Not all cancer cells are equal, they evolve in response to selective pressure driven by accumulation of mutations. Cancer cells have to out-compete nearby cells for nutrients and other resources, avoid immune cell attack, and suppress apoptotic self-destruction.
Cancer cells hijack inflammatory mechanisms to promote their own growth and survival. During a normal inflammatory response by the innate and adaptive immune system, immune cells carry out their designated task of engulfing and/or destroying foreign invaders.
Gain insight into the processes by which senescent cells contribute to tumor suppression and age-related pathologies. This webinar explores the impact of senescence on age-related dysfunction and chronic disease and introduces potential therapies targeting senescent cells.
Cancer cells invade local tissue and spread to distant sites via two distinct, but similar processes known as invasion and metastasis.
Some cancer cells adapt mechanisms to evade detection and destruction by the host's immune system. One way cells do this is by hijacking normal mechanisms of immune checkpoint control and modulation of the innate immune response via STING.
The process of epithelial-mesenchymal transition (EMT), whereby differentiated epithelial cells transform into cells with more mesenchymal characteristics, was first described by pioneering Harvard biologist Elizabeth “Betty” Hay in the 1980s.
Cellular senescence is defined by permanent cell cycle arrest. Senescent cells accumulate with age and contribute to the normal aging process as well as age-related disorders. The link between senescence, aging, and age-related pathologies, including cancer, neurodegeneration, and metabolic and cardiovascular diseases have largely fueled the senescence research field.
Topics: Cell Biology
Cancer cells resist inhibitory signals that might otherwise stop their growth. The major pathways involved are Autophagy and Death Receptor Signaling (Apoptosis), both of which can ultimately lead to cell death, and reduction in tumor growth.
Cancer cells can revert to a pre-differentiated, stem-cell-like phenotype, allowing uninhibited cellular division and other metabolic adaptations that enable survival in adverse conditions.
Cancer cells stimulate their own growth, which means they become self-sufficient in growth signals, and no longer depend on external signals (like Epidermal Growth Factor EGF/ EGFR). Proliferation depends highly on these three important pathways: Akt, MAPK/Erk, and MTOR.