Cellular senescence plays a context-dependent dual role in tumor progression. Transitioning from a tumor-suppressive barrier in premalignant stages to a tumor-promoting driver during progression, and further to double-edged effects in therapy, its functional shift involves complex molecular mechanisms and microenvironmental interactions. This review outlines the relationship between aging and cancer; describes the characteristics, functions, and clinical potential of cellular senescence in cancer; and the transition from tumor suppression to tumor promotion. Specifically, we examine how this transition is driven by immune clearance failure, NOTCH1-regulated SASP shifts, the positive feedback loop between senescence accumulation and immunosuppression, and mesenchymal drift. We also discuss the possibility that senescent cells act as a reservoir for malignant transformation, and that tumor cells escaping clearance may retain a “reversible senescence memory.” Finally, we highlight current therapeutic strategies targeting senescence, including senolytics and senomorphics, and critically assess the risks of improper senolytic use. Together, these insights offer new perspectives on the central role of senescence in tumorigenesis and progression.

Advanced age is associated with immune decline and remodeling, including loss of adaptive reserve, impaired host defense, and chronic low-grade inflammation. Yet the immune phenotype of long-lived individuals (LLIs), especially centenarians, shows that immune aging is not a uniform process. Rather than reflecting global rejuvenation, longevity-associated immunity is better understood as selective preservation of immune competence, with selected cellular features retaining youth-like characteristics under the constraints of extreme age. The most direct cellular evidence comes from innate effector functions, including preserved natural killer (NK)-cell cytotoxic surveillance and neutrophil chemotaxis, phagocytosis, and redox control. T-cell findings are more heterogeneous, including maintenance of a non-inverted CD4/CD8 ratio and partial naive CD4⁺ T-cell reserve, while T helper 17 cell (Th17)/regulatory T cell (Treg) data provide more limited support for preserved regulatory-inflammatory balance. Myeloid and antigen-presenting-cell programs may further support clearance and antigen handling, although direct functional evidence remains more limited. Molecular studies point to candidate support layers rather than proven causal mechanisms, including coordinated immune-cell states and communication, survival and apoptosis-regulatory programs, ribosome-inflammation balance, autophagy-lysosomal and mitochondrial quality control, and buffering of inflammatory and senescence-associated signals. Importantly, some immune changes reported in LLIs fall outside the youth-like frame: cytotoxic and effector-memory T-cell states and repertoire remodeling, humoral shifts, and complement changes are better interpreted as adaptive remodeling whose occurrence and significance depend on lifelong immunological experience. This framework places selective preservation of immune competence at the center of LLI immune biology while distinguishing it from experience-shaped adaptive remodeling.