2006
DOI: 10.1016/j.ijrobp.2006.02.051
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Antitransforming growth factor–β antibody 1D11 ameliorates normal tissue damage caused by high-dose radiation

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Cited by 115 publications
(89 citation statements)
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“…55 Radiation fibrosis is considered late radiation damage, and TGFb1 plays a pivotal role in the establishment of radiation fibrosis. For the purpose of neutralizing TGF-b antibodies to prevent lung fibrosis in rats 56 or using a small molecule to inhibit TGFb signaling, halofuginone was tested in mice. 57 …”
Section: Mitigators Of Radiationmentioning
confidence: 99%
“…55 Radiation fibrosis is considered late radiation damage, and TGFb1 plays a pivotal role in the establishment of radiation fibrosis. For the purpose of neutralizing TGF-b antibodies to prevent lung fibrosis in rats 56 or using a small molecule to inhibit TGFb signaling, halofuginone was tested in mice. 57 …”
Section: Mitigators Of Radiationmentioning
confidence: 99%
“…Although the treatment was well tolerated, the therapeutic results were unconvincing, and development of this compound has been stopped. Another anti-TGF␤ antibody, called 1D11, is in development (12), but no experience on its effects in patients with SSc has yet been reported. The pleiotropic nature of TGF␤ makes consequences of its use as a treatment approach difficult to predict.…”
mentioning
confidence: 99%
“…Due to the vast number of potential targets in the TGFB1 signaling pathway, multiple approaches have been adopted in vitro to prevent the binding of TGFB1 to its receptor, including specific antibody-mediated neutralization of soluble TGFB, or dominant-negative inhibition of TGFBRI and TGFBRII (71,72). The TGFB-specific approaches inhibited radiation-dependent TGFB1 secretion, the phosphorylation of SMAD and reporter gene activity, indicating that autocrine production of TGFB and the subsequent activation of TGFB1 induced these changes (54).…”
Section: Preclinical and Clinical Strategies For Targeting The Tgfb1 mentioning
confidence: 99%
“…The TGFB-specific approaches inhibited radiation-dependent TGFB1 secretion, the phosphorylation of SMAD and reporter gene activity, indicating that autocrine production of TGFB and the subsequent activation of TGFB1 induced these changes (54). After administering a single dose of 1.0 mg/kg anti-TGFB1 antibody, delivered with the final fraction of the right hemithorax irradiation, to Fischer rats, Anscher et al (72) demonstrated that, compared with in the rats receiving radiation alone, inhibited fibrosis, TGFB1 expression and TGFB1-induced signaling were observed in the rats treated with a combination of radiation and an anti-TGFB1 antibody. A TGFBRI inhibitor was also administered daily to a group of Sprague-Dawley rats with irradiated right lungs (72).…”
Section: Preclinical and Clinical Strategies For Targeting The Tgfb1 mentioning
confidence: 99%