Chemotherapy-induced metastasis: mechanisms and translational opportunities

George S. Karagiannis, John S. Condeelis, Maja H. Oktay

Research output: Contribution to journalArticle

18 Citations (Scopus)

Abstract

Tumors often overcome the cytotoxic effects of chemotherapy through either acquired or environment-mediated drug resistance. In addition, signals from the microenvironment obfuscate the beneficial effects of chemotherapy and may facilitate progression and metastatic dissemination. Seminal mediators in chemotherapy-induced metastasis appear to be a wide range of hematopoietic, mesenchymal and immune progenitor cells, originating from the bone marrow. The actual purpose of these cells is to orchestrate the repair response to the cytotoxic damage of chemotherapy. However, these repair responses are exploited by tumor cells at every step of the metastatic cascade, ranging from tumor cell invasion, intravasation and hematogenous dissemination to extravasation and effective colonization at the metastatic site. A better understanding of the mechanistic underpinnings of chemotherapy-induced metastasis will allow us to better predict which patients are more likely to exhibit pro-metastatic responses to chemotherapy and will help develop new therapeutic strategies to neutralize chemotherapy-driven prometastatic changes.

Original languageEnglish (US)
Pages (from-to)1-16
Number of pages16
JournalClinical and Experimental Metastasis
DOIs
StateAccepted/In press - Jan 6 2018

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Neoplasm Metastasis
Drug Therapy
Neoplasms
Mesenchymal Stromal Cells
Drug Resistance
Bone Marrow
Therapeutics

Keywords

  • Bone marrow-derived cells
  • Cancer cell dissemination
  • Macrophages
  • Mena
  • Mesenchymal stem cells
  • TMEM

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

Cite this

Chemotherapy-induced metastasis : mechanisms and translational opportunities. / Karagiannis, George S.; Condeelis, John S.; Oktay, Maja H.

In: Clinical and Experimental Metastasis, 06.01.2018, p. 1-16.

Research output: Contribution to journalArticle

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