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Advances in genomics have profoundly influenced drug discovery by increasing both the speed and accuracy of pharmaceutical development. Pharmacogenomics, which examines how genetic variation influences drug response, facilitates the identification of novel therapeutic targets and enables patient stratification for personalized treatment. These strategies contribute to improved drug efficacy, minimized adverse effects, and more efficient clinical trial design.Mapping genetic differences...
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The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
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Related Experiment Video

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Assessment of Resistance to Tyrosine Kinase Inhibitors by an Interrogation of Signal Transduction Pathways by Antibody Arrays
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Polypharmacology-based ceritinib repurposing using integrated functional proteomics.

Brent M Kuenzi1,2, Lily L Remsing Rix1, Paul A Stewart3

  • 1Department of Drug Discovery, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida, USA.

Nature Chemical Biology
|October 10, 2017
PubMed
Summary
This summary is machine-generated.

The anaplastic lymphoma kinase (ALK) inhibitor ceritinib shows effectiveness in ALK-negative lung cancer by targeting multiple noncanonical pathways. Combining ceritinib with paclitaxel demonstrates strong synergy, offering new therapeutic strategies.

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Kinase Inhibitor Screening In Self-assembled Human Protein Microarrays
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Area of Science:

  • Oncology
  • Pharmacology
  • Systems Biology

Background:

  • Targeted therapies are limited to diseases with defined drivers.
  • Network-based approaches can reveal novel therapeutic targets.
  • Anaplastic lymphoma kinase (ALK) inhibitors are primarily used for ALK-driven cancers.

Purpose of the Study:

  • To investigate the activity of the ALK inhibitor ceritinib in ALK-negative lung cancer.
  • To identify new targets and signaling effects of ceritinib using a systems chemical biology approach.
  • To explore synergistic drug combinations involving ceritinib.

Main Methods:

  • Integrated phenotypic screening, chemical proteomics, and phosphoproteomics.
  • Pharmacological inhibition and RNA interference to elucidate polypharmacology.
  • Functional studies involving mutations in the YB1 signaling hub.
  • Combination therapy studies with paclitaxel.

Main Results:

  • Ceritinib demonstrated activity in ALK-negative lung cancer cell lines.
  • Polypharmacology was identified, involving noncanonical targets like IGF1R, FAK1, RSK1, and RSK2.
  • Mutation of YB1 conferred resistance to ceritinib.
  • Combination of ceritinib with paclitaxel showed strong synergy, especially in cells with high FAK autophosphorylation.

Conclusions:

  • A systems chemical biology platform can elucidate multikinase inhibitor polypharmacology.
  • Ceritinib exhibits efficacy beyond its primary target, offering new avenues for ALK-negative lung cancer treatment.
  • Combination therapy with paclitaxel, guided by biomarkers like FAK autophosphorylation, presents a promising strategy.