#PATHOLOGICAL LYMPH NODE DRIVER#

Previous studies have demonstrated better therapeutic outcomes and fewer toxic effects via EGFR-TKIs compared with the traditional chemotherapies in patients with non-small cell lung cancer (NSCLC) and EGFR mutations.

#PATHOLOGICAL LYMPH NODE DRIVER#

These improvements are due to the development of targeted therapies, i.e., epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs), for lung adenocarcinoma through specific driver genes. In the past decade, significant improvements in survival rate have been observed. Traditional chemotherapies as the cornerstone of therapy in the first line setting in an advanced stage of lung cancer. Therefore, the main concern is on targeted therapies in order to increase the rate of recovery of the disease. Despite many therapies for cancer, no satisfactory clinical results have been observed because of early metastasis of tumor. GLOBOCAN reported approximately 2.21 million new lung cancer cases (11.4% of the total new cancer cases) and 1.80 million deaths (18.0% of the total cancer deaths) worldwide in 2020. This is due to diversity in lifestyles and socioeconomic development. In the recent years, the rate of incidence and mortality has significantly increased with significant gender and geographic differences. Lung cancer is one of the most common forms of cancer worldwide and also the leading cause of cancer mortalities worldwide. The findings indicated that FAM83A may play a critical role in promoting the LUAD progression and thus might serve as a novel prognostic marker in LUAD. Overexpression of FAM83A was associated with early lymph node metastasis and poor overall survival among LUAD patients. Downregulation of FAM83A led to a reduction in cell proliferation, a decrease in migration ability, and diminished epithelial-mesenchymal transition (EMT) in the lung cancer cell lines.

Compared with patients with early-stage tumors (stage I-II), those with advanced stage tumors (stage III-IV) had significantly higher FAM83A expression levels ( ). A significant increase in FAM83A protein was observed in the LUAD tissue ( ). FAM83A expression was elevated in LUAD tissues and was related to shorter overall survival ( ). The correlation between FAM83A expression and survival rate was assessed by the Kaplan-Meier and Cox regression. The mechanism of FAM83A in proliferation and migration was examined. Bioinformatics analysis, immunohistochemistry, and Western blotting were used to explore and detect the expression of FAM83A in LUAD cells. This study aimed to determine the expression pattern of FAM83A in lung adenocarcinoma (LUAD) and its correlation with the prognosis of cancer and the survival of the patients. Family with sequence similarity 83, member A (FAM83A) plays an essential and fundamental role in the proliferation, progression, and apoptosis of many malignant tumors, including lung cancer.

Pathological lymph node