Background
The efficacy of targeted therapy for colorectal cancer (CRC) is affected by hub genes of epidermal growth factor receptor (EGFR) signaling pathways, such as
KRAS
. Immune cell infiltration may lead to gene mutation, but the relationship between
KRAS
status and peripheral immune-inflammatory indices has not been clarified in CRC.
Methods
Clinical records of CRC patients were collected. The relationship between
KRAS
status and clinicopathological characteristics, peripheral immune-inflammatory indices (pan-immune inflammation value (PIV) (monocyte×neutrophil×platelet/lymphocyte), systemic immune inflammation index (SII) (platelet×neutrophil/lymphocyte), and system inflammation response index (SIRI) (monocyte×neutrophil/lymphocyte)) were analyzed.
Results
1033 CRC patients were collected, there were 514 (49.8%) patients with
KRAS
wild-type and 519 (50.2%) with
KRAS
mutation. Patients with
KRAS
mutation had higher proportions of female, III-IV stage, and lymph node metastasis and lower proportion of low grade of tumor budding (the presence of single tumor cells or small clusters of up to 5 cells in mesenchyma at the front of tumor invasion) than those with
KRAS
wild-type. The PIV, SII, and SIRI levels in
KRAS
mutation patients were significantly higher than those in
KRAS
wild-type patients. The proportion of aged ≥65 years old, dMMR, distant metastasis, and
KRAS
mutation were high in patients with high PIV, SII, and SIRI levels. Logistic regression analysis showed that non-low grade of tumor budding (odds ratio (OR): 1.970, 95% confidence interval (CI): 1.287–3.016,
p
=0.002), and high SII level (≥807.81 vs <807.81, OR: 1.915, 95% CI: 1.120–3.272,
p
=0.018) were independently associated with
KRAS
mutation.
Conclusion
Non-low grade of tumor budding, and high SII level were independently associated with
KRAS
mutation in CRC. It provides additional references for diagnosis and treatment options for patients with CRC.