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There are three main clinically relevant biological subtypes: Oestrogen/Progesterone receptor positive breast cancer (ER +/PR +), HER2 amplified (HER2 +) breast cancer and Triple Negative Breast Cancer (TNBC i.e., ER -, PR -, HER2 -). Therapy and prognosis are largely determined by the biological and molecular characteristics of the primary tumor and its size and spreading at time of diagnosis. In spite of improved management over the past 30 years, it remains the leading cause of cancer-related mortality for women world-wide. īreast cancer subtypes and adjuvant therapiesīreast cancer is the most common cancer diagnosed among women. In breast cancer, relapses occur with a peculiar bimodal distribution: a first peak appears generally 1-2 years and a second peak 4-5 years after surgery, followed by a tailed extension up to 15 years. Conversely, in prostate cancer relapses occur late, with over 90% of the patients still alive 15 years after initial diagnosis. For example, lung and colorectal cancers mostly relapse within 1-3 years after diagnosis and the 5-year survival rates for these cancers are about 20% and 60%, respectively.
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Those that progress to metastatic disease can do with strikingly different kinetic. At diagnosis, only a minority of cancers have already formed clinically overt metastases (i.e., stage IV). Tumor angiogenesis, the remodeling of the extracellular matrix, the activation of local resident cells and the recruitment of inflammatory cells provide essential contributions to the metastatic process, including in breast cancer.
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While cell autonomous processes, such as genetic evolution and epigenetic modifications, altered gene expression and metabolic adaptation, are essential to the metastatic process, the microenvironments of the primary tumor and of the metastatic site are equally critical determinants of metastasis formation. During this adaptation step at the metastatic site, cells have to establish bidirectional paracrine communication with a new tissue different from the primary site, acquire novel survival capacities and escape immune destruction. The main rate limiting step in the metastatic process appears to be the ability of tumor cells to adapt to the new environment. Metastasis formation is believed to be a highly inefficient process. With a few exceptions, as in the case of brain or liver cancer, the main cause of cancer-related death is not the primary tumor itself but rather the formation of secondary tumors, so called metastases, in vital organs, in particular lung, liver, bone or brain, leading to organ destruction and failure, resistance to therapy and cachexia. Here we will review concepts and recent developments in cancer metastasis and dormancy with emphasis on breast cancer, and elaborate strategies to exploit them therapeutically. Using this model, we identified IRF-7/Interferon type I/IFNRA as signaling axis essential for this effect. We have observed that cells surviving chemotherapy can enter a state of immunological dormancy. Thus, developing new models to identify clinically relevant mechanisms and candidate therapeutic targets may open new avenues for novel therapies to induce and prolong dormancy. Investigating mechanisms of breast cancer dormancy remains challenging, as in patients the condition is elusive and experimentally there are only a few models that recapitulate the clinical condition. How cancer cells enter, sustain and exit dormancy, are unanswered questions with relevance to cancer biology, monitoring and therapy. This discontinuous growth kinetics is consistent with the notion that disseminated cancer cells can remain dormant over a prolonged period of time before resuming growth. Relapses occur with a bimodal temporal distribution, with a first peak at 1-2 years after initial therapy and a second peak 2-3 years later. Main cause of death is the development of therapy-resistant metastases. Breast cancer remains the main cause of cancer-related mortality for women world-wide.