Abstract
Primary cancer cells exert unique capacity to disseminate and nestle in distant organs. Once seeded in secondary sites, cancer cells may enter a dormant state, becoming resistant to current treatment approaches, and they remain silent until they reactivate and cause overt metastases. To illuminate the complex mechanisms of cancer dormancy, 10 transcriptomic datasets from the literature enabling 21 dormancy–cancer comparisons were mapped on protein–protein interaction networks and gene-regulatory networks to extract subnetworks that are enriched in significantly deregulated genes. The genes appearing in the subnetworks and significantly upregulated in dormancy with respect to proliferative state were scored and filtered across all comparisons, leading to a dormancy–interaction network for the first time in the literature, which includes 139 genes and 1974 interactions. The dormancy interaction network will contribute to the elucidation of cellular mechanisms orchestrating cancer dormancy, paving the way for improvements in the diagnosis and treatment of metastatic cancer.
Highlights
Primary cancer cells exert unique capacity to disseminate and nestle in distant organs
Advances in medicine and technological developments allow treatment of many types of cancer, especially if patients were diagnosed at earlier stages; diagnosis of advanced disease, metastatic relapse and treatment at these late stages still remains as a difficult challenge
Rather than cell division versus death rates of cancer cells, in cellular dormancy, intrinsic mechanisms leading to a quiescence-like stage and cell cycle arrest are in play
Summary
Primary cancer cells exert unique capacity to disseminate and nestle in distant organs. Once seeded in secondary sites, cancer cells may enter a dormant state, becoming resistant to current treatment approaches, and they remain silent until they reactivate and cause overt metastases. Some of the disseminated tumor cells might escape immune surveillance and develop resistance against cancer treatment modalities. These single cells or micrometastases formed by disseminated tumor cells are beyond the detection limit of current cancer diagnosis techniques, and untraceable through CT scans, MRI approaches and PET-scans. Rather than cell division versus death rates of cancer cells, in cellular dormancy, intrinsic mechanisms leading to a quiescence-like stage and cell cycle arrest are in play. BioNet has been applied to data from prostate cancer[13], breast cancer[14], and hepatocellular carcinoma[15], among others
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