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Association between mutated RAS status and microvascular density (MVD) in advanced colorectal cancer
Intratumoral angiogenesis, process of development of new blood vessels from pre-existing vascular networks, is currently a well-described mechanism. It leads to the initiation and maintenance of tumors and the promotion of metastasis to secondary sites. Mutation of the KRAS gene is one of the most implicated genes in CRC. It is important to highlight the involvement of the KRAS gene in the process of tumor angiogenesis. Nevertheless, the different studies published, the precise role of the KRAS oncogene mutation in CRC angiogenesis is not yet well elucidated.
The immunostaining results showed cytoplasmic expression of the CD34 receptor in the intratumoral endothelial cells of all CRC cases and in the cytoplasm of endothelial cells within the nontumoral mucosa. Endothelial cell staining was intense, specific and easily visualized. MVD was determined by counting the number of CD34-labeled blood vessels per field under light microscopy (G, X400) in CRC cases and in non-tumor mucosa. After analyzing the results, we found that the average observed MVD corresponds to 16 labeled vessels. For this reason, we considered a high MVD those with more than 20 labeled vessels and a low MVD for those with less than 20 labeled vessels. RAS testing was assessed by fully automated Idylla TM kras mutation test.
MVD was high in 71 (83.53%) of CRC cases. The results indicated that the mean percentage of CD34-labeled blood vessels in normal mucosa is lower than the mean percentage of CD34-labeled blood vessels in CRC. This difference was highly significant (p=0.003). This high MVD-CD34 was significantly associated with mutated RAS status (p < 0.05).
The significant association of high MVD-CD34 and mutated RAS status, suggesting that mutation of the RAS gene may increase angiogenic activity in CRC.
The authors.
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All authors have declared no conflicts of interest.
