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Together with the findings that overexpression of MYC in the mouse prostate causes PIN [1], [32] that progresses to adenocarcinoma[1], and that MYC can transform isolated human prostate epithelial cells into tumorigenic cells when mixed with urogenital sinus mesenchyme [33], these results suggest MYC overexpression may also be a critical factor contributing to prostatic adenocarcinoma initiation.
Furthermore, transgenic expression of SKP2 in the mouse prostate causes low-grade prostate carcinomas that coincide with p27 downregulation [ 32].
We showed previously that PPAR γ ablation in mouse prostate causes tumorigenesis and active autophagy, suggesting PPAR γ may provide a molecular link between systemic metabolism and prostate differentiation and growth.
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Orally administration of this isothiocyanate reduced prostate tumor growth and pulmonary metastasis in transgenic adenocarcinoma of mouse prostate (TRAMP) mice without causing any side effects [ 67] and retarded the growth of PC-3 xenografts in nude mice [ 78, 79].
New proof that the mouse prostate contains stem cells could aid cancer research.
Wang, X.-D. et al. Expression profiling of the mouse prostate after castration and hormone replacement: implication of H-cadherin in prostate tumorigenesis.
Liang, Z. et al. Plasmid-based Stat3 siRNA delivered by hydroxyapatite nanoparticles suppresses mouse prostate tumour growth in vivo.
Liu, J. et al. Regenerated luminal epithelial cells are derived from preexisting luminal epithelial cells in adult mouse prostate.
Transgenic adenocarcinoma of the mouse prostate.
Transgenic mice expressing a subphysiological level of a p53(R172L) minigene (PB-p53(R172L)) in the prostate epithelium were generated and bred to the transgenic adenocarcinoma mouse prostate (TRAMP) model of prostate cancer.
Radiation and a metalloporphyrin radioprotectant in a mouse prostate tumor model.
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