F10, encoding coagulation factor X, plays a crucial role in the blood coagulation pathway. It is essential for the normal hemostasis process, converting prothrombin to thrombin, which is vital for the formation of blood clots [1,2].

In papillary thyroid carcinoma (PTC), a 2.06-fold increase in F10 expression was detected in disease-free tumors compared to recurrent PTC tumors. Also, non-Hispanic patients had approximately a 1.74-fold increase in F10 gene expression levels compared to Hispanic patients. The probability of tumor recurrence was 1.82 times higher in the cohort with low F10 expression [1].

In hereditary factor X deficiency, high-throughput sequencing identified five new F10 variants, contributing to a better understanding of the phenotype-genotype correlation in this disorder [2].

In cervical cancer, F10 mRNA and protein expressions were significantly higher in cancer tissues than adjacent normal tissues. Its expression was higher in poorly differentiated cancer and lower in patients with preoperative chemotherapy, indicating an inverse correlation with cancer differentiation [3].

In conclusion, F10 is crucial for blood coagulation. Studies on F10 in PTC, hereditary factor X deficiency, and cervical cancer show its potential as a prognostic biomarker and its significance in understanding the genotype-phenotype relationship and cancer development. These findings may contribute to improving diagnostic and treatment strategies for related diseases.