Table 3.
Domain | Disease setting | Clinical setting | Association with FCGR2/3 genetic variation | References |
---|---|---|---|---|
Autoimmune | ITP | Prognosis | 2B.4 and FCGR2C-ORF correlate are associated with transient disease; CNR1 deletion is associated with chronic disease | (65) |
Autoimmune | ITP | Treatment | 2B.4 and FCGR2C-ORF correlate with favorable IVIg response | (65) |
Autoimmune | ITP | Treatment | FCGR3A-p.176Val/Val is associated with favorable response to rituximab | (164) |
Autoimmune | Kawasaki disease | Treatment | 2B.4 correlates with favorable IVIg response | (153) |
Autoimmune | SLE | Prognosis | 2B.4 shows lower rate of lupus nephritis | (11) |
Autoimmune | SLE | Prognosis | CNR1 deletion is associated with lupus nephritis | (158) |
Autoimmune | Rheumatoid arthritis | Treatment | FCGR3A-p.176Val allele confers improved response to rituximab treatment (meta-analysis, 3 studies) | (165) |
Autoimmune | Rheumatoid arthritis | Treatment | FCGR2A-p.166Arg allele is associated with favorable response to adalimumab | (166) |
Cancer | Breast cancer | Treatment | FCGR2A-p.166His/His and FCGR3A-p.176Val/Val have higher response and progression-free survival with trastuzumab in HER2-positive metastatic disease | (167) |
Cancer | Breast cancer | Treatment | FCGR2A-p.166His/His shows better pathological response and progression-free survival after trastuzumab in HER2-positive disease | (168) |
Cancer | Breast cancer | Treatment | FCGR3A-p.176Val/Val shows improved patient outcomes and benefit from trastuzumab | (169) |
Cancer | Breast cancer | Treatment | No difference after trastuzumab observed with FCGR2A-p.166 and FCGR3A-p.176 variants | (170) |
Cancer | Lymphoma | Treatment | FCGR3A-p.176Val/Val showed better response rates to rituximab | (171) |
Cancer | Lymphoma | Treatment | FCGR3A-p.176Val/Val showed better response rates and progression-free survival to rituximab | (172) |
Cancer | Lymphoma | Treatment | Carriers of FCGR3A-p.176Val allele showed better response rates | (173) |
Cancer | Lymphoma | Treatment | Carriers of FCGR3A- p.176Val allele showed better response rates | (174) |
Cancer | Lymphoma | Treatment | No difference in response to rituximab with FCGR2A-p.166 and FCGR3A-p.176 variants | (175) |
Cancer | Lymphoma | Treatment | No difference in response to rituximab with FCGR2A- p.166 and FCGR3A-p.176 variants | (176) |
Cancer | Lymphoma | Treatment | No difference in response to rituximab with FCGR2A- p.166 and FCGR3A-p.176 variants | (177) |
Cancer | CLL | Treatment | No difference in response to rituximab with FCGR2A- p.166 and FCGR3A-p.176 variants | (178) |
Cancer | Colorectal carcinoma | Treatment | FCGR2A-p.166His/His and FCGR3A-p.176Val/Val show longer progression-free survival after cetuximab | (179) |
Cancer | Colorectal carcinoma | Treatment | FCGR2A-p.166His and FCGR3A-p.176Val alleles show increased response rates and stable disease after cetuximab | (180) |
Cancer | Colorectal carcinoma | Treatment | FCGR2A-p.166His/His and FCGR3A-p.176Phe/Phe* showed higher progression-free surival rates after cetuximab | (181) |
Cancer | Colorectal carcinoma | Treatment | FCGR3A-p.176Phe/Phe* showed higher survival rates after cetuximab | (182) |
Cancer | Colorectal carcinoma | Treatment | FCGR3A-p.176Val/Val and p.176Val/Phe show higher progression-free survival than p.176Phe/Phe after cetuximab | (183) |
Cancer | Colorectal carcinoma | Treatment | FCGR3A-p.176Val/Val showed shorter* progression-free survival compared to p.176Val/Phe or p.176Phe/Phe | (184) |
Cancer | Head and neck carcinoma | Treatment | FCGR2A-p.166His/His and FCGR3A-p.176Val/Val have longer progression-free survival with cetuximab | (185) |
Transplant | Liver transplant | Treatment | After rituximab, FCGR2A-p.166His/His shows stronger B cell suppression, bacterial infections, and poor prognosis | (186) |
CLL, chronic lymphocytic leukemia.
Result is in contrary direction to other studies.