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VEGF

Liver-Specific Overexpression of Gab2 Accelerates Hepatocellular Carcinoma Progression by Activating Immunosuppression of Myeloid-Derived Suppressor Cells

[Oncogene] Liver-specific overexpression of GRB2-associated-binding protein 2 (Gab2) mice accelerated hepatoma progression possibly through activating IL-6-initiated the activation of myeloid-derived suppressor cells.

Liver-Specific Overexpression of Gab2 Accelerates Hepatocellular Carcinoma Progression by Activating Immunosuppression of Myeloid-Derived Suppressor Cells

[Oncogene] Liver-specific overexpression of GRB2-associated-binding protein 2 (Gab2) mice accelerated hepatoma progression possibly through activating IL-6-initiated the activation of myeloid-derived suppressor cells.

Attenuating Adaptive VEGF-A and IL8 Signaling Restores Durable Tumor Control in AR Antagonist–Treated Prostate Cancers

[Molecular Cancer Research] Hypoxia increased androgen receptor expression and transcriptional activity in prostate cells in vitro.

Protrudin Regulates FAK Activation, Endothelial Cell Migration and Angiogenesis

[Cellular and Molecular Life Sciences] Researchers investigated the role of the endoplasmic reticulum-anchored protein, Protrudin, in endothelial cell protrusion, migration and angiogenesis.

Inhibition of Triple Negative Breast Cancer-Associated Inflammation, Tumor Growth and Brain Colonization by Targeting Monoacylglycerol Lipase

[Scientific Reports] Scientists targeted Monoacylglycerol lipase (MAGL) in TNBCs, using a potent carbamate-based inhibitor AM9928 with prolonged pharmacodynamic effects. AM9928 blocked TNBC cell adhesion and transmigration across human brain microvascular endothelial cells in 3D co-cultures.

Doxorubicin Induced Immune Abnormalities and Inflammatory Responses via HMGB1, HIF1-α and VEGF Pathway in Progressive of Cardiovascular Damage

[Annals of Medicine] The authors comprehensively review the role of high-mobility group box 1 (HMGB1), hypoxia-inducible factor-1α (HIF-1α), and VEGF in doxorubicin-induced cardiovascular disease and its molecular mechanisms.

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