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Neoadjuvant chemoimmunotherapy is becoming an increasingly important part of the management of lung cancer to facilitate surgical resection. This study aimed to summarize the treatment-related adverse events (TRAEs) and wound complications of neoadjuvant chemoimmunotherapy in non-small cell lung cancer (NSCLC). Eligible studies of neoadjuvant chemoimmunotherapy for NSCLC were identified from PubMed, Embase and Web of Science. The endpoints mainly included TRAEs and wound complications. Stata18 software was used for statistical analysis with p < 0.05 considered statistically significant. Twenty studies including a total of 1072 patients were eligible for this study. Among the patients who received neoadjuvant chemoimmunotherapy, the pooled prevalence of any grade TRAEs was 77% (95% confidence interval [CI] [0.64–0.86]), grade 1–2 TRAEs was 77% (95% CI [0.58–0.89]) and grade ≥3 TRAEs was 26% (95% CI [0.16–0.38]). Surgery-related complications rate was 22% (95% CI [0.14–0.33]). Among the wound complications, the pooled rate of air leakage was 10% (95% CI [0.04–0.23]), pulmonary/wound infection was 8% (95% CI [0.05–0.13]), bronchopleural fistula was 8% (95% CI [0.02–0.27]), bronchopulmonary haemorrhage was 3% (95% CI [0.01–0.05]), pneumonia was 5% (95% CI [0.02–0.10]), pulmonary embolism was 1% (95% CI [0.01–0.03]), pleural effusion was 7% (95% CI [0.03–0.14]) and chylothorax was 4% (95% CI [0.02–0.09]). Overall, neoadjuvant chemoimmunotherapy in NSCLC results a high incidence of grade 1–2 TRAEs but a low risk of increasing the incidence of ≥3 grade TRAEs and wound complications. These results need to be confirmed by more large-scale prospective randomized controlled trials and studies.
Transforming Growth Factor-Beta (TGF-β) signalling pathway is of paramount importance in the processes of wound healing, epidermal integrity maintenance and development of skin cancer. The objective of this research endeavour was to clarify the impact of gene mutations and variations in expression within TGF-β family on mechanisms of tissue repair, as well as to identify potential targets for therapeutic purposes in non-melanoma skin cancer (NMSC). The methods utilized in this study involved obtaining RNA-seq data from 224 NMSC patients and paired normal skin tissues from the PRJNA320473 and PRJEB27606 databases. The purpose of the differential gene expression analysis was to identify genes whose expression had changed significantly. In order to evaluate the effects and interrelationships of identified gene variants, structural analysis with AlphaFold and PDB data and network analysis with the STRING database were both utilized. Critical gene expression was externally validated through the utilization of the GEPIA database. Tumour tissues exhibited a notable upregulation of genes associated with the TGF-β pathway, specifically MMP1, MMP3, MMP9, EGF, COL3A1 and COL1A2, in comparison with normal tissues. As indicated by the central node status of these genes in the network analysis, they play a crucial role in the progression of NMSCs. The results of the structural analysis suggested that mutations might cause functional disruptions. External validation of the upregulation confirmed the expression trends and emphasized the biomarker potential of the upregulated genes. In conclusion, this research offered thorough examination of molecular modifications that occur in TGF-β family genes, which are linked to cutaneous wound healing and NMSC. The modified expression of the identified hub genes may represent innovative targets for therapeutic intervention.
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