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Deletion of Smad4 in the Pten-null mouse prostate led to highly proliferative, invasive, metastatic and lethal tumors.
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Considering that targeted expression of ETK in mouse prostate leads to the development of PIN [13], it is possible that ETK may also play a role in oncogenic transformation in bladder urothelial cells.
Moreover, overexpression of Skp2 in mouse prostate leads to prostate intraepithelial neoplasia (PIN) [50].
For example, it is now well-established that inactivation of PTEN in prostate leads to the development of cancer, however, deletion of mTOR in prostate cells inhibited tumor development in mouse PTEN-deficient prostates (42).
A recent study showed that P. acnes can lead to a chronic inflammation of the mouse prostate; introduction of P. acnes into the mouse prostate via transurethral catheterization and inoculation led to chronic inflammation of the dorsal lobe of the prostate that persisted for at least 8 weeks after inoculation [ 27].
Furthermore, loss of ADAM9 in a prostate cancer mouse model led to the development of well-differentiated prostate tumours as opposed to poorly differentiated tumours in control littermates (Peduto et al, 2005).
Transgenic adenocarcinoma of the mouse prostate.
We used animals designed to develop this disease, Transgenic Adenocarcinoma of the Mouse Prostate (TRAMP) mice, to investigate the potential role of AHR signaling in prostate cancer development.
To further define the role of 15-LO-1 in prostate carcinogenesis, we established a novel GEM model with targeted overexpression of h15-LO-1 in the prostate [human fifteen lipoxygenase-1 in mouse prostate (FLiMP)].
Primary prostate colonies from DsRED transgenic mouse prostate cells were trypsinized and dissociated into single cells.
Study of tumor development in mouse prostate cancer models can be instrumental in understanding human prostate cancer.
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