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.
Our immune system has the ability to detect and fight infectious pathogens. It can also detect when normal cells become cancerous and kill those cells, preventing cancer progression. But over time, cancers can evolve and evade the immune response.
Researchers use chromatin immunoprecipitation, or ChIP, to identify and characterize protein-DNA interactions in the context of chromatin. ChIP experiments can use varying input samples, chromatin fragmentation methods, and provide ChIP-qPCR or ChIP-seq readouts.
Immunohistochemistry, or IHC, remains the simplest method for detecting biomarker expression while maintaining spatial context within tissues. You know that getting reliable IHC staining results hinges on the specificity and performance of your antibody. These are high stakes experiments, and you want to be 100% confident your antibody will detect the target of interest.
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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.
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.
In collaboration with Cell Press, we are excited to announce a new educational resource that will make it easier for biology students and researchers to navigate their careers, get published, and strengthen their laboratory skills to enable experimental success. That new resource is called Cell Mentor™.