Environmental eustress inhibits CCL2 to overcome doxorubicin-induced cardiotoxicity and alleviate tumor growth
Peer-Reviewed Publication
Updates every hour. Last Updated: 23-Oct-2026 07:16 ET (23-Oct-2026 11:16 GMT/UTC)
A team led by Academician Ge Junbo and Professor Sun Aijun at Fudan University reveals that environmental eustress attenuates doxorubicin-induced cardiotoxicity while enhancing antitumor effects via a hypothalamus-heart-tumor axis. Eustress upregulates hypothalamic BDNF, which activates TrkB receptors on cardiac resident macrophages to inhibit CCL2 secretion, thereby reducing pro-inflammatory Ly6Chigh monocyte/macrophage infiltration into heart tissue. In hepatocellular carcinoma models, eustress also downregulates tumor microenvironment CCL2, decreasing immunosuppressive G-MDSCs and M2 macrophages while increasing cytotoxic CD8+ T cells and M1 macrophages. CCL2 is identified as a core dual target for cardio-oncology intervention, providing a safe and accessible non-pharmacological strategy for preventing chemotherapy-related cardiac toxicity in cancer patients.
After treatment for metastatic prostate cancer, a drop in prostate-specific antigen (PSA) levels in the blood is an indicator that the treatment is working. A recent real-world study published by Wiley online in CANCER indicates that reaching a PSA level below 0.2 ng/mL is an indicator of improved patient survival.
Researchers from Keio University have found that D-serine increases the growth of gastric cancer by creating an immunosuppressive and anti-inflammatory tumor microenvironment. Higher levels of D-serine in serum correlated with greater immune checkpoint inhibitor therapy resistance in tumors. Suppressing D-serine in circulation could improve the efficacy of immunotherapies against gastric cancer. These findings position D-serine within the broader field of cancer amino acid metabolism and point to it as a possible target for tumor evasion.
The tissue microenvironments surrounding HIV-infected immune cells look a lot like those surrounding cancerous tumors, reports a new Northwestern University study.
The findings help explain why HIV has been so difficult to cure. Scientists found that viral reservoirs exist within tissue microenvironments that resemble immune-suppressive tumor microenvironments, suggesting that future HIV cure strategies may benefit from approaches traditionally used in cancer therapy.