Fig. 7

P1C1M-PNU limits growth of mutant p53-expressing HT29 xenograft in vivo. HLA-A24 expressing a HT29 (p53^R273H) and HepG2 (p53^wt) cells were injected subcutaneously into NSG mice. After tumours reached an average size of ≥100 mm³, mice were treated with a single dose of either P1C1TM-PNU ADC (1 or 0.3 mg kg⁻¹) or unconjugated P1C1TM only (1 mg kg⁻¹) as indicated by the arrows. P1C1TM-PNU significantly delayed tumour growth as compared to the unconjugated P1C1TM (* represents significant differences with p ≤ 0.05. Statistical analyses were done by Student’s t test with Holm–Šidák method of multiple comparison.). b Mice bearing HT29 (p53^R273H) tumours were treated with a loading dose of 1 mg kg⁻¹ of either P1C1TM-PNU or unconjugated P1C1TM only, followed by two more doses at 0.3 mg kg⁻¹ 7 days apart. c HT29 cells were introduced i.v. into NSG mice and treated with 1 mg kg⁻¹ P1C1TM-PNU or unconjugated P1C1TM 24 h post introduction. P1C1TM-PNU-treated mice showed significantly prolonged survival compared to unconjugated P1C1TM-treated mice (*p = 0.0339. Statistical analysis was done with a log-rank test for survival.). Tumour sizes were calculated as V = ½(length × width²). Data are means of triplicates ± SEM.