Figure 2From: p27Kip1deficiency promotes prostate carcinogenesis but does not affect the efficacy of retinoids in suppressing the neoplastic process Effects of 9cRA on cell proliferation and senescence in DLP of p27 deficient mice. Fig. 2A: Cell proliferation, as determined by Ki-67 antibody in DLP of 9-month-old p27+/+ mice. Note several Ki-67-positive cells (brawn-stained, arrows) in glandular structures which are covered by a single layer of epithelial cells. The slide is counterstained by hematoxylin × 200. 2B: Ki-67 positive cells (arrows) in anterior (large left) and DLP (two right glands) of 9-month-old p27-/- mice. Note the thick connective tissue surrounding glandular structures. The slide is counterstained by hematoxylin × 200. 2C: Ki-67 positive cells in PIN of MNU-treated mice. The number of Ki-67 positive cells is higher (arrow), as compared to those in Fig. 2B. The slide is counterstained by hematoxylin × 200. 2D: Treatment of p27-/- mice with 9cRA for 6 months reduced the number of Ki-67 positive cells in PIN (arrow). Note the inflammation associated cells in PINs' lumen. The slide is counterstained by hematoxylin × 200. 2E: Senescent cells (blue stained) determined by SA-β-Gal staining in glandular and ductal structures of DLP of 9-month-old p27+/- mice. Senescent cells are also detectable among myoepithelial and stroma cells (arrows). The slide is counterstained by nuclear fast red × 200. 2F: Treatment of animals with 9cRA increased senescent cells (blue stained) in DLP and AP of a p27+/- mice. The slide is counterstained by nuclear fast red × 200. 2G: 9cRA increased senescent cells in low grade PIN (arrows) as compared to non-PIN areas of a 10-month-old p27+/- animal. The slide is counterstained by nuclear fast red × 200. 2H: 9cRA also increased senescent cells in high grade PIN as shown in the right glandular structure. The slide is counterstained by nuclear fast red × 200.Back to article page