OBJECTIVE To establish an evaluation index system for the selection of therapeutic drugs for colorectal carcinoma， providing a basis for clinical medication decision-making. METHODS A preliminary framework for the evaluation index system for the selection of therapeutic drugs for colorectal carcinoma was constructed through literature research and expert surveys. Using the Delphi method， consultations were conducted with 40 experts engaged in the use and evaluation of antitumor drugs， ultimately forming the evaluation system for selecting therapeutic drugs for colorectal carcinoma. RESULTS The effective recovery rate of questionnaires for both rounds of inquiries was 100%， with the reliability coefficients of 0.82 and 0.85. The Kendall’s W coordination coefficients were 0.251 and 0.252 （the P values of χ 2 tests were both less than 0.05）. The final evaluation system constructed included 6 first-level indicators （safety， efficacy， cost-effectiveness， suitability， innovation， and accessibility） and 29 second-level indicators （such as disease control rate， precise treatment of target diseases， objective remission rate， and whether clinical medication complies with authoritative recommendations）. Among these， efficacy and accessibility received high average importance scores （4.60， 4.30 points）， with “disease control rate” and “precision treatment for target disease” carrying relatively high weights （both were 0.035 2）. CONCLUSIONS This study successfully established a drug evaluation index system for the selection of therapeutic drugs for colorectal cancer that aligns with clinical practice.

Objective To construct eukaryotic expression vector of wild type E 4F1 and the mutant deleting amino acid region 32-81, and to detect the interaction between wild type or mutant E 4F1 and p53 and to study the effect of E4F1 on the expression level of p21.Methods Wild type and mutant sequences of E 4F1 were amplified from the mammary library using standard PCR and recombinant PCR .The sequences were cloned into pXJ 40-MYC vector to generate the MYC-E4F1 and MYC-E4F1(Δ32-81) recombinant plasmids that were transfected into 293T cells and identified by Western blotting . FLAG-p53 and MYC-E4F1 or MYC-E4F1(Δ32-81) were co-transfected into 293T cells and immunoprecipitation assay was performed to detect the interaction of wild type or mutant E 4F1 with p53.Wild type and mutant E4F1 expressing vec-tors were co-transfected into osteosarcoma U2OS cells and the expression of p21was detected.Results Recombinant plas-mids of MYC-E4F1 and MYC-E4F1(Δ32-81) were successfully constructed.Both wild type and mutant E4F1 interacted with p53.Deletion of amino acid region 32-81 of E4F1 increased the interaction .The expression level of p21 was in-creased by wild-type E4F1, but not by mutant E4F1.Conclusion The eukaryotic expression vector of wild type E4F1 and its deletion mutant is successfully constructed .Both of them interact with p53.Deletion of amino acid region 32-81 of E4F1 increases the interaction .This study contributes to further studies on the regulation and mechanism of E 4F1 on p53.