatment. Tyrosine kinases (TKs) play a pivotal role in intercellular signal transduction and regulate crucial processes of tumor cell biological activities in GBM. This information provides the basis for the molecular target therapies for GBMs. TK inhibitors (TKIs) are expected to be effective therapeutic strategies. However, one important limitation is that GBMs exhibit marked resistance to the TKIs currently available, yet the mechanisms underlying TKI resistance have not been fully characterized. In the current review, we will address the varieties of chemoresistance mechanisms against TKIs in GBM. The mechanisms responsible for TKI refractoriness in GBMs are divided into 2 aspects. The first includes tumor-related concerns, such as a lack of target expression, the multiplicity of targets, redundancy, the appearance of resistant cells, and tumor changes in characteristics. The second includes drug-related concerns, such as inefficient drug effects, delivery, pharmacokinetics, and intolerable side effects. A better understanding of these mechanisms is needed to develop accurate tests to predict the lack of response to TKIs and for developing novel approaches aimed at overcoming the resistance to TKIs.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Education
  • Science
  • Health & Fitness

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 7,643,078 visitors per month in the current month.

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

We see no obvious way the site makes money.

The purpose of some websites isn't monetary gain; they're meant to inform, educate, or foster collaboration. Everyone has unique reasons for building websites. This could be an example. Link.springer.com could be getting rich in stealth mode, or the way it's monetizing isn't detectable.

Keywords {🔍}

pubmed, article, google, scholar, cas, cancer, glioblastoma, central, tyrosine, kinase, glioma, tumor, resistance, inhibitors, nakada, cell, drug, cells, receptor, oncol, egfr, brain, kinases, access, clin, inhibitor, erlotinib, privacy, cookies, content, malignant, kita, watanabe, therapeutic, role, tkis, response, recurrent, prados, phase, patients, science, protein, abcg, breast, invasion, information, publish, research, search,

Topics {✒️}

yutaka hayashi & jun-ichiro hamada pten/pi3k/akt pathway regulates month download article/chapter dna damage response tumor-specific peptide vaccination mesenchymal-epithelial transition inhibitor p-glycoprotein-mediated efflux includes drug-related concerns includes tumor-related concerns egfr gene amplification—rearrangement met-amplified recurrent glioblastoma receptor tyrosine kinases full article pdf targeting tyrosine kinases human glioblastoma multiforme tyrosine kinase inhibitors privacy choices/manage cookies rich jn egfr kinase inhibitors glioblastoma defines subpopulations glioma tumor stem effective therapeutic strategies friedman hs invasive glioma cells blood–brain barrier article nakada inefficient drug effects normalizes tumor vasculature cancer stem cells integrated genomic analysis haas-kogan da abcg2 multidrug transporter individualized targeted therapy european economic area intercellular signal transduction regulate crucial processes develop accurate tests variable proportions reflective abc multidrug transporters mellinghoff ik john-williams ls ethyl]amino}methyl atp-binding cassette individual tumor heterogeneity restrict brain accumulation tyrosine kinases article log phase ii study short-term treatment conditions privacy policy

Questions {❓}

  • Hatzikirou H, Basanta D, Simon M, Schaller K, Deutsch A (2012) ‘Go or grow’: the key to the emergence of invasion in tumour progression?
  • Tanaka S, Louis DN, Curry WT, Batchelor TT, Dietrich J (2013) Diagnostic and therapeutic avenues for glioblastoma: no longer a dead end?
  • Weller M, Stupp R, Hegi M, Wick W (2012) Individualized targeted therapy for glioblastoma: fact or fiction?

Schema {🗺️}

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         headline:The mechanism of chemoresistance against tyrosine kinase inhibitors in malignant glioma
         description:Glioblastoma (GBM) is one of the most lethal malignancies in humans, and novel therapeutic strategies are urgently required for its treatment. Tyrosine kinases (TKs) play a pivotal role in intercellular signal transduction and regulate crucial processes of tumor cell biological activities in GBM. This information provides the basis for the molecular target therapies for GBMs. TK inhibitors (TKIs) are expected to be effective therapeutic strategies. However, one important limitation is that GBMs exhibit marked resistance to the TKIs currently available, yet the mechanisms underlying TKI resistance have not been fully characterized. In the current review, we will address the varieties of chemoresistance mechanisms against TKIs in GBM. The mechanisms responsible for TKI refractoriness in GBMs are divided into 2 aspects. The first includes tumor-related concerns, such as a lack of target expression, the multiplicity of targets, redundancy, the appearance of resistant cells, and tumor changes in characteristics. The second includes drug-related concerns, such as inefficient drug effects, delivery, pharmacokinetics, and intolerable side effects. A better understanding of these mechanisms is needed to develop accurate tests to predict the lack of response to TKIs and for developing novel approaches aimed at overcoming the resistance to TKIs.
         datePublished:2014-01-08T00:00:00Z
         dateModified:2014-01-08T00:00:00Z
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            Cancer Research
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      headline:The mechanism of chemoresistance against tyrosine kinase inhibitors in malignant glioma
      description:Glioblastoma (GBM) is one of the most lethal malignancies in humans, and novel therapeutic strategies are urgently required for its treatment. Tyrosine kinases (TKs) play a pivotal role in intercellular signal transduction and regulate crucial processes of tumor cell biological activities in GBM. This information provides the basis for the molecular target therapies for GBMs. TK inhibitors (TKIs) are expected to be effective therapeutic strategies. However, one important limitation is that GBMs exhibit marked resistance to the TKIs currently available, yet the mechanisms underlying TKI resistance have not been fully characterized. In the current review, we will address the varieties of chemoresistance mechanisms against TKIs in GBM. The mechanisms responsible for TKI refractoriness in GBMs are divided into 2 aspects. The first includes tumor-related concerns, such as a lack of target expression, the multiplicity of targets, redundancy, the appearance of resistant cells, and tumor changes in characteristics. The second includes drug-related concerns, such as inefficient drug effects, delivery, pharmacokinetics, and intolerable side effects. A better understanding of these mechanisms is needed to develop accurate tests to predict the lack of response to TKIs and for developing novel approaches aimed at overcoming the resistance to TKIs.
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         Tyrosine kinase inhibitor
         Chemoresistance
         Neurosurgery
         Neurology
         Pathology
         Oncology
         Cancer Research
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               type:PostalAddress
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External Links {🔗}(192)

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4.04s.