TY - JOUR
T1 - Chemotherapy-induced metastasis
T2 - mechanisms and translational opportunities
AU - Karagiannis, George S.
AU - Condeelis, John S.
AU - Oktay, Maja H.
N1 - Funding Information:
MHO and JSC are inventors on a patent application (#96700/2505) submitted by the Albert Einstein College of Medicine that covers methods detecting and reducing chemotherapy-induced prometastatic changes in breast tumors. GSK declares no competing interests.
Funding Information:
Funding This article is supported by grants from the NIH (CA100324, CA150344 and CA216248), the SIG 1S10OD019961-01, the
Publisher Copyright:
© 2017, Springer Science+Business Media B.V., part of Springer Nature.
PY - 2018/4/1
Y1 - 2018/4/1
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
VL - 35
SP - 269
EP - 284
JO - Clinical and Experimental Metastasis
JF - Clinical and Experimental Metastasis
SN - 0262-0898
IS - 4
ER -
