TY - JOUR
T1 - Regulation of tumor cell dormancy by tissue microenvironments and autophagy.
AU - Sosa, Maria Soledad
AU - Bragado, Paloma
AU - Debnath, Jayanta
AU - Aguirre-Ghiso, Julio A.
N1 - Funding Information:
This work is supported by grants from the Samuel Waxman Cancer Research Foundation Tumor Dormancy Program, NIH/National Cancer Institute (CA109182, CA163131), NIEHS (ES017146), and NYSTEM to J.A.A-G, DoD Breast Cancer Postdoctoral Fellowship to M.S.S. and NIH RO1 CA126792, CA126792-S1 (ARRA), and a DOD BCRP Era of Hope Scholar Award (W81XWH-11-1-0310) to J.D.
PY - 2013
Y1 - 2013
N2 - The development of metastasis is the major cause of death in cancer patients. In certain instances, this occurs shortly after primary tumor detection and treatment, indicating these lesions were already expanding at the moment of diagnosis or initiated exponential growth shortly after. However, in many types of cancer, patients succumb to metastatic disease years and sometimes decades after being treated for a primary tumor. This has led to the notion that in these patients residual disease may remain in a dormant state. Tumor cell dormancy is a poorly understood phase of cancer progression and only recently have its underlying molecular mechanisms started to be revealed. Important questions that remain to be elucidated include not only which mechanisms prevent residual disease from proliferating but also which mechanisms critically maintain the long-term survival of these disseminated residual cells. Herein, we review recent evidence in support of genetic and epigenetic mechanisms driving dormancy. We also explore how therapy may cause the onset of dormancy in the surviving fraction of cells after treatment and how autophagy may be a mechanism that maintains the residual cells that are viable for prolonged periods.
AB - The development of metastasis is the major cause of death in cancer patients. In certain instances, this occurs shortly after primary tumor detection and treatment, indicating these lesions were already expanding at the moment of diagnosis or initiated exponential growth shortly after. However, in many types of cancer, patients succumb to metastatic disease years and sometimes decades after being treated for a primary tumor. This has led to the notion that in these patients residual disease may remain in a dormant state. Tumor cell dormancy is a poorly understood phase of cancer progression and only recently have its underlying molecular mechanisms started to be revealed. Important questions that remain to be elucidated include not only which mechanisms prevent residual disease from proliferating but also which mechanisms critically maintain the long-term survival of these disseminated residual cells. Herein, we review recent evidence in support of genetic and epigenetic mechanisms driving dormancy. We also explore how therapy may cause the onset of dormancy in the surviving fraction of cells after treatment and how autophagy may be a mechanism that maintains the residual cells that are viable for prolonged periods.
UR - http://www.scopus.com/inward/record.url?scp=84875804581&partnerID=8YFLogxK
U2 - 10.1007/978-1-4614-1445-2_5
DO - 10.1007/978-1-4614-1445-2_5
M3 - Review article
C2 - 23143976
AN - SCOPUS:84875804581
SN - 0065-2598
VL - 734
SP - 73
EP - 89
JO - Advances in Experimental Medicine and Biology
JF - Advances in Experimental Medicine and Biology
ER -