Adjuvant hormonotherapy, as indicated, was given simultaneously with SSPBI. Patient, tumour and treatment related characteristics are listed in Table 1, respectively. In Table 2, we reported the abbreviations for the polymorphic sites. The genotyping selleck inhibitor procedure was successful in 57 patients. The observed allele frequencies of the polymorphic genes analyzed were comparable to those reported for European populations in the dbSNP database and are shown in Figure 1. Table 1 Main patient and tumor characteristics Age (years) median (range) 66 (51-87) Tumor stage Tis/T1/T2 1/48/8 Nodal stage N0/N1 54/3 Chemotherapy yes/no 15/42 Hormone-therapy
yes/no 52/5 Follow-up (months) selleck products median (range) 38 (19-50) Table 2 Polymorphism abbreviations Gene NCBI ds SNP ID homozygote wt heterozygote Homozygote mut XRCC1 G28152A (Arg399Gln) rs25487 GG (399 Arg/Arg) GA(399Arg/Gln) AA
(399 Gln/Gln) XRCC3 C18067T (Thr241Met) rs861539 CC (241Thr/Thr) CT(241Thr/Met) TT (241Met/Met) XRCC3 A4541G (5′UTR) rs1799794 AA AG GG GSTP1A313G (Ile105Val) rs1695 AA (105 Ile/Ile) AG (105 Ile/Val) GG (105 Val/Val) RAD51 G135C (5′UTR) rs1801320 GG GC CC Abbreviations: NCBI = National Center for Biotechnology Information, ID = identification Figure 1 Polymorphism distribution. With a median follow-up 38 months (range: 19-50 months), the G1, G2 and G3 subcutaneous fibrosis, corresponding to a marked increased density and firmness on palpation with/without retraction/fixation, were observed in 23 see more (40%), 18 (32%) and 7 (12%) patients, respectively. While the G2 and
G3 fat necrosis were observed in 1 (2%) and 1 (2%) patient, respectively. Late moderate-to-severe (≥ G2) subcutaneous fibrosis or fat necrosis were more frequent (64% vs 38%) in patients with the mutation or heterozygote (aa/Aa) genotype of GSTP1 (Ile105Val) with greater odds (OR = 2.9; 95% CI, 0.88-10.14, p = 0.047 Chi-square test). No statistical significant increase/decrease of ORs was observed with other SNPs or their combination. In particular, no correlation was found between late toxicity and mut/het XRCC1 Arg399Gln, mut/het XRCC3 A4541G or mut/het XRCC3 Phosphatidylethanolamine N-methyltransferase Thr241Met or mut/het RAD51. Table 3 shows a summary of a statistical analysis. Table 3 ORs of ≥ G2 fibrosis or fat necrosis for different polymorphisms and their combination Polymorphisms Genotype ≥ G2 fibrosis or fat necrosis OR (95% CI) p-value (*) p-value (§) XRCC1 (Arg399Gln) AA 45% 1 aa/Aa 54% 1.41 (0.44-4.58) 0.514 0.599 XRCC3(A4541G) aa/Aa 44% 1 AA 53% 1.43 (0.45-4.71) 0.494 0.596 XRCC3(C18067T) AA/Aa 51% 1 aa 33% 0.49 (0.04-3.75) 0.413 0.670 GSTP1 AA 38% 1 aa/Aa 64% 2.9 (0.88-10.14) 0.047 0.064 RAD51 AA 48% 1 aa/Aa 67% NA # 0.9751 0.
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