Esophageal cancer is a highly lethal malignancy with high incidence and mortality rates, which continue to pose a significant threat to public health worldwide. Despite the adoption of multidisciplinary treatments, improving long-term survival rates remains a major challenge. Therefore, conducting in-depth research into the molecular mechanisms of esophageal cancer, identifying predictive biomarkers, and developing personalized treatment and monitoring strategies are crucial to enhancing clinical outcomes and patient prognosis. This study utilized advanced bioinformatics techniques to construct a gene co-expression network for esophageal cancer and compared it with sequencing data from real-world esophageal cancer samples. This approach successfully identified four key genes closely associated with the progression of esophageal cancer: MARCKSL1, MCM6, RFC4, and PLAU. A risk assessment model based on these genes demonstrated high predictive accuracy, particularly in assessing the risk of early-stage esophageal cancer, highlighting its significant potential for clinical application. Functional validation experiments and clinical data analysis further revealed that these genes play critical roles in esophageal cancer cell metastasis, glycolysis, and response to radiation therapy. These findings provide a new molecular basis for radiotherapy prognosis, helping to formulate more precise radiotherapy protocols and optimize treatment outcomes. Additionally, the regulatory networks of these genes revealed a complex molecular regulatory mechanism, offering new perspectives for precision treatment in esophageal cancer. In summary, these genes not only offer new insights into the early diagnosis and personalized treatment of esophageal cancer but also improve patient prognosis by correlating with radiotherapy response, thus laying a solid scientific foundation for future advancements.
Tendon Sheath Giant Cell Tumor (TGCT) is a benign tumor that primarily grows within joints and bursae. However, it has a high postoperative recurrence rate, ranging from 15% to 45%. Although radiotherapy may reduce this recurrence rate, its applicability as a standard treatment is still controversial. Furthermore, the pathogenic mechanisms of TGCT are not clear, which limits the development of effective treatment methods. The unpredictable growth and high recurrence rate of TGCT adds to the challenges of disease management. Currently, our understanding of TGCT mainly depends on pathological slice analysis due to a lack of stable cell models. In this study, we first reviewed the medical records of two female TGCT patients who had undergone radiotherapy. Then, by combining bioinformatics and machine learning, we interpreted the pathogenesis of TGCT and its associations with other diseases from multiple perspectives. Based on a deep analysis of the case data, we provided empirical support for postoperative radiotherapy in TGCT patients. Additionally, our further analysis revealed the signaling pathways of differentially expressed genes in TGCT, as well as its potential associations with osteoarthritis and synovial sarcomas.