Targeting the microenvironment in high grade serous ovarian cancer

Nkechiyere G. Nwani, Livia E. Sima, Wilberto Nieves-Neira, Daniela Matei*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

26 Scopus citations


Cancer–stroma interactions play a key role in cancer progression and response to standard chemotherapy. Here, we provide a summary of the mechanisms by which the major cellular components of the ovarian cancer (OC) tumor microenvironment (TME) including cancer-associated fibroblasts (CAFs), myeloid, immune, endothelial, and mesothelial cells potentiate cancer progression. High-grade serous ovarian cancer (HGSOC) is characterized by a pro-inflammatory and angiogenic signature. This profile is correlated with clinical outcomes and can be a target for therapy. Accumulation of malignant ascites in the peritoneal cavity allows for secreted factors to fuel paracrine and autocrine circuits that augment cancer cell proliferation and invasiveness. Adhesion of cancer cells to the mesothelial matrix promotes peritoneal tumor dissemination and represents another attractive target to prevent metastasis. The immunosuppressed tumor milieu of HGSOC is permissive for tumor growth and can be modulated therapeutically. Results of emerging preclinical and clinical trials testing TME-modulating therapeutics for the treatment of OC are highlighted.

Original languageEnglish (US)
Article number266
Issue number8
StatePublished - Aug 10 2018


  • Angiogenesis
  • High-grade serous ovarian cancer
  • Immune response
  • Metastasis
  • Therapeutic targeting strategies
  • Tumor microenvironment

ASJC Scopus subject areas

  • Oncology
  • Cancer Research


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