Abstract
Breast cancer is the most commonly diagnosed cancer in women worldwide, and >90% of breast cancer-related deaths are associated with metastasis. Breast cancer spreads preferentially to the lung, brain, bone and liver; termed organ tropism. Current treatment methods for metastatic breast cancer have been ineffective, compounded by the lack of early prognostic/predictive methods to determine which organs are most susceptible to developing metastases. A better understanding of the mechanisms that drive breast cancer metastasis is crucial for identifying novel biomarkers and therapeutic targets. Lung metastasis is of particular concern as it is associated with significant patient morbidity and a mortality rate of 60–70%. This review highlights the current understanding of breast cancer metastasis to the lung, including discussion of potential new treatment approaches for development.
Highlights
Breast cancer is the most common malignancy in women, and 626,679 deaths worldwide in 2018 were attributed to it [1]
We summarize current advancements in the understanding of molecular mechanisms that drive breast cancer metastasis to the lung
The process of generating the pre-metastatic niche in lung is highly reliant on immune-suppression to ensure that CD8+ T cells, natural killer (NK) cells and patrolling monocytes are masked from the presence of tumor cells trying to establish themselves as metastatic lesions in the lung [57,58]
Summary
Breast cancer is the most common malignancy in women, and 626,679 deaths worldwide in 2018 were attributed to it [1]. Lung metastases in particular tend to occur within 5 years of initial breast cancer diagnosis and have a significant impact on patient morbidity and mortality. These metastases disrupt normal lung function, resulting in coughing, labored breathing, hemoptysis, and eventual death. First described by Perou et al (2000), breast cancer can be subdivided into four main clinical subtypes on the basis of gene expression profiles and receptor status (estrogen receptor [ER], progesterone receptor [PR], human epidermal growth factor receptor 2 [HER2]) and proliferation status as assessed by Ki67 [10]. By integrating the complex body of work that surrounds this topic, we highlight key therapeutic targets and potential/emerging treatment approaches
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