Translational Health Reports

Abstract Background: Stereotactic Body Radiation Therapy (SBRT) represents the standard treatment for inoperable early-stage non-small cell lung cancer (NSCLC) and is increasingly utilized for oligometastatic disease. Its distinct radiobiological profile, involving high doses per fraction, triggers complex tumor-killing effects and systemic biological reactions not fully detectable through conventional imaging.
Objective: This review aims to summarize and critically assess current evidence regarding dynamic alterations in circulating, tissue, and imaging biomarkers after SBRT for lung cancer, and to explore their clinical significance.
Methods: A narrative synthesis of scientific literature from PubMed, Scopus, and Google Scholar was conducted, focusing on studies published between 2005 and 2024. Key search terms included "SBRT," "SABR," "lung cancer," "biomarker," "ctDNA," "immunotherapy," "cytokines," and "radiation pneumonitis."
Results: SBRT prompts a rapid, biphasic shift in tumor-derived biomarkers such as circulating tumor DNA (ctDNA), characterized by an initial post-treatment surge followed by reduction in responders. It significantly influences the immune system, inducing immunogenic cell death, expanding tumor-specific T-cell populations, and increasing checkpoint molecule expression like PD-L1. Additionally, SBRT modifies levels of cytokines (e.g., IL-6, TGF-β) and angiogenic factors (e.g., VEGF), which correlate with both treatment effectiveness and side effects like radiation-induced lung injury. Certain genetic polymorphisms also appear promising for predicting toxicity risk.
Conclusion: SBRT induces a dynamic and multifaceted change in the biomarker profile of lung cancer patients. These biomarkers offer considerable potential for personalizing treatment, predicting outcomes, monitoring response, and rationally planning combination therapies, especially with immunotherapy. Future prospective and validated studies are necessary to integrate these findings into clinical practice.

Abstract Background: The established first-line treatment for newly diagnosed Glioblastoma Multiforme (GBM) involves maximal surgical removal of the tumor, followed by a regimen of radiotherapy (RT) together with concurrent and maintenance temozolomide (TMZ) chemotherapy. Patient response to this combined approach varies widely and is closely associated with the tumor's molecular characteristics.
Objective: This analysis compiles current research on how the RT/TMZ combination modifies crucial GBM biomarkers over time, focusing on therapy-induced alterations rather than their initial prognostic significance.
Methods: A systematic review of literature from January 2000 to July 2024 was performed using PubMed, Scopus, and Web of Science. Search keywords included "glioblastoma," "radiotherapy," "temozolomide," "MGMT," "IDH," "biomarker," and related terms. Emphasis was placed on clinical trials and key preclinical studies.
Results: The RT/TMZ protocol imposes significant selective pressure, dynamically influencing GBM biomarkers. MGMT promoter methylation is the primary predictor of TMZ efficacy, but treatment often leads to the expansion of MGMT-active, resistant tumor clones at recurrence. IDH1/2 mutations are strong prognostic indicators, and their associated metabolic changes may increase tumor sensitivity to DNA-damaging therapies. Treatment substantially reshapes the tumor immune microenvironment; RT can stimulate anti-tumor immune responses but also increase PD-L1 expression, while TMZ often causes severe lymphocyte depletion. Additionally, therapy promotes the selection of cells with enhanced DNA damage repair mechanisms and activates survival pathways such as EGFR, fostering treatment resistance.
Conclusion: RT and TMZ induce continuous, adaptive changes in GBM biomarkers. Recognizing this dynamic process is essential for personalizing treatment, assessing response, and developing new combination therapies to combat resistance.

Abstract Background: Chemoradiation therapy (CRT) is fundamental for treating locally advanced and high-risk breast cancer. Although effective, it significantly impacts systemic physiology, which can be tracked through fluctuations in serum biomarkers. This review consolidates existing research on how CRT affects circulating tumor cells (CTCs), circulating tumor DNA (ctDNA), inflammatory cytokines, and tissue injury markers, assessing their value for predicting outcomes and guiding treatment.
Methods: A systematic search of PubMed, Embase, Scopus, and Web of Science was conducted for studies to 2025. Keywords included "breast cancer," "chemoradiation," "serum biomarker," "ctDNA," "CTC," and related terms. Eligible studies reported serum biomarker levels in breast cancer patients before, during, or after CRT and linked them to clinical results.
Results: Analysis of studies indicates that CRT causes a predictable but individualized alteration in serum biomarkers. A swift decrease in CTCs and ctDNA levels during neoadjuvant or definitive CRT strongly correlates with pathological complete response (pCR) and better survival. In contrast, detectable ctDNA after treatment is a powerful indicator of minimal residual disease (MRD) and impending relapse. Inflammatory markers such as IL-6 and CRP generally increase during therapy; prolonged elevation is linked to poorer prognosis and greater toxicity. Additionally, biomarkers like high-sensitivity Troponin I and TGF-β1 enable early identification of subclinical cardiotoxicity and radiation-induced skin damage, respectively.
Conclusion: Serum biomarkers offer a real-time, dynamic reflection of tumor response and host toxicity during CRT. Incorporating liquid biopsy components (CTCs, ctDNA) and host-response markers into clinical practice shows great potential for personalizing treatment, facilitating early intervention, and enhancing long-term results. Prospective studies are urgently required to standardize testing methods and confirm their clinical utility in guiding treatment strategies.