Therapy-induced senescence (TIS) generates an immunogenic state in cancer cells
First-pass extracted concept
therapy-induced senescence
Aliases
TIS
Evidence Snippets
Supporting Sources
Linked Claims
BH3 profiling assessments have revealed that therapy-induced senescent cancer cells are globally less primed for apoptosis than their proliferating precursors.
recent assessments of mitochondrial apoptotic signaling via BH3 profiling ... have revealed that TIS cancer cells are globally less primed for apoptosis than their proliferating precursors
Therapy-induced senescent cancer cells exhibit a conserved, druggable dependence on specific BCL-2 family members for survival.
TIS cancer cells exhibit a conserved, druggable dependence on specific members of the BCL-2 family for survival.
Pre-existing mitochondrial priming and anti-apoptotic dependencies of parental non-senescent cells are retained after senescence induction, suggesting an inherited mitochondrial memory.
the pre-existing priming and anti-apoptotic addictions of parental, non-senescent cells, are retained upon induction of senescence. This suggests an "inherited" mitochondrial memory
Therapy-induced senescence generates an immunogenic state in cancer cells by altering antigen presentation, cytokine production, and surfaceome organization.
Therapy-induced senescence (TIS) generates an immunogenic state in cancer cells by altering how they present antigens, produce cytokines, and organize their surfaceome.
Therapy-induced senescence can be therapeutically exploited using immunosenolytic strategies including CAR-engineered T cells and NK cells.
TIS can be exploited for therapeutic purposes using "immunosenolytic" strategies, including adoptive cellular therapies such as chimeric antigen receptor (CAR)-engineered T and natural killer (NK) cells.