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. 2015 Mar 17;10(3):e0120628. doi: 10.1371/journal.pone.0120628

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© 2015 Linn et al

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.

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Fig 2 — A. Representative anterior prostate (AP) histology of male mice with the indicated combinations of Nkx3.1 ^+/-, Pten ^+/-, and T-ERG knockin. Note HG-PIN lesions developed in all prostate lobes of T-ERG;Pten ^+/- and T-ERG;Pten ^+/- ;Nkx3.1 ^+/- males due to cooperation between Pten ^+/- and T-ERG. Representative HG-PIN lesions developed in the APs of T-ERG;Pten ^+/- and T-ERG;Pten ^+/- ;Nkx3.1 ^+/- males are shown (red arrows). Scale bars represent 100 μm. B. Histology summary of aged Pten ^+/- (left) and Pten ^+/- ;Nkx3.1 ^+/- (right) male mice with or without the T-ERG knockin allele. Notable cooperation was detected with T-ERG (p = 0.05 under the Pten ^+/- background and p = 0.04 under the Pten ^+/- ;Nkx3.1 ^+/- background). HG-PIN in any prostate lobe was diagnosed by a trained rodent pathologist.