Role of the tumor microenvironment in digestive neuroendocrine tumors

Thomas Cuny1,2,3, Wouter de Herder1, Anne Barlier2,3

  • 1Division Endocrinology, Department of Internal Medicine, Erasmus Medical Center, Rotterdam, The Netherlands.

Endocrine-Related Cancer
|October 12, 2018
PubMed

Insights

Gastroenteropancreatic neuroendocrine tumors (GEP-NETs) are increasing, with many patients diagnosed with metastatic disease. The tumor microenvironment (TME) hinders treatment efficacy and promotes GEP-NETs progression.

Area of Science:

  • Oncology
  • Cancer Biology
  • Tumor Microenvironment Research

Background:

  • Gastroenteropancreatic neuroendocrine tumors (GEP-NETs) incidence is rising, with approximately 50% of patients presenting with metastatic disease at diagnosis.
  • Current cytotoxic and targeted therapies show limited efficacy in metastatic GEP-NETs due to treatment resistance.
  • The tumor microenvironment (TME) is increasingly recognized as a critical factor influencing GEP-NETs progression and therapeutic resistance.

Purpose of the Study:

  • To review current knowledge on the tumor microenvironment (TME) in gastroenteropancreatic neuroendocrine tumors (GEP-NETs).
  • To discuss existing therapeutic agents targeting GEP-NETs.
  • To explore potential future therapeutic strategies targeting the TME in GEP-NETs.

Main Methods:

  • Literature review of current research on GEP-NETs and their tumor microenvironment.
  • Analysis of existing therapeutic approaches for metastatic GEP-NETs.
  • Exploration of emerging therapeutic targets within the TME.

Main Results:

  • The TME plays a dual role in GEP-NETs, supporting tumor growth, metastasis, and treatment resistance.
  • Limited efficacy of current therapies suggests a need for novel treatment strategies.
  • The TME presents potential targets for future GEP-NETs therapies.

Conclusions:

  • Understanding the TME is crucial for improving treatment outcomes in GEP-NETs.
  • Targeting the TME offers a promising avenue for overcoming therapeutic resistance in metastatic GEP-NETs.
  • Future research should focus on developing novel therapies that modulate the GEP-NETs TME.

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