Abstract
Breast cancer metastasis is the leading cause of cancer deaths in women and is difficult to combat due to the long periods in which disseminated cells retain a potential to be re-activated and start the relapse. Assessing the number and molecular profile of circulating tumor cells (CTCs) in breast cancer patients, especially in early breast cancer, should help in identifying the possibility of relapse in time for therapeutic intervention to prevent or delay recurrence. While metastatic breast cancer is considered incurable, molecular analysis of CTCs still have a potential to define particular susceptibilities of the cells representing the current tumor burden, which may differ considerably from the cells of the primary tumor, and offer more tailored therapy to the patients. In this review we inspect the routes to metastasis and how they can be linked to specific features of CTCs, how CTC analysis may be used in therapy, and what is the current status of the research and efforts to include CTC analysis in clinical practice.
Highlights
Breast cancer (BC) has the highest incidence rate and is the leading cause of cancer death in women, the overall mortality is not as high as in the other types of cancer [1]
circulating tumor cells (CTCs)’ expression prolife display intra-patient heterogeneity, which suggest the existence of some distinct population of metastasis-initiating cells; the work of Baccelli et al [35] demonstrated, using a mouse xenograft assay, that such a population in luminal breast cancer CTCs is enriched with EPCAM, CD44, CD47 and MET
It was demonstrated in mouse models that breast cancer metastases are of polyclonal origin [68,69], which is inconsistent with the dissemination and expansion of a single cell, but can be explained by the dissemination of CTC clusters
Summary
Breast cancer (BC) has the highest incidence rate and is the leading cause of cancer death in women, the overall mortality is not as high as in the other types of cancer [1]. Triple-negative breast cancer (TNBC, ER- PR- HER2-), which constitutes about 15% of all cases, is heterogeneous itself, comprising different subtypes, including basal like, immune-modulatory, luminal androgen receptor, mesenchymal and claudin low. Despite these differences, it is always highly aggressive, associated with chemotherapeutic resistance and low survival rates. Different timelines and dynamics of breast cancer metastasis in different subtypes might suggest differences in the mode of dissemination, but more convincing evidence is needed to prove that it is the case At the moment it seems that parallel progression is better described for HER2-positive tumors [11,12] and occurs in ER-positive type [13]. Clarification of the factors determining the CTC release pattern is an important goal that can be achieved only by systematic longitudinal studies of CTC numbers in a large patients’ cohorts
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