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Scott Lonning

Researcher at Genzyme

Publications -  34
Citations -  3738

Scott Lonning is an academic researcher from Genzyme. The author has contributed to research in topics: Transforming growth factor beta & Metastasis. The author has an hindex of 24, co-authored 34 publications receiving 3403 citations.

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Protection from obesity and diabetes by blockade of TGF-β/Smad3 signaling

TL;DR: It is demonstrated that TGF-β signaling regulates glucose tolerance and energy homeostasis and suggested that modulation of T GF-β activity might be an effective treatment strategy for obesity and diabetes.
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Tumor Evasion of the Immune System by Converting CD4+CD25− T Cells into CD4+CD25+ T Regulatory Cells: Role of Tumor-Derived TGF-β

TL;DR: It is demonstrated that tumor cells directly convert CD4+CD25− T cells to Treg cells through production of high levels of TGF-β, suggesting a possible mechanism through which tumor cells evade the immune system.
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Transforming growth factor beta subverts the immune system into directly promoting tumor growth through interleukin-17.

TL;DR: Using transplantable models of breast and colon cancer, the unexpected finding that CD8+ cells in tumor-bearing animals can directly promote tumorigenesis, by a mechanism that is dependent on TGF-beta is made.
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Resistance of Glioblastoma-Initiating Cells to Radiation Mediated by the Tumor Microenvironment Can Be Abolished by Inhibiting Transforming Growth Factor-β

TL;DR: The use of TGF-β inhibitors with radiation to improve therapeutic response in patients with GBM is motivated by data that suggest GIC promotes effective DNA damage response and self-renewal, which creates microenvironment-mediated resistance.
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An Anti–Transforming Growth Factor β Antibody Suppresses Metastasis via Cooperative Effects on Multiple Cell Compartments

TL;DR: It is shown that efficacy of the anti-TGF-beta antibody 1D11 in suppressing metastasis was dependent on a synergistic combination of effects on both the tumor parenchyma and microenvironment and the absence of a major effect of TGF- beta antagonism on any one cell compartment may be critical for a good therapeutic window and the avoidance of autoimmune complications.