Context-aware monitoring: rethinking comprehensive screening in the era of AI.

Breast cancer is a major global health challenge, being the most commonly diagnosed cancer and the fifth leading cause of cancer-related mortality worldwide. Breast cancer development and progression are influenced not only by tumor-intrinsic factors but also by systemic host factors such as chronic low-grade inflammation and dysregulated cytokines. Obesity and physical inactivity are associated with an inflammatory milieu that can promote breast cancer pathogenesis and worsen survival. In overweight or obese subjects, adipose tissue releases pro-inflammatory cytokines (e.g., interleukin-6 [IL-6], tumor necrosis factor-alpha [TNF-α]), and adipokines (e.g., leptin), contributing to a chronic inflammatory environment that promotes tumor progression by enhancing angiogenesis and impairing anti-tumor immune responses. Raised IL-6, TNF-α, and C-reactive protein (CRP) are linked to poorer prognosis in breast cancer, correlating with higher rates of recurrence, metastasis, and mortality. In contrast, anti-inflammatory factors like interleukin-10 (IL-10) and adiponectin may exert protective effects. Adiponectin, an adipocyte-derived hormone, promotes an anti-inflammatory, insulin-sensitizing state and can directly inhibit breast cancer cell growth via activation of AMP-activated protein kinase (AMPK) and downregulation of proliferative pathway PI3K/Akt. Higher adiponectin is associated with lower breast cancer risk, whereas leptin, a pro-inflammatory adipokine upregulated in obesity, enhances breast cancer cell proliferation and survival, angiogenesis, and invasion through estrogen-dependent and -independent mechanisms. A leptin/adiponectin imbalance observed in obesity (characterized by hyperleptinemia and hypoadiponectinemia) is a major factor linking excess adiposity to breast cancer progression. Thus, targeting chronic inflammation and adipocytokine dysregulation is increasingly recognized as an important strategy in breast cancer management. Exercise training is emerging as a potent lifestyle intervention to attenuate chronic inflammation and favorably modulate adipocytokines in both healthy and clinical populations, with regular exercise exerting anti-inflammatory effects. Exercise reduces visceral and total body fat mass, thereby decreasing the source of pro-inflammatory adipokines including IL-6, TNF-α, and leptin, often with increases in adiponectin. On the other hand, each acute bout of exercise provokes a transient release of muscle-derived cytokines (myokines), notably IL-6, which paradoxically mediates anti-inflammatory effects by stimulating IL-10 production and inhibiting TNF-α and IL-1β signaling through AMPK activation. Exercise also shifts immune cell profiles toward a less inflammatory state—such as increasing anti-inflammatory M2 macrophages over pro-inflammatory M1 in adipose tissue—and improves metabolic factors like insulin resistance that are closely linked to inflammation. These multifactorial actions help explain why long-term (chronic) exercise is associated with reduced systemic inflammation and improved outcomes in cancer survivors. In breast cancer patients and survivors, numerous randomized controlled trials (RCTs) have examined the effects of exercise on inflammatory markers. Many reports exercise reduces circulating IL-6 and CRP, and in some cases, downregulates TNF-α and leptin while upregulating adiponectin, although such findings have not been uniform. The heterogeneity in inflammatory outcomes may relate to differences in exercise modes, intensities, and durations, as well as patient factors. Notably, prior meta-analyses have provided evidence that overall, exercise has beneficial effects on inflammatory biomarkers in breast cancer. Similarly, structured exercise can induce small-to-moderate improvements in pro-inflammatory cytokines in this population. However, these reviews have typically evaluated exercise in general and have not directly compared different exercise modes (e.g., aerobic vs. resistance vs. combined training). It remains unclear whether certain modes of exercise confer superior anti-inflammatory effects in breast cancer patients, which represents a critical knowledge gap for exercise oncology. We present a systematic review along with the first network meta-analysis comparing the efficacy of different exercise modalities on key pro- and anti-inflammatory cytokines and adipokines (IL-6, TNF-α, IL-10, CRP, leptin, and adiponectin) in patients with breast cancer. By integrating direct and indirect evidence, this approach enables the ranking of exercise interventions based on their anti-inflammatory effects. Our objectives are to quantify the overall effects of exercise training and identify which modes offer the greatest benefits. We have also examined the potential effect modifiers, such as the patients’ clinical status (during vs. post-treatment) and intervention durations. This work addresses a key evidence gap and aims to refine exercise prescriptions by ident