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Systemic jnk2 deletion enhances tumor development.

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posted on 2013-02-21, 01:32 authored by Peila Chen, Jamye F. O'Neal, Nancy D. Ebelt, Michael A. Cantrell, Shreya Mitra, Azadeh Nasrazadani, Tracy L. Vandenbroek, Lynn E. Heasley, Carla L. Van Den Berg

PyV MT/jnk2+/+ (n = 12), PyV MT/jnk2+/− (n = 16), and PyV MT/jnk2−/− (n = 19) mice were palpated for mammary tumors thrice weekly. Once palpated, tumor growth was recorded thrice weekly. A). Kaplan Meier graph showing age of first tumor palpation (median age was day 55 for PyV MT/jnk2−/− vs. day 70 for PyV MT/jnk2+/+, p = .11); B). Total number of tumors palpated per mouse at the time of harvest was higher in PyV MT/jnk2−/− mice compared to PyV MT/jnk2+/+ mice, p = 0.0192); C). Paraffin embedded, non-target tumor sections were probed with cleaved caspase 3 primary antibody and detected using FITC labeled secondary antibody. Nuclei were stained with propidium iodide. The total number of cells staining positive for cleaved caspase 3 were scored and divided by the total number of nuclei (n = 5 tumors in each group); D). Paraffin embedded tissue sections were probed with Ki-67 primary antibody and detected using DAB. Cells staining positive for Ki-67 were counted and divided by the total number of nuclei (Hematoxylin) per field. Five fields per tumor were counted (n = 5 per genotype, p = 0.0159); E). Paraffin embedded tissue sections were probed with p-c-Jun (Ser63) primary antibody and detected using DAB. Hematoxylin was used as a nuclear stain.

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