Skip to main content
. 2020 Feb 24;9(2):514. doi: 10.3390/cells9020514

Table 6.

Basic research studies showing the associations between KIR and HLA in CRC patients.

Reference Type of Experiment/Objective Conclusions
[19] 109 CRC patients (70 bladder and 34 laryngeal) and 100 controls. HLA and KIR genotyping. No differences in KIR/HLA frequencies was observed between patients and controls.
[20] 128 CRC patients and 255 controls. KIR and HLA genotyping. The data showed no significant differences between KIR gene frequencies in CRC patients versus controls.
[21] 241 CRC patients and 159 controls from Korean populations. KIR and HLA-C genotyping The activating KIR2DS5 was more frequent in Korean CRC patients, showing a risk for the disease. The frequencies of KIR3DL1, KIR2DS2 and KIR2DS4 were lower in the rectal cancer subgroup, and they could have a protective effect against CRC. Also, the lower frequency of KIR2DS2 in patients with HLA-C1 homozygote, may be a protective effect too.
[22] 52 CRC patients and 70 controls from Saudi population. KIR and HLA-C genotyping. Activating KIRs (2DS1, 2DS2, 2DS3, 2DS5 and 3DS1) was more frequent in CRC patients, suggesting their presence a risk for disease.
[23] 470 CRC patients and 483 controls. KIR genotyping. The presence of KIR2DS5 was associated with CRC like as a non-protective gene. This result explains the inflammatory basis of this cancer.
[24] 154 CRC patients and 216 controls from Caucasian Brazilian population. KIR and HLA genotyping. No associations between KIRs and HLA in CRC was observed. However, the Bx haplotype was more frequent in controls than in patients, being a possible mechanism of protection to CRC.
[25] 165 colorectal adenocarcinoma patients and 165 controls. KIR genotyping. The presence of activating KIRs (≥ 4) and KIR3DL1, 3DS1, 2DS1 and 2DS4, were associated with protection against metastasis in CRC patients.
[26] 29 CRC recurrent patients (in 5 years) vs. 58 CRC non-recurrent patients (in 5 years) after surgery and 154 controls. KIR and HLA-class I genotyping. The increment of activating KIRs (in particularly 2DS2 and 2DS3) and the lack of inhibitory KIRs (in particularly 2DL1) was associated with long term disease-free survival and this was independent of tumor localization or stage. Also, HLA-A-Bw4 was associated with recurrent disease.