Abstract
Chemotherapy offers long-term clinical benefits to many patients with advanced cancer. However, recent evidence has linked the cytotoxic effects of chemotherapy with the de novo elicitation of a prometastatic tumor microenvironment. This "modified" tumor microenvironment is triggered by a chemotherapy-driven cytokine storm or through direct effects of certain chemotherapeutics on stromal and/or immune cells, the most critical being tumor-associated macrophages. These chemotherapy-educated cells act as facilitators in tumor-host cell interactions promoting the establishment of distant metastasis. Certain clinical studies now offer substantial evidence that prometastatic changes are indeed identified in the tumor microenvironment of certain patient subpopulations, especially those that do not present with any pathologic response after neoadjuvant chemotherapy. Deciphering the exact contextual prerequisites for chemotherapy-driven metastasis will be paramount for designing novel mechanism-based treatments for circumventing chemotherapy-induced metastasis.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 4567-4577 |
| Number of pages | 11 |
| Journal | Cancer Research |
| Volume | 79 |
| Issue number | 18 |
| DOIs | |
| State | Published - Sep 15 2019 |
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ASJC Scopus subject areas
- Oncology
- Cancer Research
Cite this
Chemotherapy-induced metastasis : Molecular mechanisms, clinical manifestations, therapeutic interventions. / Karagiannis, George S.; Condeelis, John S.; Oktay, Maja H.
In: Cancer Research, Vol. 79, No. 18, 15.09.2019, p. 4567-4577.Research output: Contribution to journal › Review article
}
TY - JOUR
T1 - Chemotherapy-induced metastasis
T2 - Molecular mechanisms, clinical manifestations, therapeutic interventions
AU - Karagiannis, George S.
AU - Condeelis, John S.
AU - Oktay, Maja H.
PY - 2019/9/15
Y1 - 2019/9/15
N2 - Chemotherapy offers long-term clinical benefits to many patients with advanced cancer. However, recent evidence has linked the cytotoxic effects of chemotherapy with the de novo elicitation of a prometastatic tumor microenvironment. This "modified" tumor microenvironment is triggered by a chemotherapy-driven cytokine storm or through direct effects of certain chemotherapeutics on stromal and/or immune cells, the most critical being tumor-associated macrophages. These chemotherapy-educated cells act as facilitators in tumor-host cell interactions promoting the establishment of distant metastasis. Certain clinical studies now offer substantial evidence that prometastatic changes are indeed identified in the tumor microenvironment of certain patient subpopulations, especially those that do not present with any pathologic response after neoadjuvant chemotherapy. Deciphering the exact contextual prerequisites for chemotherapy-driven metastasis will be paramount for designing novel mechanism-based treatments for circumventing chemotherapy-induced metastasis.
AB - Chemotherapy offers long-term clinical benefits to many patients with advanced cancer. However, recent evidence has linked the cytotoxic effects of chemotherapy with the de novo elicitation of a prometastatic tumor microenvironment. This "modified" tumor microenvironment is triggered by a chemotherapy-driven cytokine storm or through direct effects of certain chemotherapeutics on stromal and/or immune cells, the most critical being tumor-associated macrophages. These chemotherapy-educated cells act as facilitators in tumor-host cell interactions promoting the establishment of distant metastasis. Certain clinical studies now offer substantial evidence that prometastatic changes are indeed identified in the tumor microenvironment of certain patient subpopulations, especially those that do not present with any pathologic response after neoadjuvant chemotherapy. Deciphering the exact contextual prerequisites for chemotherapy-driven metastasis will be paramount for designing novel mechanism-based treatments for circumventing chemotherapy-induced metastasis.
UR - http://www.scopus.com/inward/record.url?scp=85072234819&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85072234819&partnerID=8YFLogxK
U2 - 10.1158/0008-5472.CAN-19-1147
DO - 10.1158/0008-5472.CAN-19-1147
M3 - Review article
VL - 79
SP - 4567
EP - 4577
JO - Cancer Research
JF - Cancer Research
SN - 0008-5472
IS - 18
ER -