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Tumor cell lysis via selective oncolytic replication refers to a therapeutic mechanism in which oncolytic viruses—either genetically engineered or naturally occurring—are designed or selected to infect, replicate within, and lyse tumor cells while typically sparing normal tissue. The selectivity arises from cancer-specific defects in antiviral pathways, such as the interferon response or apoptotic signaling, enabling viruses to proliferate and destroy malignant cells directly. Simultaneously, this lytic process releases tumor antigens and danger signals (DAMPs), which can stimulate dendritic cell recruitment, adaptive immune activation, and systemic anti-tumor immunity. This dual effect makes oncolytic virotherapy distinct from many other cancer strategies, and it serves both as a local cytotoxic agent and as an immunotherapy platform. Representative agents include talimogene laherparepvec (T-VEC) and JX-594. Key challenges include immune clearance of the virus, ensuring tumor specificity, and overcoming resistance mechanisms within the tumor microenvironment.
Selective viral infection and replication in tumor cells; Direct cell lysis resulting in tumor destruction; Release of tumor antigens/DAMPs stimulating the immune system; Transgene expression for additional toxicity or immune stimulation; Disruption of tumor immune evasion mechanisms; Modulation of cell cycle and apoptotic signaling pathways
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