We are analyzing https://link.springer.com/article/10.1007/s40268-017-0180-1.

Title:
Revisiting CDK Inhibitors for Treatment of Glioblastoma Multiforme | Drugs in R&D
Description:
Despite extensive efforts and continual progress in research and medicine, outcomes for patients with high-grade glioma remain exceptionally poor. Over the past decade, research has revealed a great deal about the complex biology behind glioma development, and has brought to light some of the major barriers preventing successful treatment. Glioblastoma multiforme (GBM) (stage 4 astrocytoma) is a highly dynamic tumour and one of the most extreme examples of intratumoural heterogeneity, making targeting with specific therapeutics an inefficient and highly unpredictable goal. The cancer stem cell hypothesis offers a new view on the possible mechanisms dictating the heterogeneous nature of this disease and contributes to our understanding of glioma resistance and recurrence. Revealing cell division characteristics of initiating cell populations within GBM may represent novel treatment targets and/or the effective repurposing of existing therapies. In this review, we discuss the potential role of targeting the cyclin-dependent kinases (CDKs) driving this specific population. We also describe developments using multi-omic approaches that may aid in stratifying patient populations for CDK inhibitor therapy.
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Keywords {🔍}

pubmed, article, google, scholar, cas, cell, cdk, glioma, cancer, cells, glioblastoma, stem, central, gbm, brain, analysis, kinase, tumour, genomic, treatment, cyclindependent, therapy, human, nature, inhibitor, heterogeneity, inhibitors, study, ckis, resistance, populations, combination, growth, cycle, model, proteins, specific, potential, cdks, clinical, molecular, protein, expression, multiforme, population, tumours, pathways, subtypes, data, research,

Topics {✒️}

epidermal growth factor aacr-nci-eortc international conference multipotent stem cells egf + fibroblast growth factor cyclin d1-cdk4/6-rb pathway cyclin-dependent kinase activators cyclin-dependent kinase inhibitor single-cell proteomic chip nf-kappab-dependent manner 5-dihydro-1h-py razolo[4 neural stem cells neural-specific regulatory subunit mammalian cell cycle cyclin-dependent kinase inhibitors bcl-2/bcl-xl inhibitors [43] cell cycle regulator single-cell analysis approach primary patient-derived cultures steady-state tumour genomic article download pdf cancer stem cells diffuse lower-grade gliomas glial cells tmz-mediated selective pressure glioma stem cells key goal anti-aging drug today cyclin-dependent kinases cdc2 cell cycle arrest central nervous system seek molecular-based reasons common cancers—therapeutic implications multi-omic approaches transit amplifying cells multi-kinase inhibitor human glioblastoma multiforme article lubanska single-cell analysis transit amplifying state integrated genomic analysis glioma-initiating cells patient-derived gbm model cyclin-dependent kinase 5 cyclin-dependent kinase 4/6 related subjects single tumor cells human glioma cells environmental pressure induced privacy choices/manage cookies arrest tumour growth

Questions {❓}

Breast cancer stem cells: eradication by differentiation therapy?

Schema {🗺️}

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         headline:Revisiting CDK Inhibitors for Treatment of Glioblastoma Multiforme
         description:Despite extensive efforts and continual progress in research and medicine, outcomes for patients with high-grade glioma remain exceptionally poor. Over the past decade, research has revealed a great deal about the complex biology behind glioma development, and has brought to light some of the major barriers preventing successful treatment. Glioblastoma multiforme (GBM) (stage 4 astrocytoma) is a highly dynamic tumour and one of the most extreme examples of intratumoural heterogeneity, making targeting with specific therapeutics an inefficient and highly unpredictable goal. The cancer stem cell hypothesis offers a new view on the possible mechanisms dictating the heterogeneous nature of this disease and contributes to our understanding of glioma resistance and recurrence. Revealing cell division characteristics of initiating cell populations within GBM may represent novel treatment targets and/or the effective repurposing of existing therapies. In this review, we discuss the potential role of targeting the cyclin-dependent kinases (CDKs) driving this specific population. We also describe developments using multi-omic approaches that may aid in stratifying patient populations for CDK inhibitor therapy.
         datePublished:2017-03-21T00:00:00Z
         dateModified:2017-03-21T00:00:00Z
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            Glioblastoma Multiforme
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            Internal Medicine
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      headline:Revisiting CDK Inhibitors for Treatment of Glioblastoma Multiforme
      description:Despite extensive efforts and continual progress in research and medicine, outcomes for patients with high-grade glioma remain exceptionally poor. Over the past decade, research has revealed a great deal about the complex biology behind glioma development, and has brought to light some of the major barriers preventing successful treatment. Glioblastoma multiforme (GBM) (stage 4 astrocytoma) is a highly dynamic tumour and one of the most extreme examples of intratumoural heterogeneity, making targeting with specific therapeutics an inefficient and highly unpredictable goal. The cancer stem cell hypothesis offers a new view on the possible mechanisms dictating the heterogeneous nature of this disease and contributes to our understanding of glioma resistance and recurrence. Revealing cell division characteristics of initiating cell populations within GBM may represent novel treatment targets and/or the effective repurposing of existing therapies. In this review, we discuss the potential role of targeting the cyclin-dependent kinases (CDKs) driving this specific population. We also describe developments using multi-omic approaches that may aid in stratifying patient populations for CDK inhibitor therapy.
      datePublished:2017-03-21T00:00:00Z
      dateModified:2017-03-21T00:00:00Z
      pageStart:255
      pageEnd:263
      sameAs:https://doi.org/10.1007/s40268-017-0180-1
      keywords:
         Epidermal Growth Factor Receptor
         Cancer Stem Cell
         Glioblastoma Multiforme
         Flavopiridol
         Epidermal Growth Factor Stimulation
         Pharmacotherapy
         Pharmacology/Toxicology
         Internal Medicine
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