bims-meluca 2025-03-30 papers

on Metabolism of non-small cell lung carcinoma

Issue of 2025–03–30
twelve papers selected by
the Muñoz-Pinedo/Nadal (PReTT) lab, L’Institut d’Investigació Biomèdica de Bellvitge

The prognostic value of a laboratory cachexia score (LCAS) defined by LDH, CRP and albumin in patients with advanced lung cancer.
A Dynamic Time Warping Extension to Consensus Weight-Based Cachexia Criteria Improves Prediction of Cancer Patient Outcomes.
The influence of fatty acid metabolism on T cell function in lung cancer.
Predictive and therapeutic value of the ferroptosis gene CISD1 in non?small cell lung cancer.
Serum VEGF-A as a biomarker for the addition of bevacizumab to chemo-immunotherapy in metastatic NSCLC.
GDF-15 as a biomarker for diagnosis and prognosis of lung cancer: a meta-analysis.
Anti-EGFR therapy can overcome acquired resistance to the third-generation ALK-tyrosine kinase inhibitor lorlatinib mediated by activation of EGFR.
Arachidonic acid suppresses lung cancer cell growth and modulates lipid metabolism and the ERK/PPARγ signaling pathway.
Hyperglycemia and Lung Cancer-A Possible Relationship.
Metabolomics for early-stage lung adenocarcinoma: diagnostic biomarker screening.
Nutritional conditions and PFS and OS in cancer immunotherapy: the MOUSEION-010 meta-analysis.
Serum Interleukin Levels Predict Occurrence of Acute Radiation Pneumonitis and Overall Survival in Thoracic Tumours.

BMC Cancer. 2025 Mar 25. 25(1): 543

The prognostic value of a laboratory cachexia score (LCAS) defined by LDH, CRP and albumin in patients with advanced lung cancer.

Joshua J Thompson, Nicholas MacLeod, Sarah Will, Fraser O'Rourke, Josh McGovern, Campbell Roxburgh, Joanne Edwards, Ross D Dolan, Donald C McMillan.

   BACKGROUND: Systemic inflammation has prognostic value in cancer and is considered aetiological of cachexia by the Global Leadership Initiative on Malnutrition (GLIM). Lactate dehydrogenase (LDH) also has recognized prognostic value. The present study aimed to evaluate the ability of a laboratory cachexia score (LCAS) defined by LDH, CRP and albumin, to identify cachexia and predict outcome in advanced lung cancer.
METHODS: Patients (n = 261) with serum LDH, CRP and albumin measurement receiving palliative radiotherapy for advanced lung cancer between 2009 and 2015 were identified. Subjects were stratified by LDH and LCAS. This was compared to GRIm and LIPI, two previously described LDH based prognostic scores, which do not incorporate CRP.
RESULTS: On follow up there were 201 deaths. LDH and LCAS were associated with 1-year survival independent of ECOG-PS, MUST, weight loss, BMI, SMI, SMD, metastases, mGPS or NLR (all p < 0.001). On multivariate analysis LCAS (1.36, 1.13-1.63, p = 0.001), LIPI (1.50, 1.17-1.92, p = 0.02), metastases (1.53, 1.15-2.04, p = 0.004) and ECOG-PS (1.28, 1.04-1.57, p = 0.019) were independently associated with poorer overall survival.
CONCLUSION: LCAS appears to identify cachexia and stratify survival. This may represent a useful aetiological criterion within the GLIM framework and a more powerful prognostic tool than the phenotypic criteria.

Keywords:  Cachexia; GLIM. CRP; Lactate Dehydrogenase; Lung Cancer; Performance status; mGPS

DOI:  https://doi.org/10.1186/s12885-025-13426-3
JCSM Commun. 2025 Jan-Jun;8(1):8(1): e107

A Dynamic Time Warping Extension to Consensus Weight-Based Cachexia Criteria Improves Prediction of Cancer Patient Outcomes.

Noah Forrest, Steven Tran, Khizar R Nandoliya, Ethan J Houskamp, Tomasz Gruchala, Vijeeth Guggilla, Zequn Sun, Rimas Lukas, Derek Wainwright, Al'ona Furmanchuk, Jodi L Johnson, Ishan Roy, Theresa L Walunas.

   Background: Cachexia is a complex syndrome that impacts up to half of patients with cancer. Criteria systems have been developed for the purpose of diagnosing and grading cachexia severity in clinical settings. One of the most widely known is those developed by Fearon et al. in 2011, which utilizes body mass loss and body mass index (BMI) to determine the presence and extent of cachexia. One limitation of this system and other clinical cachexia scales is the lack of systematic methods for assessing cachexia severity longitudinally. We sought to develop an extension to the 2011 consensus criteria that categorizes cancer patients with respect to their temporal cachexia progression and assess its predictive capacity relative to the current time-agnostic system.
Methods: Two cancer cohorts were identified in electronic health record data: lung cancer and glioblastoma. We extracted weight and BMI measures from the time of cancer diagnosis until death or loss to follow-up and computed cachexia severity according to the consensus criteria. Subgroups of cachexia progression were uncovered using dynamic time warping (DTW) followed by unsupervised clustering. This system and baseline consensus criteria measurements were each assessed for their ability to stratify patient outcomes utilizing Kaplan-Meier curves and Cox proportional hazards and subsequently compared with model concordance and inverse probability of censoring weighting (IPCW).
Results: Significant differences were observed in overall survival Kaplan-Meier curves of 1023 patients with lung cancer when stratified by baseline cachexia classification (p = 0.0002, N events = 592) but not in a cohort of 545 patients with glioblastoma (p = 0.16, N events = 353). DTW uncovered three patterns of cachexia progression in each subgroup with features described as 'smouldering', 'rapid with recovery' or 'persistent/recurrent'. Significant differences were observed in Kaplan-Meier curves when stratified by cachexia longitudinal patterns in lung cancer (p < 0.0001) and glioblastoma (p < 0.0001). Adjusted hazards ratios comparing the 'persistent/recurrent' cluster to referent subgroups in Cox models were 4.8 (4.1-5.8, p < 0.05) and 1.9 (1.4-2.4, p < 0.05) among patients with lung cancer and glioblastoma, respectively. Areas under the curve at multiple time points and Cox model concordances were greater when patients were stratified by progression pattern compared with baseline consensus criteria.
Conclusions: Our results suggest that accounting for cachexia's longitudinal progression in a systematic way can improve upon the prognostic capacity of a widely used consensus criteria set. These findings are important for the future development of systems that recognize concerning patterns of cachexia progression in clinical settings and aid clinicians in cachexia-related decision making.

Keywords:  cancer cachexia; dynamic time warping; electronic health records

DOI:  https://doi.org/10.1002/rco2.107
FEBS J. 2025 Mar 25.

The influence of fatty acid metabolism on T cell function in lung cancer.

Jessica Petiti, Ludovica Arpinati, Alessio Menga, Giovanna Carrà.

  The tumor microenvironment (TME) is a complex ecosystem, encompassing a variety of cellular and non-cellular elements surrounding and interacting with cancer cells, overall promoting tumor growth, immune evasion, and therapy resistance. In the context of solid tumors, factors, such as hypoxia, nutritional competition, increased stress responses, glucose demand, and PD-1 signals strongly influence metabolic alterations in the TME, highly contributing to the maintenance of a tumor-supportive and immune-suppressive milieu. Cancer cell-induced metabolic alterations partly result in an increased fatty acid (FA) metabolism within the TME, which strongly favors the recruitment of immune-suppressive M2 macrophages and myeloid-derived suppressor cells, crucial contributors to T-cell exhaustion, tumor exclusion, and decreased effector functions. The drastic pro-tumoral changes induced by the tumor metabolic rewiring result in signaling loops that support tumor progression and metastatic spreading, and negatively impact therapy efficacy. As tumor- and immune metabolism are increasingly gaining attention due to their potential therapeutic implications, we discuss the effects of altered lipid metabolism on tumor progression, immune response, and therapeutic efficacy in the context of lung cancer. In particular, we focus our analysis on the tumor-induced metabolic alterations experienced by T lymphocytes and the possible strategies to overcome immunotherapy resistance by targeting specific metabolic pathways in T cells.

Keywords:  T‐cell function; cancer metabolism; fatty acid metabolism; lung cancer

DOI:  https://doi.org/10.1111/febs.70081
Oncol Lett. 2025 May;29(5): 235

Predictive and therapeutic value of the ferroptosis gene CISD1 in non?small cell lung cancer.

Tao Wang, Xiaoyu Xiao, Zhe Zhang, Xiang Li.

  The present study aimed to investigate the expression of ferroptosis genes in non-small cell lung cancer and their relationship with prognosis, and to analyze the relationship between ferroptosis genes and tumor immunity. To evaluate the expression levels of ferroptosis genes and their association with prognosis in lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC), The Cancer Genome Atlas LUAD and LUSC data were downloaded, patient clinical information and ferroptosis gene expression profiles were extracted, and differential gene expression, survival and correlation analyses were performed using R. Using immune correlation analysis, the value of ferroptosis genes for immunotherapy was explored. The potential application of ferroptosis genes in immunotherapy was further validated by immunohistochemical staining. A number of ferroptosis-associated genes were differentially expressed in tumor tissues compared with in non-tumor tissues. CDGSH iron-sulfur domain-containing protein 1 (CISD1) was upregulated in both LUAD and LUSC tumor tissues, and was associated with tumor Tumor-Node-Metastasis stage. Notably, high levels of CISD1 in LUAD indicated a poor prognosis, and CISD1 was negatively correlated with CD4+ T cells based on the immune score. Furthermore, CISD1 may be involved in pathways such as cellular response to hypoxia, DNA repair, extracellular matrix-related genes, epithelial-mesenchymal transition markers, oxidative phosphorylation and PI3K-AKT-mTOR pathway. Immunohistochemical staining indicated that CISD1 was highly expressed in LUAD tissues, it was associated with a poor prognosis of patients with LUAD, and it was negatively associated with CD4 and CD20. In conclusion, the ferroptosis gene CISD1 may be associated with the prognosis of LUAD, and high levels of CISD1 could indicate a shorter survival time. Furthermore, CISD1 has potential applications in immunotherapy. These findings may provide novel theoretical insights into the treatment of LUAD.

Keywords:  CDGSH iron-sulfur domain-containing protein 1; ferroptosis; immune correlation; lung adenocarcinoma; prognosis

DOI:  https://doi.org/10.3892/ol.2025.14981
Nat Commun. 2025 Mar 22. 16(1): 2825

Serum VEGF-A as a biomarker for the addition of bevacizumab to chemo-immunotherapy in metastatic NSCLC.

Kentaro Tanaka, Jun Sugisaka, Yoshimasa Shiraishi, Yasutaka Watanabe, Haruko Daga, Koichi Azuma, Kazumi Nishino, Masahide Mori, Takayo Ota, Haruhiro Saito, Akito Hata, Tadashi Sakaguchi, Toshiyuki Kozuki, Hiroaki Akamatsu, Hirotaka Matsumoto, Motoko Tachihara, Kazushige Wakuda, Yuki Sato, Tomohiro Ozaki, Yuko Tsuchiya-Kawano, Nobuyuki Yamamoto, Kazuhiko Nakagawa, Isamu Okamoto.

Anti-vascular endothelial growth factor (VEGF) agents in combination with immunotherapies have improved outcomes for cancer patients, but predictive biomarkers have not been elucidated. We report here a preplanned analysis in the previously reported APPLE study, a phase 3 trial evaluating the efficacy of the bevacizumab in combination with atezolizumab, plus platinum chemotherapy in metastatic, nonsquamous non-small cell lung cancer (NSCLC). We investigated the correlation of serum VEGF-A and its isoforms at baseline with treatment response by using an enzyme-linked immunosorbent assay. We reveal that the addition of bevacizumab significantly improves the progression-free survival in patients with the low VEGF-A level. Our results demonstrate that measuring serum VEGF-A or its isoforms may identify NSCLC patients who are likely to benefit from the addition of bevacizumab to immunotherapy. These assays are easy to measure and have significant potential for further clinical development.

DOI: https://doi.org/10.1038/s41467-025-58186-7
Front Oncol. 2025 ;15 1447990

GDF-15 as a biomarker for diagnosis and prognosis of lung cancer: a meta-analysis.

Teng Pan, Rui Duan, Zihan Xu, Xiaohan He, Xiaojin Luo, Guanglin Zhou, Yu Song, Jinhai Deng, Xuerui Tan, Fengxiang Wei.

   Introduction: Due to the tendency of lung cancer to be diagnosed at advanced stages, many patients are not eligible for curative surgery. Identifying early detection and prognosis biomarkers is crucial for improving outcomes. This study explores the potential of Growth Differentiation Factor 15 (GDF-15) as a biomarker for these purposes.
Methods: A thorough review and meta-analysis of literature from PubMed, Embase, the CENTRAL, and the CNKI was performed. We analyzed the diagnostic accuracy of GDF-15, focusing on its sensitivity, specificity, and AUC. Additionally, we investigated the association between three-year overall survival and GDF-15 levels in lung cancer patients. Our analysis included nine studies, encompassing 1296 patients with lung cancer and 1182 healthy controls.
Results: GDF-15 showed high diagnostic performance with a sensitivity of 0.80 (95% Confidence Interval (CI): 0.71-0.87), specificity of 0.92 (95% CI: 0.85-0.96), diagnostic odds ratio of 45 (95% CI: 25-79), and an AUC of 0.93 (95% CI: 0.90-0.95). Moreover, the prognosis analysis revealed that the plasma GDF-15 levels were significantly higher in patients than controls (standardized mean difference: 2.91, CI 2.79-3.04 and P < 0.00001), and the odds ratio of 3-year overall survival rate was 4.05 (95% CI: 1.92-8.51 and P = 0.0002).
Discussion: GDF-15 exhibits strong potential as both a diagnostic and prognostic biomarker in lung cancer, distinguishing effectively between patients and healthy individuals. These findings support its further exploration and potential integration into clinical practice.
Systematic Review Registration: https://www.crd.york.ac.uk/PROSPERO/, identifier CRD42024519807.

Keywords:  GDF-15; biomarkers; diagnostic utility; lung cancer; meta-analysis; prognostic value

DOI:  https://doi.org/10.3389/fonc.2025.1447990
Acta Pharmacol Sin. 2025 Mar 21.

Anti-EGFR therapy can overcome acquired resistance to the third-generation ALK-tyrosine kinase inhibitor lorlatinib mediated by activation of EGFR.

Chen Hu, Cong-Hua Lu, Jie Zheng, Jun Kang, Dai-Juan Huang, Chao He, Yi-Hui Liu, Zhan-Rui Liu, Di Wu, Yuan-Yao Dou, Yi-Min Zhang, Cai-Yu Lin, Rui Han, Yong He.

  Non-small cell lung cancer (NSCLC) is a leading cause of cancer-related mortality. Anaplastic lymphoma kinase (ALK) tyrosine kinase inhibitors (TKIs) are standard treatments for EML4-ALK-positive NSCLC, but resistance to these agents remains a challenge. This study aimed to determine the mechanisms of acquired resistance to the third-generation ALK-TKI lorlatinib. Lorlatinib-resistant cell lines were established by prolonged exposure to a high concentration of lorlatinib. Activation of epidermal growth factor receptor (EGFR) caused by a decrease in endocytosis and degradation of protein was demonstrated to play an essential role in acquired resistance to lorlatinib. The interaction between the EGFR and ALK was investigated to identify binding sites and conformational changes in ALK. We performed high-throughput compound screening using a small-molecule drugs library comprising 510 antitumor agents in an effort to discover small-molecule compounds that target EGFR in lorlatinib-resistant cells. Combination treatment with ALK-TKI and anti-EGFR agents suppressed acquired resistance to ALK-TKIs caused by activation of EGFR in vitro and in vivo, suggesting that the combination of lorlatinib and an anti-EGFR agent could be effective in patients with lorlatinib-resistant NSCLC. This research provides insights into the mechanism of resistance to lorlatinib and suggests that it can be overcome by anti-EGFR treatment, offering a promising approach for treating resistance to lorlatinib mediated by EGFR activation in patients with ALK-positive NSCLC.

Keywords:  anaplastic lymphoma kinase; epidermal growth factor receptor; non-small cell lung cancer; resistance; tyrosine kinase inhibitor

DOI:  https://doi.org/10.1038/s41401-025-01511-z
Lipids Health Dis. 2025 Mar 27. 24(1): 114

Arachidonic acid suppresses lung cancer cell growth and modulates lipid metabolism and the ERK/PPARγ signaling pathway.

Lin Wang, Lanlan Wei, Xueling Chen, Jiali Xiong.

  Lung cancer remains the leading cause of cancer-related mortality worldwide, necessitating the development of new treatment strategies. Arachidonic acid (ARA), a polyunsaturated fatty acid, shows promise in cancer therapy due to its potential anti-tumor effects, although its role in lung cancer remains unclear. This study investigated the effects and underlying mechanism of ARA on A549 and NCI-H1299 lung cancer cells. In vitro assays were used to assess cell viability, apoptosis, colony formation, lipid droplet formation, and changes in cellular lipid content. ARA dose-dependently suppressed cell viability, facilitated apoptosis, and suppressed colony formation in both lung cancer cell lines. Network pharmacology analysis was performed to identify potential gene targets and pathways, uncovering 61 overlapping genes between ARA and lung cancer-related targets, with mitogen-activated protein kinase 1 (MAPK1) emerging as a key gene. Enrichment analyses suggested that the effects of ARA might be mediated through lipid metabolism and the extracellular signal-regulated kinase (ERK)/peroxisome proliferator-activated receptor gamma (PPARγ) signaling pathway. In both lung cancer cell lines, ARA treatment inhibited lipid droplet formation and decreased the cellular lipids. Immunoblotting further confirmed that ARA treatment significantly increased ERK phosphorylation while reducing PPARγ and fatty acid synthase (FASN) protein levels. In vitro experiments using GW9662, a PPARγ antagonist, confirmed that inhibiting lipid droplet formation impairs lung cancer cell viability and promotes apoptosis. Furthermore, in vivo experiments demonstrated that ARA significantly reduced tumor size and weight in a lung cancer xenograft model, further validating its anti-tumor effects. The potential of ARA as a therapeutic agent for lung cancer might involve lipid metabolism and relevant signaling pathways. A future study exploring the full therapeutic potential of ARA and underlying mechanisms in lung cancer is needed.

Keywords:  Arachidonic acid (ARA); Lipid metabolism; Lung cancer; Mitogen-activated protein kinase 1 (MAPK1); The extracellular signal-regulated kinase (ERK)/peroxisome proliferator-activated receptor gamma (PPARγ) pathway

DOI:  https://doi.org/10.1186/s12944-025-02490-0
Diagnostics (Basel). 2025 Mar 07. pii: 651. [Epub ahead of print]15(6):

Hyperglycemia and Lung Cancer-A Possible Relationship.

Spasoje Popevic, Nikola Maric, Branislav Ilic, Slobodan Belic, Ivana Sekulovic Radovanovic, Sanja Dimic-Janjic, Mihailo Stjepanovic.

  Glucose is the main source of energy in human cells. Elevated levels of glucose are one of the most common metabolic disorders, and it has been shown to have a significant, mostly negative, effect on multiple chronic and acute diseases. Lung cancer remains one of the biggest challenges for treatment in modern medicine, with a high prevalence, incidence and mortality. Hyperglycemia is not uncommon in patients with lung cancer; however, it is usually overlooked. Patients with unregulated glycemia and lung cancer have been shown to have worse outcomes, reduced therapeutic effect and more complications during treatment. Studies have identified multiple molecular pathways common in both hyperglycemia and lung cancer; however, no clear correlation has been identified. By understanding these signaling pathways, we can influence the outcome therapeutically and thereby improve the survival of patients with lung cancer.

Keywords:  hyperglycemia; lung cancer; molecular pathways; treatment

DOI:  https://doi.org/10.3390/diagnostics15060651
Front Oncol. 2025 ;15 1535525

Metabolomics for early-stage lung adenocarcinoma: diagnostic biomarker screening.

Danxiong Sun, Yanhong Du, Rufang Li, Yunhui Zhang.

   Objective: This study aimed to identify specific metabolic markers in the blood that can diagnose early-stage lung adenocarcinoma.
Methods: An untargeted metabolomics study was performed, and the participants were divided into four groups: early-stage lung adenocarcinoma group (E-LUAD; n = 21), healthy control group (HC, n = 17), non-cancerous lung disease group (NCC; n = 17), and advanced lung adenocarcinoma group (A-LUAD; n = 25). Plasma metabolite levels that differed in the E-LUAD group compared to the other three groups were identified via liquid chromatography-mass spectrometry (LC-MS). Principal component analysis (PCA) and partial least squares discriminant analysis (PLS-DA) were performed at metaX for statistical analysis. A Venn diagram was constructed to identify overlapping differential metabolites of the class comparisons. The data were randomly divided into a training set and a validation set. Based on the overlapping differential metabolites, the diagnostic model was constructed. The discrimination of the model was evaluated using the area under the curve (AUC).
Results: A total of 527 metabolites were tentatively identified in positive ion mode and 286 metabolites in negative ion mode. Compared with the HC group, 121 differential metabolites were identified. Compared with the NCC group, 67 differential metabolites were identified. Compared with the A-LUAD group, 54 differential metabolites were identified. The Venn diagram showed that 29 metabolites can distinguish E-LUAD from HC and NCC and that four metabolites can distinguish E-LUAD from HC, NCC, and A-LUAD. The feature metabolites were selected to establish the diagnostic model for E-LUAD. The AUC value of the training set was 0.918, and it was 0.983 in the validation set.
Conclusion: Blood metabolomics has potential diagnostic value for E-LUAD. More medical studies are needed to verify whether the metabolic markers identified in the current research can be applied in clinical practice.

Keywords:  biomarker; diagnostic model; early-stage lung adenocarcinoma; liquid chromatography-mass spectrometry; metabolomics

DOI:  https://doi.org/10.3389/fonc.2025.1535525
Immunotherapy. 2025 Mar 25. 1-13

Nutritional conditions and PFS and OS in cancer immunotherapy: the MOUSEION-010 meta-analysis.

Elsa Vitale, Lorenza Maistrello, Alessandro Rizzo, Oronzo Brunetti, Raffaella Massafra, Veronica Mollica, Francesco Massari, Matteo Santoni.

   BACKGROUND: The MOUSEION-010 Meta-Analysis assessed the association between nutritional status and clinical outcomes such as Progression Free Survival (PFS) and Overall Survival (OS) among cancer patients treated with immune checkpoint inhibitors (ICIs).
METHODS: Nutritional status was assessed based on the Prognostic Nutrition Index (PNI), Geriatric Nutritional Risk Index (GNRI) and Controlling Nutritional Status (CONUT) indexes. Databases consulted were: Embase, PubMed, Scopus and Web of Science.
RESULTS: PNI and GNRI indexes did not show a significant association with both PFS and OS, while CONUT index displayed a significant difference in PFS between the two groups, in favor of the control group (Z = 4.04; p < 0.01) also without any publication bias (β= -1.27; 95% CI = [-2.13; -0.42]; p = 0.10]). The same trend was recorded in OS, too (Z = 4.24; p < 0.01). However, publication bias was present (β = 1.89; 95% CI = [1.26; 2.54]; p = 0.028]) and the numerosity of the studies did not reveal the sufficient statistical power to obtain reliable results.
CONCLUSION: Malnutrition could negatively impact cancer patients, especially in advanced phases. Our findings could be associated with the reduction of physical ability and daily activity performance, lower compliance with treatment protocols, and shorter survival outcomes.

Keywords:  Body mass index; disease progression; immunotherapy; mortality; survival

DOI:  https://doi.org/10.1080/1750743X.2025.2483656
Clin Invest Med. 2025 Mar;48(1): 29-38

Serum Interleukin Levels Predict Occurrence of Acute Radiation Pneumonitis and Overall Survival in Thoracic Tumours.

Yan Zhang, Wen-Xiang Shen, Ping Li, Min-Bin Chen, Li-Na Zhou.

   BACKGROUND: Radiation-induced lung injury (RILI) is a significant adverse effect of thoracic radiotherapy, potentially impacting patient prognosis. The risk factors for acute radiation pneumonitis (RP) have not been fully clarified. The present study evaluated the predictive value of serum interleukins (ILs) in the occurrence of RP and overall survival in patients with thoracic cancers.
METHODS: This single-centre retrospective observational study enrolled 435 thoracic cancer patients who underwent chest radiation therapy. Serum levels of IL-1β, IL-2, IL-4, IL-5, IL-6, IL-8, IL-10, IL-12p70, IL-17, TNF-α, IFN-γ, IFN-α were measured by cytometric bead array before radiotherapy. The relationship between clinical characteristics, serum IL levels and the occurrence of RP were analyzed. Cox regression and Kaplan-Meier methods were also performed to investigate the prognostic role of serum IL levels in these patients.
RESULTS: The incidence of RP in these patients was 17.01%. Elevated serum levels of IL-1β, IL-2, IL-4, IL-6, IL-8, IL-10, IL-12p70, TNF-α, IFN-α were all associated with the occurrence of RP. High levels of IL-1β, IL-4, and IL-12p70 were correlated with more severe pneumonitis. Univariate and multivariate logistic regression analysis identified serum IL-6 level as an independent prognostic factor in patients receiving thoracic radiotherapy.
CONCLUSIONS: Serum interleukin levels are linked to the development of acute RP in patients receiving thoracic radiotherapy. Serum IL-6 could serve as a valuable biomarker in identifying patients at high risk for RP, potentially guiding individualized therapeutic strategies and improving patient management in radiotherapy. Future research should focus on validating IL-6's role in larger cohorts and exploring its integration into clinical practice for the early prediction of RILI.

Keywords:  Interleukin; Prognosis; Radiation pneumonitis; Radiotherapy-induced lung injury; Thoracic malignancies

DOI:  https://doi.org/10.3138/cim-2024-0262