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Looking for Driver Pathways of Acquired Resistance to Targeted Therapy: Drug Resistant Subclone Generation and Sensitivity Restoring by Gene Knock-down
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Resistant to Targeted Therapy - Aim for Metabolic Liabilities

André Lima Queiroz1, Helin Vakifahmetoglu-Norberg1, Erik Norberg1

  • 1Department of Physiology and Pharmacology, Karolinska Institutet, Nanna Svartz väg 2, SE-171 77, Stockholm, Sweden.

Theranostics
|March 24, 2018
PubMed

Insights

Lung tumors resistant to EGFR-inhibitor Erlotinib reprogram metabolism. Targeting Phosphoglycerate Dehydrogenase (PHGDH) eliminates these resistant tumors.

Area of Science:

  • Oncology
  • Molecular Biology
  • Metabolic Pathways

Background:

  • Targeted therapies offer promise but face challenges with acquired resistance.
  • Epidermal Growth Factor Receptor (EGFR) inhibitors like Erlotinib are used for lung cancer treatment.
  • Tumor resistance mechanisms often involve metabolic reprogramming.

Discussion:

  • This study investigates metabolic adaptations in Erlotinib-resistant lung tumors.
  • Focuses on the role of Phosphoglycerate Dehydrogenase (PHGDH) in tumor survival.
  • Explores PHGDH as a potential therapeutic target for overcoming resistance.

Key Insights:

  • Erlotinib-resistant lung tumors exhibit altered metabolic dependencies.
  • Phosphoglycerate Dehydrogenase (PHGDH) is crucial for the pro-survival of resistant cells.
  • Targeting PHGDH can effectively eliminate Erlotinib-resistant lung tumors.

Outlook:

  • PHGDH inhibition represents a promising strategy to overcome Erlotinib resistance in lung cancer.
  • Further research into metabolic vulnerabilities can guide the development of next-generation therapies.
  • Combination therapies targeting both EGFR and metabolic pathways may improve patient outcomes.
Keywords:
EGFRLung AdenocarcinomasLung CancerNon-small Cell Lung CarcinomasPHGDHSerineTumor Metabolism

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