Researchers identified 9 genes that showed increased expression with an increased risk of gastrointestinal stromal tumor (GIST) formation and published their results in the International Journal of General Medicine. The expression of these genes therefore can be used as biomarkers to assess the risk of GIST.

The genes encode proteins that regulate cell division, proliferation, and apoptosis, the researchers said. The genes and their related signaling pathways were identified using bioinformatics tools to assess differentially expressed genes in GIST samples.

Fulai Gao and colleagues used primary tumor samples from 59 patients with GISTs They divided them into high, intermediate, and low-risk groups and identified 2988 differentially expressed genes when they compared the high and low-risk groups. They identified a further 682 genes when they compared the high and intermediate-risk groups.


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A total of 577 genes were overlapped between the 2 comparisons. From this set of 577 genes, the researchers identified 270 genes, that were highly differentially expressed. Finally, they identified 9 top genes potentially associated with the risk classification of GIST. These were CENPA, CDK1, TPX2, CCNB1, CCNA2, BUB1, AURKA, KIF11, and NDC80.

These differentially expressed genes encode proteins that are involved in the PI3K-Akt, P53, cell cycle, mitogen-activated protein kinase, and WNT signaling pathways, which play a role in the cell cycle, apoptosis, and cellular senescence.

Statistical analysis also revealed that the expression level of P21-activated kinase 4 (PAK4) was significantly higher in GIST compared to normal tissues. It is known that PAK4 can induce tumor cell proliferation and metastasis by increasing the phosphorylation of tumor signaling proteins and that PAK4 is overexpressed in cancer cells. However, it had not previously been reported in GIST.

Reference

Gao F, Wang J, Li C, et al. Risk-related genes and associated signaling pathways of gastrointestinal stromal tumors. Int J Gen Med. 2022;15:3839-3849. doi:10.2147/IJGM.S357224