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. 2016 Jul 19;50(3):289–296. doi: 10.1515/raon-2016-0031

Table 3.

Genotype frequencies in patients with Hurthle cell neoplasms

Gene Polymorphism Genotype All patients (%) PHWE HCTA+HCTN (%) HCTC (%)
SOD2 rs4880; c.47C>T; p.Val16Ala CC 26 (21.7) 0.903 12 (17.9) 14 (26.4)
CT 59 (49.2) 34 (50.7) 25 (47.2)
TT 35 (29.2) 21 (31.3) 14 (26.4)
CAT rs1001179; c.-262C>T; c.-262G>A CC 70 (58.3) 0.907 35 (52.2) 35 (66.0)
CT 43 (35.8) 30 (44.8) 13 (24.5)
TT 7 (5.8) 2 (3) 5 (9.4)
GPX1 rs1050450; c.599C>T; p.Pro200Leu CC 63 (52.1) 0.424 35 (51.5) 28 (52.8)
CT 51 (42.1) 32 (47.1) 19 (35.8)
TT 7 (5.8) 1 (1.5) 6 (11.3)
GSTP1 rs1695; c.341C>T; p.Ile105Val CC 54 (44.6) 0.653 28 (41.2) 26 (49.1)
CT 52 (43.0) 32 (47.1) 20 (37.7)
TT 15 (12.4) 8 (11.8) 7 (13.2)
GSTP1 rs1138272; c.313A>G; p.Ala114Val AA 103 (85.1) 0.159 58 (85.3) 45 (84.9)
AG 16 (13.2) 8 (11.8) 8 (15.1)
GG 2 (1.7) 2 (2.9) 0 (0)
GSTM1 Gene deletion Wild type 55 (50.9) /a 33 (50.8) 22 (51.2)
Gene deletion 53 (49.1) 32 (49.2) 21 (48.8)
GSTT1 Gene deletion Wild type 93 (86.1) /a 54 (83.1) 39 (90.7)
Gene deletion 15 (13.9) 11 (16.9) 4 (9.3)
a

HWE could not be evaluated for GSTM1 and GSTT1 as we were not able to distinguish between carriers of one or two copies of each gene.

HCTA = Hurthle cell thyroid adenoma; HCTC = Hurthle cell thyroid carcinoma; HCTN = Hurthle cell thyroid nodule; HWE = Hardy-Weinberg equilibrium