***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Purpose ERCC1 and ERCC2 play critical roles in the nucleotide excision repair pathway that effectively repairs DNA damage induced by chemotherapeutic agents . Therefore , functional single nucleotide polymorphisms ( SNPs ) in these genes could have an impact on clinical outcomes in cancer patients who received chemotherapy .  However , few studies have simultaneously investigated the roles of ERCC1 and ERCC2 SNPs in clinical outcomes in gastric cancer patients . Experimental Design We genotyped by the TaqMan assay three common , potentially functional ERCC1 ( rs3212986 ) and ERCC2 SNPs ( rs13181 and rs1799793 ) in 360 gastric cancer patients . We used both Kaplan-Meier tests and Cox proportional hazards models to evaluate the effects of ERCC1 and ERCC2 genotypes and haplotypes on clinical outcomes . Results We found that , compared with ERCC2 rs1799793 GG+AG genotypes , the homozygous variant AA genotype was associated with significantly poorer overall survival ( OS ) ( AA vs. GG+AG , log-rank P = 0.012 ) and significantly higher risk of death ( AA vs. GG+AG , Adjusted hazards ratio [ HR ] 2.13 ; 95 % CI , 1.28 to 3.56 ; P = 0.004 ) . In combined analyses , patients with any one of the three unfavorable genotypes ( i.e. ERCC1 rs3212986 TT , ERCC2 rs13181 GG and rs1799793 AA ) had statistically significant hazards of poor prognosis ( Adjusted HR , 1.54 ; 95 % CI , 1.06 to 2.25 ; P = 0.025 ) , compared with those without any unfavorable genotypes . Furthermore , the haplotype A-G-G ( rs1799793/rs13181/rs3212986 ) had a significant impact on OS ( Adjusted HR , 1.57 ; 95 % CI , 1.11 to 2.21 ; P = 0.011 ) , compared with the common haplotype G-T-G. Conclusion ERCC1 and ERCC2 functional SNPs may jointly affect OS in Caucasian gastric cancer patients . Additional large prospect i ve studies are essential to confirm our findings Background The objective of this study was to evaluate the efficacy and toxicity of infusional 5-fluorouracil ( 5-FU ) , folinic acid and oxaliplatin ( modified FOLFOX-6 ) in patients with advanced gastric cancer ( AGC ) , as first-line palliative combination chemotherapy . We also analyzed the predictive or prognostic value of germline polymorphisms of c and i date genes associated with 5-FU and oxaliplatin . Methods Seventy-three patients were administered a 2 hour infusion of oxaliplatin ( 100 mg/m2 ) and folinic acid ( 100 mg/m2 ) followed by a 46 hour continuous infusion of 5-FU ( 2,400 mg/m2 ) . Genomic DNA from the patients ' peripheral blood mononuclear cells was extracted . Ten polymorphisms within five genes were investigated including TS , GSTP , ERCC , XPD and XRCC . Results The overall response rate ( RR ) was 43.8 % . Median time to progression ( TTP ) and overall survival ( OS ) were 6.0 months and 12.6 months , respectively . Toxicities were generally tolerable and manageable . The RR was significantly higher in patients with a 6-bp deletion homozygote ( -6 bp/-6 bp ) in TS-3'UTR ( 55.0 % vs. 30.3 % in + 6 bp/+6 bp or + 6 bp/-6 bp , p = 0.034 ) , and C/A or A/A in XPD156 ( 52.0 % vs. 26.1 % in C/C , p = 0.038 ) . The -6 bp/-6 bp in TS-3'UTR was significantly associated with a prolonged TTP and OS . In a multivariate analysis , the 6-bp deletion in TS-3'UTR was identified as an independent prognostic marker of TTP ( hazard ratio = 0.561 , p = 0.032 ) . Conclusion Modified FOLFOX-6 chemotherapy appears to be active and well tolerated as first line chemotherapy in AGC patients . The 6-bp deletion in TS-3'UTR might be a c and i date to select patients who are likely to benefit from 5-FU based modified FOLFOX-6 in future large scale trial CONTEXT AND OBJECTIVE Oxaliplatin is one of the chemotherapy regimens most used for treating colorectal cancer . One of the main limitations to its use is induction of peripheral neuropathy . Previous studies have shown that vitamin E can reduce the incidence of peripheral neuropathy by 50 % . This study aim ed to assess the effectiveness of vitamin E for prevention of oxaliplatin-induced peripheral neuropathy . DESIGN AND SETTING Prospect i ve , phase II , r and omized pilot study developed at a university hospital in the Greater ABC region . METHODS Patients were r and omized five days before starting oxaliplatin treatment , to receive either vitamin E or placebo until the end of the chemotherapy regimen . The outcome was evaluated using the Common Terminology Criteria for Adverse Events ( CTCAE ) , version 3 , and specific gradation scales for oxaliplatin-induced peripheral neuropathy .  Patients with colorectal and gastric cancer who had been scheduled to receive oxaliplatin-based chemotherapy were included . Both groups received calcium and magnesium supplementation before and after oxaliplatin infusions . RESULTS Eighteen patients were r and omized to the vitamin E group and 16 to the placebo group .  Cumulative incidence of 83 % with peripheral neuropathy grade s 1/2 was observed in the vitamin E group , versus 68 % in the placebo group ( P = 0.45 ) . A trend towards more diarrhea was observed among patients who received vitamin E ( 55.6 % vs. 18.8 % ; P = 0.06 ) . There were no other significant differences in toxicity between the groups . CONCLUSIONS No significant decrease in the incidence of acute oxaliplatin-induced peripheral neuropathy was demonstrated through vitamin E use In this marker evaluation study , we tested whether distinct patterns of functional genomic polymorphisms in genes involved in drug metabolic pathways and DNA repair that predict clinical outcome to 5-fluorouracil (5-FU)/oxaliplatin chemotherapy in patients with advanced colorectal cancer could be identified . Functional polymorphisms in DNA-repair genes XPD , ERCC1 , XRCC1 , XPA , and metabolising genes glutathione S-transferase GSTP1 , GSTT1 , GSTM1 , and thymidylate synthase ( TS ) were assessed retrospectively in 106 patients with refractory stage IV disease who received 5-FU/oxaliplatin combination chemotherapy , using a polymerase chain reaction-based RFLP technique .  Favourable genotypes from polymorphisms in XPD-751 , ERCC1 - 118 , GSTP1 - 105 , and TS-3′-untranslated region ( 3′UTR ) that are associated with overall survival were identified . After adjustment for performance status , the relative risks of dying for patients who possessed the unfavourable genotype were : 3.33 for XPD-751 ( P=0.037 ) , 3.25 for GSTP1 - 105 ( P=0.072 ) , 2.05 for ERCC1 - 118 ( P=0.037 ) , and 1.65 for TS-3′UTR ( P=0.091 ) when compared to their respective beneficial genomic variants . Combination analysis with all four polymorphisms revealed that patients possessing ⩾2 favourable genotypes survived a median of 17.4 months ( 95 % confidence interval ( CI ) : 9.4 , 26.5 ) compared to 5.4 months ( 95 % CI : 4.3 , 6.0 ) in patients with no favourable genotype . Patients who carried one favourable genotype demonstrated intermediate survival of 10.2 months ( 95 % CI : 6.8 , 15.3 ; P<0.001 ) . Polymorphisms in the TS-3′UTR and GSTP1 - 105 gene were also associated with time to progression . After adjustment for performance status , patients with an unfavourable TS-3′UTR genotype had a relative risk of disease progression of 1.76 ( P=0.020 ) and those with the unfavourable GSTP1 - 105 genotype showed a relative risk of progression of 2.00 ( P=0.018 ) . The genomic polymorphisms XPD-751 , ERCC1 - 118 , GSTP1 - 105 , and TS-3′UTR may be useful in predicting overall survival and time to progression of colorectal cancer in patients who receive 5-FU/oxaliplatin chemotherapy .  These findings require independent prospect i ve confirmation Background : While single nucleotide polymorphisms ( SNP ) in genes involved in DNA repair or drug metabolism have been shown to influence survival of metastatic colon cancer patients treated with FOLFOX  , data on adjuvant setting are scarce . Methods : This study evaluated the correlation between disease-free survival ( DFS ) of 210 unselected stage III colon cancer patients receiving FOLFOX chemotherapy , and ERCC1 - 118 ( rs11615 , c.354T > C ) , XRCC1 - 399 ( rs25487 , c.1196G  > A  ) and GSTP1 - 105 ( rs1695 , c.313A > G ) polymorphisms .  SNP were determined on tumor DNA using a PCR-based RFLP technique . Results : In univariate analysis , a trend towards longer DFS was observed for ERCC1 ( C/T + T/T ) versus ( C/C ) ( HR=2.29 ; p=0.06 ) , and XRCC1 ( A/A ) versus ( G/G + G/A ) ( HR=1.61 ; p=0.16 ) , but not for GSTP1 genotypes ; a statistically significant p value was obtained when combining ERCC1 and XRCC1 favorable genotypes ( 0 versus ≥ 1 favorable genotypes , HR=2.42 ; p=0.02 ) . After adjustment on tumor stage , lymph node ratio and differentiation grade , multivariate analysis showed that combining ERCC1 and XRCC1 genotypes gave a p value slightly above the threshold for statistical significance ( HR=2.03 ; p=0.06 ) , which was lower than for tumor stage , lymph node ratio or differentiation grade . Conclusion : The association of ERCC1 and XRCC1 polymorphisms may influence the prognosis of stage III colon cancer patients treated  with FOLFOX adjuvant chemotherapy . Yet , these findings need to be confirmed in independent prospect i ve studies Background : The FAST was a factorial trial in first-line treatment of advanced non-small-cell lung cancer ( NSCLC ) , addressing the role of replacing cisplatin with a non-platinum agent . The prognostic and predictive effect of ERCC1/BRCA1 expression and ERCC1/XPD/XRCC1–3 gene polymorphisms on outcomes of patients was examined . Methods : Patients were r and omised to receive treatment with or without cisplatin .  ERCC1/BRCA1 expression was determined by immunohistochemistry . ERCC1 ( C8092A , C118 T ) , XPD ( Lys751Gln ) , XRCC1 ( Arg399Gln ) and XRCC3 ( Thr241Met ) gene polymorphisms were evaluated on tumour DNA by TaqMan allelic discrimination assay . Results : Tumour sample s were available from 110 of 433 patients enrolled : 54.7 % were ERCC1 positive and 51.4 % were BRCA1 positive . Overall , ERCC1-negative patients had better response rate ( P=0.004 ) , progression-free survival ( P=0.023 ) and overall survival ( P=0.012 ) compared with positive ones , with no statistically significant treatment interaction . The BRCA1-positive patients showed numerically better outcomes , although not statistically significant , with no treatment interaction . Among DNA repair gene polymorphisms , only XRCC1 Gln/Gln genotype evidence d a potential prognostic role ( P=0.036 ) . Conclusion : This study confirms the prognostic role of ERCC1 expression and XRCC1 ( Arg399Gln ) polymorphism in advanced NSCLC treated with first-line chemotherapy . None of these biomarkers was shown to be a specific predictive factor of cisplatin efficacy Purpose The aim of this study was to assess whether genetic polymorphisms in p53 , glutathione S-transferase P1 ( GSTP1 ) , GSTM1 , excision repair cross complementing group 1 ( ERCC1 ) and X-ray repair cross-complementing group 1 ( XRCC1 ) genes are associated with clinical outcome of gastric cancer patients treated with oxaliplatin-based adjuvant chemotherapy .  Methods The genetic polymorphisms in p5 
    Output:
    
Conclusion The ERCC1 rs11615 polymorphism was closely associated with the clinical outcomes of GC and CRC patients treated with oxaliplatin-based chemotherapy