Chapter

Systems Biology of Tumor Dormancy

Volume 734 of the series Advances in Experimental Medicine and Biology pp 73-89

Date:

Regulation of Tumor Cell Dormancy by Tissue Microenvironments and Autophagy

  • Maria Soledad SosaAffiliated withDepartments of Medicine and Otolaryngology, Tisch Cancer Institute, Black Family Stem Cell Institute, Mount Sinai School of Medicine
  • , Paloma BragadoAffiliated withDepartments of Medicine and Otolaryngology, Tisch Cancer Institute, Black Family Stem Cell Institute, Mount Sinai School of Medicine
  • , Jayanta DebnathAffiliated withDepartment of Pathology, Helen Diller Family Comprehensive Cancer Center, University of California San Francisco
  • , Julio A. Aguirre-GhisoAffiliated withDepartments of Medicine and Otolaryngology, Tisch Cancer Institute, Black Family Stem Cell Institute, Mount Sinai School of Medicine Email author 

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Abstract

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.

Keywords

Quiescence Minimal residual disease Cellular stress p38 MAPK Metastasis