Abstract
Brain metastases (BMs) are the most common brain tumor in adults, developing in about 10% of adult cancer patients. It is not the incidence of BM that is alarming, but the poor patient prognosis. Even with aggressive treatments, median patient survival is only months. Despite the high rate of BM-associated mortality, very little research is conducted in this area. Lack of research and staggeringly low patient survival is indicative that a novel approach to BMs and their treatment is needed. The ability of a small subset of primary tumor cells to produce macrometastases is reminiscent of brain tumor-initiating cells (BTICs) or cancer stem cells (CSCs) hypothesized to form primary brain tumors. BTICs are considered stem cell-like due to their self-renewal and differentiation properties. Similar to the subset of cells forming metastases, BTICs are most often a rare subpopulation. Based on the functional definition of a TIC, cells capable of forming a BM could be considered to be brain metastasis-initiating cells (BMICs). These putative BMICs would not only have the ability to initiate tumor growth in a secondary niche, but also the machinery to escape the primary tumor, migrate through the circulation, and invade the neural niche.
Highlights
IntroductionAdvancements in the treatment of systemic diseases along with timely screening and imaging protocols have led to an increase in the overall and progression-free survival of primary malignancies
Advancements in the treatment of systemic diseases along with timely screening and imaging protocols have led to an increase in the overall and progression-free survival of primary malignancies.for many of these patients who have won their battle with cancer, their war remains far from over as recent epidemiological studies have shown an increase in the incidence and prevalence of brain metastasis (BM) [1,2]
We focus on evidence from the metastatic process, the recent identification of brain tumor-initiating cells (BTICs), the presence of activated developmental signaling pathways in BMs, and how these cell-intrinsic pathways may promote tumor heterogeneity while presenting novel therapeutic targets
Summary
Advancements in the treatment of systemic diseases along with timely screening and imaging protocols have led to an increase in the overall and progression-free survival of primary malignancies. BMs occur in up to 40% of cancer patients [4], representing an incidence that is ten times greater than that of primary brain tumors [5,6] Aside from their frequency, the burden of BMs is further illustrated by a median survivorship of 1–2 months in palliative patients with multimodal therapy extending survival to only 4–6 months [7]. In contrast to their uniformly fatal prognosis, the localization, tissue-specific primary origin, and clinical presentation of BMs are all quite variable. Multiple lesions form in the cortex as opposed to the grey-white junction, associated with hemorrhage
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