Serum markers for prediction of pulmonary radiation syndromes. Part I: Surfactant apoprotein

Rubin, Philip; McDonald, Sandra; Maasilta, Paula; Finkelstein, Jacob N.; Shapiro, Donald L.; Penney, David P.; Gregory, Philip K.

doi:10.1016/0360-3016(89)90106-5

Cited by 21 publications

(5 citation statements)

References 25 publications

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“…Type II pneumocyte damage has been demonstrated by ultrastmctural study as early as 1 hour after radiation and results in the immediate release of surfactant (1). Plasma surfactant apoprotein level has been shown to increase after radiation in a dose-dependent manner and has been proposed as a marker for the later development of pulmonary fibrosis (27). Pretreatment with keratinocyte growth factor (KGF), a potent type II pneumocyte growth factor in vivo (28), has been shown to prevent the bleomycin-induced lung fibrosis in rats (29), suggesting that type II pneumocytes are important in the regulation of development of fibrosis.…”

Section: Discussionmentioning

confidence: 99%

Radiation-induced lung injury in vivo: Expression of transforming growth factor?Beta precedes fibrosis

Bedoya

Lee

et al. 1996

Inflammation

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Cytokine release from irradiated cells has been postulated to start soon after irradiation preceding detectable clinical and pathological manifestation of lung injury. The expression of transforming growth factor beta (TGF beta), a fibrogenic and radiation-inducible cytokine, was studied from 1-16 weeks after the 15 and 30 Gray (Gy) of thoracic irradiation to rats. Thoracic irradiation caused an increase in TGF beta protein in bronchoalveolar lavage (BAL) fluid peaking at 3-6 weeks as compared to sham-irradiated control rats. Steady state TGF beta mRNA expression as shown by whole lung northern blot assay paralleled the TGF beta protein expression in BAL fluid. The peak of TGF beta protein increase in BAL fluid between 3 and 6 weeks coincided with the initial influx of inflammatory cells in BAL fluid, but preceded histologically discernable pulmonary fibrosis that was not apparent until 8-10 weeks after irradiation. In conclusion. TGF beta and mRNA and protein upregulation preceded the radiation-induced pulmonary fibrosis, suggesting a pathogenetic role in the development of radiation fibrosis.

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Section: Discussionmentioning

confidence: 99%

Radiation-induced lung injury in vivo: Expression of transforming growth factor?Beta precedes fibrosis

Bedoya

Lee

et al. 1996

Inflammation

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“…A series of experiments using a rabbit model reported these leaked pulmonary surfactant apoproteins in the serum to be an accurate marker and predictor for later lethal radiation pneumonitis. 38 Serum pulmonary surfactant proteins A (SP-A) and D (SP-D) were reported to be useful markers for the early detection of radiation pneumonitis after thoracic irradiation. Serum SP-D levels in patients with radiation pneumonitis were sequentially higher than in patients without radiation pneumonitis.…”

Section: Pulmonary Surfactant Proteinsmentioning

confidence: 99%

The Use of Blood Biomarkers to Predict Radiation Lung Toxicity: A Potential Strategy to Individualize Thoracic Radiation Therapy

Kong

Wang

et al. 2008

Cancer Control

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“…After radiation, surfactant levels in the blood quickly rise as do the levels of surfactant in the exposed lung tissue [11, 39, 40]. The mechanism of acute respiratory distress syndrome that can occur following lung radiation is thought to be a result of impaired metabolism of surfactant from high density to low density forms [41].…”

Section: Metabolic Markers Of Normal Tissue Response To Radiation mentioning

confidence: 99%

“…They include growth factors, angiogenesis and angiostatic proteins, interleukins, adhesion molecules and chemokines. High, low, or prolonged expression of angiogenic or angiostatic cytokines have been associated with human diseases that pathologically simulate radiation toxicity [10, 39, 40, 75]. Chemokines are chemotactic proteins that recruit inflammatory cells to irradiated tissues and, like interleukins, can activate inflammatory cells.…”

Section: Physiological Processesmentioning

confidence: 99%

Molecular markers of radiation-related normal tissue toxicity

Okunieff

Chen

Maguire

et al. 2008

Cancer Metastasis Rev

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Over the past five decades, those interested in markers of radiation effect have focused primarily on tumor response. More recently, however, the view has broadened to include irradiated normal tissues -markers that predict unusual risk of side-effects, prognosticate during the prodromal and therapeutic phases, diagnose a particular toxicity as radiation-related, and, in the case of bioterror, allow for tissue-specific biodosimetry. Currently, there are few clinically useful radiation-related biomarkers. Notably, levels of some hormones such as thyroid-stimulating hormone (TSH) have been used successfully as markers of dysfunction, indicative of the need for replacement therapy, and for prevention of cancers. The most promising macromolecular markers are cytokines: TGFβ, IL-1, IL-6, and TNFα being lead molecules in this class as both markers and targets for therapy. Genomics and proteomics are still in nascent stages and are actively being studied and developed.

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Serum markers for prediction of pulmonary radiation syndromes. Part I: Surfactant apoprotein

Cited by 21 publications

References 25 publications

Radiation-induced lung injury in vivo: Expression of transforming growth factor?Beta precedes fibrosis

Radiation-induced lung injury in vivo: Expression of transforming growth factor?Beta precedes fibrosis

The Use of Blood Biomarkers to Predict Radiation Lung Toxicity: A Potential Strategy to Individualize Thoracic Radiation Therapy

Molecular markers of radiation-related normal tissue toxicity

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