Fig. 1: PyMT ProTracer/Deleter for modeling breast cancer relapse.
From: Modeling tumor relapse using proliferation tracing and ablation transgenic mouse
a Schematic of Ki67-based proliferation tracing and deletion in the PyMT spontaneous breast cancer model. Tamoxifen-induced DreER/Rox recombination activates Ki67 promoter-driven Cre, enabling continuous labeling of proliferating cells. b Experimental workflow for fluorescent labeling of organoids derived from the PyMT ProTracer/Deleter model (4-OH-TAM: 4-Hydroxytamoxifen; IF: immunofluorescence; FC: flow cytometry). IF staining (c) and FC quantification (d) of tdTomato+ cells after 4-OH-TAM treatment. e EdU incorporation and Ki67 IF staining in cultured organoids. White arrowheads denote rare non-proliferative single cells or small clusters (scale bar, 50 μm). f Tumor growth kinetics post-palpation. Mice were administered with 2 mg tamoxifen (Tam) via oral gavage on Day 58, and 200 ng diphtheria toxin (DT) intraperitoneally on Day 60. g (Upper) Experimental design for fluorescent labeling and genetic ablation of tumor cells proliferating within a two-day time window. (Lower) IF analysis of tdTomato+ cell abundance in primary versus relapsed tumors (scale bar, 50 μm). In the TamPost approach, Tam was administered both before DT (initial labeling) and during relapse, enabling detection of repopulating cancer cells that were not labeled during the original 2-day labeling window. Mean ± s.e.m. shown. P values were calculated by comparing individual animals using two-tailed paired (d, g) Student’s t-test.
