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 language | English (US) |
|---|---|
| Pages (from-to) | 1-16 |
| Number of pages | 16 |
| Journal | Clinical and Experimental Metastasis |
| DOIs | |
| State | Accepted/In press - Jan 6 2018 |
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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 journal › Article
}
TY - JOUR
T1 - Chemotherapy-induced metastasis
T2 - mechanisms and translational opportunities
AU - Karagiannis, George S.
AU - Condeelis, John S.
AU - Oktay, Maja H.
PY - 2018/1/6
Y1 - 2018/1/6
N2 - 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.
AB - 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.
KW - Bone marrow-derived cells
KW - Cancer cell dissemination
KW - Macrophages
KW - Mena
KW - Mesenchymal stem cells
KW - TMEM
UR - http://www.scopus.com/inward/record.url?scp=85040056181&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85040056181&partnerID=8YFLogxK
U2 - 10.1007/s10585-017-9870-x
DO - 10.1007/s10585-017-9870-x
M3 - Article
C2 - 29307118
AN - SCOPUS:85040056181
SP - 1
EP - 16
JO - Clinical and Experimental Metastasis
JF - Clinical and Experimental Metastasis
SN - 0262-0898
ER -