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. Author manuscript; available in PMC: 2009 Aug 10.
Published in final edited form as: Clin Cancer Res. 2008 Jul 15;14(14):4543–4549. doi: 10.1158/1078-0432.CCR-07-4230

Table I.

Genotype and allele frequencies of the the studied variants

Genotype Frequenciesa Allele Frequenci
Allelic Variantc Effectd Ne Wtf Het Var p
Docetaxel alone (N = 23)g
ABCB1 1236C>T G411G 23 13 (56.5) 8 (34.8) 2 (8.7) 0.739 0.
ABCB1 2677G>T A893S 23 11 (47.8) 9 (39.1) 2 (8.7) 0.674 0.
ABCB1 2677G>A A893Th 23 11 (47.8) 1 (4.3) 0 (0) 0.674 0.
ABCB1 3435C>T I1145I 23 7 (30.4) 10 (43.5) 6 (26.1) 0.522 0.
Docetaxel Plus Thalidomide (N = 50)
ABCB1 1236C>T G411G 46 12 (26.1) 18 (39.1) 16 (34.8) 0.457 0.
ABCB1 2677G>T A893S 50 15 (30.0) 20 (40.0) 15 (30.0) 0.500 0.
ABCB1 3435C>T I1145I 45 10 (22.2) 23 (51.1) 12 (26.6) 0.478 0.
a

Number represent number of patients with percentage in parenthesis; the difference in the total number of patients is due Hardy-Weinberg notation for allele frequencies (p, frequency for wild type allele and q, frequency for variant allele);

c

Num represents position in nucleotide sequence;

d

Number represents amino acid codon;

e

genotype data were not available in all patients as not all samples yielded sufficient DNA or PCR amplified;

f

WT, Homozygous wild-type allele patient; Het, Heterozygous patient; Var, Homozygous variant patient;

g

A single Hispanic male was also included, and his genotype was 1236C>T, unknown; 2677G>T/A, wild-type; 3435C>T, wild-type;

h

The 2677G>T/A polymorphism is triallelic and two d SNPs are therefore presented.