Targeting the microenvironment in high grade serous ovarian cancer

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

Research output: Contribution to journalReview article

4 Citations (Scopus)

Abstract

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
JournalCancers
Volume10
Issue number8
DOIs
StatePublished - Aug 10 2018
Externally publishedYes

Fingerprint

Ovarian Neoplasms
Tumor Microenvironment
Neoplasms
Peritoneal Cavity
Ascites
Cell Adhesion
Therapeutics
Endothelial Cells
Cell Proliferation
Clinical Trials
Neoplasm Metastasis
Drug Therapy
Growth

Keywords

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

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

Cite this

Nwani, N. G., Sima, L. E., Nieves-Neira, W., & Matei, D. (2018). Targeting the microenvironment in high grade serous ovarian cancer. Cancers, 10(8), [266]. https://doi.org/10.3390/cancers10080266

Targeting the microenvironment in high grade serous ovarian cancer. / Nwani, Nkechiyere G.; Sima, Livia E.; Nieves-Neira, Wilberto; Matei, Daniela.

In: Cancers, Vol. 10, No. 8, 266, 10.08.2018.

Research output: Contribution to journalReview article

Nwani, NG, Sima, LE, Nieves-Neira, W & Matei, D 2018, 'Targeting the microenvironment in high grade serous ovarian cancer', Cancers, vol. 10, no. 8, 266. https://doi.org/10.3390/cancers10080266
Nwani, Nkechiyere G. ; Sima, Livia E. ; Nieves-Neira, Wilberto ; Matei, Daniela. / Targeting the microenvironment in high grade serous ovarian cancer. In: Cancers. 2018 ; Vol. 10, No. 8.
@article{3dc4d6e593724ae89d4eeaedd4734695,
title = "Targeting the microenvironment in high grade serous ovarian cancer",
abstract = "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.",
keywords = "Angiogenesis, High-grade serous ovarian cancer, Immune response, Metastasis, Therapeutic targeting strategies, Tumor microenvironment",
author = "Nwani, {Nkechiyere G.} and Sima, {Livia E.} and Wilberto Nieves-Neira and Daniela Matei",
year = "2018",
month = "8",
day = "10",
doi = "10.3390/cancers10080266",
language = "English (US)",
volume = "10",
journal = "Cancers",
issn = "2072-6694",
publisher = "Multidisciplinary Digital Publishing Institute (MDPI)",
number = "8",

}

TY - JOUR

T1 - Targeting the microenvironment in high grade serous ovarian cancer

AU - Nwani, Nkechiyere G.

AU - Sima, Livia E.

AU - Nieves-Neira, Wilberto

AU - Matei, Daniela

PY - 2018/8/10

Y1 - 2018/8/10

N2 - 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.

AB - 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.

KW - Angiogenesis

KW - High-grade serous ovarian cancer

KW - Immune response

KW - Metastasis

KW - Therapeutic targeting strategies

KW - Tumor microenvironment

UR - http://www.scopus.com/inward/record.url?scp=85051411693&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85051411693&partnerID=8YFLogxK

U2 - 10.3390/cancers10080266

DO - 10.3390/cancers10080266

M3 - Review article

AN - SCOPUS:85051411693

VL - 10

JO - Cancers

JF - Cancers

SN - 2072-6694

IS - 8

M1 - 266

ER -