Abstract
The mechanisms driving dormancy of disseminated tumor cells (DTCs) remain largely unknown. Here, we discuss experimental evidence and theoretical frameworks that support three potential scenarios contributing to tumor cell dormancy. The first scenario proposes that DTCs from invasive cancers activate stress signals in response to the dissemination process and/or a growth suppressive target organ microenvironment inducing dormancy. The second scenario asks whether therapy and/or micro-environmental stress conditions (e.g. hypoxia) acting on primary tumor cells carrying specific gene signatures prime new DTCs to enter dormancy in a matching target organ microenvironment that can also control the timing of DTC dormancy. The third and final scenario proposes that early dissemination contributes a population of DTCs that are unfit for immediate expansion and survive mostly in an arrested state well after primary tumor surgery, until genetic and/or epigenetic mechanisms activate their proliferation. We propose that DTC dormancy is ultimately a survival strategy that when targeted will eradicate dormant DTCs preventing metastasis. For these non-mutually exclusive scenarios we review experimental and clinical evidence in their support.
| Original language | English (US) |
|---|---|
| Title of host publication | Recent Results in Cancer Research |
| Pages | 25-39 |
| Number of pages | 15 |
| Volume | 195 |
| DOIs | |
| State | Published - 2012 |
Publication series
| Name | Recent Results in Cancer Research |
|---|---|
| Volume | 195 |
| ISSN (Print) | 00800015 |
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ASJC Scopus subject areas
- Oncology
- Cancer Research
Cite this
Microenvironments dictating tumor cell dormancy. / Bragado, Paloma; Sosa, Maria Soledad; Keely, Patricia; Condeelis, John S.; Aguirre-Ghiso, Julio A.
Recent Results in Cancer Research. Vol. 195 2012. p. 25-39 (Recent Results in Cancer Research; Vol. 195).Research output: Chapter in Book/Report/Conference proceeding › Chapter
}
TY - CHAP
T1 - Microenvironments dictating tumor cell dormancy
AU - Bragado, Paloma
AU - Sosa, Maria Soledad
AU - Keely, Patricia
AU - Condeelis, John S.
AU - Aguirre-Ghiso, Julio A.
PY - 2012
Y1 - 2012
N2 - The mechanisms driving dormancy of disseminated tumor cells (DTCs) remain largely unknown. Here, we discuss experimental evidence and theoretical frameworks that support three potential scenarios contributing to tumor cell dormancy. The first scenario proposes that DTCs from invasive cancers activate stress signals in response to the dissemination process and/or a growth suppressive target organ microenvironment inducing dormancy. The second scenario asks whether therapy and/or micro-environmental stress conditions (e.g. hypoxia) acting on primary tumor cells carrying specific gene signatures prime new DTCs to enter dormancy in a matching target organ microenvironment that can also control the timing of DTC dormancy. The third and final scenario proposes that early dissemination contributes a population of DTCs that are unfit for immediate expansion and survive mostly in an arrested state well after primary tumor surgery, until genetic and/or epigenetic mechanisms activate their proliferation. We propose that DTC dormancy is ultimately a survival strategy that when targeted will eradicate dormant DTCs preventing metastasis. For these non-mutually exclusive scenarios we review experimental and clinical evidence in their support.
AB - The mechanisms driving dormancy of disseminated tumor cells (DTCs) remain largely unknown. Here, we discuss experimental evidence and theoretical frameworks that support three potential scenarios contributing to tumor cell dormancy. The first scenario proposes that DTCs from invasive cancers activate stress signals in response to the dissemination process and/or a growth suppressive target organ microenvironment inducing dormancy. The second scenario asks whether therapy and/or micro-environmental stress conditions (e.g. hypoxia) acting on primary tumor cells carrying specific gene signatures prime new DTCs to enter dormancy in a matching target organ microenvironment that can also control the timing of DTC dormancy. The third and final scenario proposes that early dissemination contributes a population of DTCs that are unfit for immediate expansion and survive mostly in an arrested state well after primary tumor surgery, until genetic and/or epigenetic mechanisms activate their proliferation. We propose that DTC dormancy is ultimately a survival strategy that when targeted will eradicate dormant DTCs preventing metastasis. For these non-mutually exclusive scenarios we review experimental and clinical evidence in their support.
UR - http://www.scopus.com/inward/record.url?scp=84860595935&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84860595935&partnerID=8YFLogxK
U2 - 10.1007/978-3-642-28160-0_3
DO - 10.1007/978-3-642-28160-0_3
M3 - Chapter
SN - 9783642281594
VL - 195
T3 - Recent Results in Cancer Research
SP - 25
EP - 39
BT - Recent Results in Cancer Research
ER -