Markers Useful in Monitoring Radiation-Induced Lung Injury in Lung Cancer Patients: A Review

Śliwińska-Mossoń, Mariola; Wadowska, Katarzyna; Trembecki, Łukasz; Bil‐Lula, Iwona

doi:10.3390/jpm10030072

Cited by 15 publications

(10 citation statements)

References 75 publications

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“…Several studies have evaluated the cytokine levels related to lung damage secondary to radiation exposure. The evaluation timing and patients’ characteristics were diverse, and the significant findings reported were inconclusive [ 9 , 10 , 11 ]. Therefore, it has been difficult to apply a consistent criterion for cytokines as predictive factors for RP.…”

Section: Discussionmentioning

confidence: 99%

Cytokine Profiles of Non-Small Cell Lung Cancer Patients Treated with Concurrent Chemoradiotherapy with Regards to Radiation Pneumonitis Severity

Jeong

Kim

Jung

et al. 2021

JCM

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The immunologic aspects of radiation pneumonitis (RP) are unclear. We analyzed variations in cytokine profiles between patients with grade (Gr) 0–1 and Gr ≥ 2 RP. Fifteen patients undergoing concurrent chemoradiotherapy for non-small cell lung cancer were included. Blood samples of 9 patients with Gr 0–1 and 6 with Gr ≥ 2 RP were obtained from the Biobank. Cytokine levels were evaluated using an enzyme linked immunosorbent assay at before radiotherapy (RT) initiation, 1, 3, and 6 weeks post-RT initiation, and 1 month post-RT completion. Concentrations of granulocyte colony-stimulating factor (G-CSF), interleukin (IL)-6, IL-10, IL-13, IL-17, interferon (IFN)-γ, tumor necrosis factor (TNF)-α, and transforming growth factor (TGF)-β were analyzed; none were related to the occurrence of Gr ≥ 2 RP at pre-RT initiation. At 3 weeks, relative changes in the G-CSF, IL-6, and IFN-γ levels differed significantly between the groups (p = 0.026, 0.05 and 0.026, respectively). One month post-RT completion, relative changes of IL-17 showed significant differences (p = 0.045); however, relative changes in TNF-α, IL-10, IL-13, and TGF-β, did not differ significantly. Evaluation of changes in IL-6, G-CSF, and IFN-γ at 3 weeks after RT initiation can identify patients pre-disposed to severe RP. The mechanism of variation in cytokine levels in relation to RP severity warrants further investigation.

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Section: Discussionmentioning

confidence: 99%

Cytokine Profiles of Non-Small Cell Lung Cancer Patients Treated with Concurrent Chemoradiotherapy with Regards to Radiation Pneumonitis Severity

Jeong

Kim

Jung

et al. 2021

JCM

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“…Since the clinical symptoms or imaging changes identifying toxicity do not appear in the early stage, ideal biomarkers are crucial for early diagnosis and intervention in order to prevent lung complications. Previous studies have discovered complicated intercellular interactions, signaling pathways, and dynamic cytokine cascades throughout the RILI process [ 14 ]. Nevertheless, no biological factors have been found to dynamically monitor RILI in cancer patients, and no reliable early predictors or accurate risk models are currently available in clinical practice.…”

Section: Introductionmentioning

confidence: 99%

Promising Biomarkers of Radiation-Induced Lung Injury: A Review

Liu

Shao

2021

Biomedicines

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Radiation-induced lung injury (RILI) is one of the main dose-limiting side effects in patients with thoracic cancer during radiotherapy. No reliable predictors or accurate risk models are currently available in clinical practice. Severe radiation pneumonitis (RP) or pulmonary fibrosis (PF) will reduce the quality of life, even when the anti-tumor treatment is effective for patients. Thus, precise prediction and early diagnosis of lung toxicity are critical to overcome this longstanding problem. This review summarizes the primary mechanisms and preclinical animal models of RILI reported in recent decades, and analyzes the most promising biomarkers for the early detection of lung complications. In general, ideal integrated models considering individual genetic susceptibility, clinical background parameters, and biological variations are encouraged to be built up, and more prospective investigations are still required to disclose the molecular mechanisms of RILI as well as to discover valuable intervention strategies.

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“…Although radiotherapy plays a necessary role in the primary and adjuvant treatment of lung cancer, normal lung tissue outside the tumour is sensitive to ionizing radiation and is susceptible to harmful effects, including radiation pneumonia and lung fibrosis [ 4 , 5 , 6 ] and oxidative stress damage. Approximately 30–40% of lung cancer patients suffer from radiation pneumonitis following radiotherapy, which remains a major challenge for the successful management of lung cancer treatment for local recurrence and distant metastasis [ 7 ]. Radiation-induced pneumonitis is characterized by the appearance of a large number of inflammatory cells causing inflammation [ 8 ].…”

Section: Introductionmentioning

confidence: 99%

Gut Microbiota-Derived PGF2α Fights against Radiation-Induced Lung Toxicity through the MAPK/NF-κB Pathway

et al. 2021

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Radiation pneumonia is a common and intractable side effect associated with radiotherapy for chest cancer and involves oxidative stress damage and inflammation, prematurely halting the remedy and reducing the life quality of patients. However, the therapeutic options for the complication have yielded disappointing results in clinical application. Here, we report an effective avenue for fighting against radiation pneumonia. Faecal microbiota transplantation (FMT) reduced radiation pneumonia, scavenged oxidative stress and improved lung function in mouse models. Local chest irradiation shifted the gut bacterial taxonomic proportions, which were preserved by FMT. The level of gut microbiota-derived PGF2α decreased following irradiation but increased after FMT. Experimental mice with PGF2α replenishment, via an oral route, exhibited accumulated PGF2α in faecal pellets, peripheral blood and lung tissues, resulting in the attenuation of inflammatory status of the lung and amelioration of lung respiratory function following local chest irradiation. PGF2α activated the FP/MAPK/NF-κB axis to promote cell proliferation and inhibit apoptosis with radiation challenge; silencing MAPK attenuated the protective effect of PGF2α on radiation-challenged lung cells. Together, our findings pave the way for the clinical treatment of radiotherapy-associated complications and underpin PGF2α as a gut microbiota-produced metabolite.

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Markers Useful in Monitoring Radiation-Induced Lung Injury in Lung Cancer Patients: A Review

Cited by 15 publications

References 75 publications

Cytokine Profiles of Non-Small Cell Lung Cancer Patients Treated with Concurrent Chemoradiotherapy with Regards to Radiation Pneumonitis Severity

Cytokine Profiles of Non-Small Cell Lung Cancer Patients Treated with Concurrent Chemoradiotherapy with Regards to Radiation Pneumonitis Severity

Promising Biomarkers of Radiation-Induced Lung Injury: A Review

Gut Microbiota-Derived PGF2α Fights against Radiation-Induced Lung Toxicity through the MAPK/NF-κB Pathway

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