1. UVA Induces Lesions Resembling Seborrheic Keratoses in Mice with Keratinocyte- Specific PTEN Downregulation 
Mei Ming, Christopher R. Shea, Li Feng, Keyoumars Soltani, Yu-Ying He 
Journal of Investigative Dermatology 
Volume 131, Issue 7, Pages (July 2011)
DOI: /jid
Copyright © 2011 The Society for Investigative Dermatology, Inc Terms and Conditions

2. Figure 1
PTEN (phosphatase and tensin homolog deleted on chromosome 10) hemizygosity is a predisposing factor for skin tumorigenesis following UVA irradiation. (a) Immunoblot analysis of PTEN protein levels in the epidermis from K14Cre;Pten+/+ (+/+) and K14Cre;Ptenfl/+ (+/-) mice. (b) Percentage of tumor-free mice (n=15). (c) Incidence of seborrheic keratosis (SK) and squamous cell carcinoma (SCC). (d) A mouse with an SK (indicated by a red arrow) developing in its skin. (e–h) Hematoxylin and eosin staining of the mouse specimens with SK and SCC. (e) SK at × 2.5 magnification. (f) SK at original magnification × 10. (g) SCC at original magnification × 10. (h) SCC at original magnification × 10, with a smaller field of view. (e) Scale bar=400μm and (f–h) scale bar=100μm. The green arrow in (h) indicates a multinucleated cell.
Journal of Investigative Dermatology  , DOI: ( /jid )
Copyright © 2011 The Society for Investigative Dermatology, Inc Terms and Conditions

3. Figure 2
The PTEN (phosphatase and tensin homolog deleted on chromosome 10)/AKT (a serine–threonine kinase) pathway is involved in UVA-induced tumorigenesis in Pten+/- mice. (a–e) Immunohistochemical analysis of PTEN in nontumor and tumor samples using an anti-PTEN antibody. Scale bar=50μm. (a, b) Sham-irradiated normal epidermis from (a) Pten+/+ and (b) Pten+/- mouse. (c) UVA-irradiated nontumor epidermis, (d) seborrheic keratosis (SK), and (e) squamous cell carcinoma (SCC) from Pten+/- mouse. (f) Immunoblot analysis of PTEN, p-AKT (serine 473), AKT, and GAPDH (equal loading control) in +/+, +/-, SK, and SCC. (g) Quantification of PTEN protein levels in (f). (h) Quantification of the ratio of p-AKT/AKT in (f). N in (g, h), normal Pten+/- skin. (i) Real-time RT-PCR analysis of the GLTSCR2 mRNA levels in +/+, +/-, and SK (n=3). (j) Immunoblot analysis of p-AKT, AKT, p-ERK (extracellular signal-regulated kinase), ERK, PTEN, and β-actin (equal loading control) in individual +/+ and +/- mouse epidermis (n=3) at 6 and 24h post-UVA (15Jcm−2). (k) Cell growth analysis of neonatal primary Pten+/- keratinocytes infected with empty vector (EV) alone or wild-type PTEN adenovirus (Ad-PTEN) at a multiplicity of infection of 50 at different times post sham or UVA irradiation (5Jcm−2) (n=3). The right panel shows immunoblot analysis of PTEN and β-actin. Error bars show standard error (SE). (g, h) *P<0.05, significant difference between comparison groups. NS, not statistically significant, P>0.05. (k) *P<0.05, significant difference between sham-irradiated +/-/EV and +/-/Ad-PTEN groups. +/+, K14Cre;Pten+/+; +/-, K14Cre;Ptenfl/+; EP, epidermis; D, dermis; HF, hair follicle; S, stroma; T, tumor.
Journal of Investigative Dermatology  , DOI: ( /jid )
Copyright © 2011 The Society for Investigative Dermatology, Inc Terms and Conditions