In response to a variety of cancer-inducing stresses, cells may engage a stable cell cycle arrest mechanism, termed cellular senescence, to suppress the proliferation of preneoplastic cells. Despite this cell intrinsic tumor suppression, senescent cells have also been implicated as active contributors to tumorigenesis by extrinsically promoting many hallmarks of cancer, including evasion of the immune system. Here, we discuss these dual, and seemingly contradictory, roles of senescence during tumorigenesis. Furthermore, we highlight findings of how senescent cells can influence the immune system and discuss the possibility that immune cells themselves may be acquiring senescence-associated alterations. Lastly, we discuss how senescent cell avoidance or clearance may impact pathology.

Cellular senescence is the dynamic process of durable cell-cycle arrest. Senescent cells remain metabolically active and often acquire a distinctive bioactive secretory phenotype. Much of our molecular understanding in senescent cell biology comes from studies using mammalian cell lines exposed to stress or extended culture periods. While less well understood mechanistically, senescence in vivo is becoming appreciated for its numerous biological implications, both in the context of beneficial processes, such as development, tumor suppression, and wound healing, and in detrimental conditions, where senescent cell accumulation has been shown to contribute to aging and age-related diseases. Importantly, clearance of senescent cells, through either genetic or pharmacological means, has been shown to not only extend the healthspan of prematurely and naturally aged mice but also attenuate pathology in mouse models of chronic disease. These observations have prompted an investigation of how and why senescent cells accumulate with aging and have renewed exploration into the characteristics of cellular senescence in vivo. Here, we highlight our molecular understanding of the dynamics that lead to a cellular arrest and how various effectors may explain the consequences of senescence in tissues. Lastly, we discuss how exploitation of strategies to eliminate senescent cells or their effects may have clinical utility.

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Despite many advancements in brain cancer therapeutics, brain cancer remains one of the most elusive diseases with high migratory capacity and a dismal prognosis. It is well established that tumor stem cells utilize the same available migratory machinery that normal cells employ. Some of the major determinants of brain tumor stem cell migration are their cytoskeletal rearrangements and adhesion dynamics. This phenomenon allows brain tumor stem cells to perpetually migrate, invade, and repopulate in a vicious cycle leading to tumor expansion and invasion at tumor boundaries. In order to dissect the enabling factors that allow for this process to be hijacked, we have identified relevant assays to enable measurements of neoplastic migration such as Boyden Chamber, 3D chemogradient chamber, Nanopattern, and wound healing assays. Our purpose is to report the complex experimental platforms seen in the literature today and provide an optimal platform to kick off your studies in this field.