UNASSIGNED: A high body mass index (BMI) can indicate overweight or obesity and is a crucial risk factor for breast cancer survivors. However, the association between high BMI and prognosis in early-stage breast cancer (EBC) remains unclear. We aimed to assess the effects of high BMI on the prognosis of patients with EBC.
UNASSIGNED: The PubMed, Embase, and Cochrane Library databases and proceedings of major oncological conferences related to the effects of BMI on the prognosis of breast cancer were searched up to November 2021. Fixed- and random-effects models were used for meta-analyses. Pooled hazard ratios (HRs) and 95% confidence intervals (CIs) for disease-free survival (DFS) and overall survival (OS) were extracted from the included literature.
UNASSIGNED: Twenty retrospective cohort studies with 33,836 patients with EBC were included. Overweight patients had worse DFS (HR: 1.16, 95% CI: 1.05-1.27, P = 0.002) and OS (HR: 1.20; 95% CI: 1.09-1.33, P < 0.001). Obesity also had adverse effects on DFS (HR: 1.17, 95% CI: 1.07-1.29, P = 0.001) and OS (HR: 1.30, 95% CI: 1.17-1.45, P < 0.001). Likewise, patients with high BMI had worse DFS (HR: 1.16, 95% CI: 1.08-1.26, P < 0.001) and OS (HR: 1.25, 95% CI: 1.14-1.39, P < 0.001). In subgroup analyses, overweight had adverse effects on DFS (HR: 1.11, 95% CI: 1.04-1.18, P = 0.001) and OS (HR: 1.18, 95% CI: 1.11-1.26, P < 0.001) in multivariate analyses, whereas the relationship that overweight had negative effects on DFS (HR: 1.21, 95% CI: 0.99-1.48, P = 0.058) and OS (HR: 1.39, 95% CI: 0.92-2.10, P = 0.123) was not statistically significant in univariate analysis. By contrast, obesity had adverse effects on DFS (HR: 1.21, 95% CI: 1.06-1.38, P = 0.004 and HR: 1.14, 95% CI: 1.08-1.22, P < 0.001) and OS (HR: 1.33, 95% CI: 1.15-1.54, P < 0.001 and HR: 1.23, 95% CI: 1.15-1.31, P < 0.001) in univariate and multivariate analyses, respectively.
UNASSIGNED: Compared with normal weight, increased body weight (overweight, obesity, and high BMI) led to worse DFS and OS in patients with EBC. Once validated, these results should be considered in the development of prevention programs.

Obesity poses deleterious consequences on every organ system, especially the lymphatic network. However, the underlying cellular mechanisms through which obesity causes lymphatic dysfunction remains unclear. We aimed to summarize experimental studies that evaluated the effect of obesity on the lymphatic system on animal models.
We used the following terms to search the Ovid EMBASE, Ovid MEDLINE(R), Cochrane, and Scopus databases: \"lymphedema\", \"lymphatic diseases\", \"lymphatic system/complications* \", \"lymphatic system/injuries* \", \"lymphatic system/abnormalities* \", AND \"obesity/complications* \", \"diet/high-fat\", \"adipogenesis\" and \"lipid metabolism disorder\". From a total of 166 articles identified in the initial search, 13 met our eligibility criteria.
Long-term exposure to high-fat diet in mice demonstrated significant amount of adipose tissue deposition which sets off an inflammatory cascade resulting in disruption of the chemokine gradient, inhibition of lymphangiogenesis, and changes in gene expression of lymphatic endothelial cells, that alter vessel permeability and induce cell death. Reduced contractile properties of lymphatic collectors, dilated capillaries, increased tissue pressure, and reduced hydraulic conductivity collectively contribute to reduced impaired lymphatic drainage. Aerobic exercise has shown reversal of lymphatic dysfunction in the obese and pharmacological interventions targeting T-cells, iNOS and VEGFR-3 signaling have the potential to combat acquired lymphedema.
Scientists should focus their future experiments on developing therapies that regulate expression of T-cell derived cytokines and VEGFR-3 expression whereas clinicians are urged to counsel their patients to reduce weight through aerobic exercise.