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1.
Figure 5

Figure 5. From: Distinct mechanisms of TGF-?1-mediated epithelial-to-mesenchymal transition and metastasis during skin carcinogenesis.

Immunohistochemistry for pSmad2. Scale bar: 40 μm for all panels.

Gangwen Han, et al. J Clin Invest. 2005 July 1;115(7):1714-1723.
2.
Figure 3

Figure 3. From: Distinct mechanisms of TGF-?1-mediated epithelial-to-mesenchymal transition and metastasis during skin carcinogenesis.

TGF-β1 expression levels in mouse tumors with different genotypes. (A) Results of RT-PCR for TGF-β1 transgene expression in TGF-β1– and TGF-β1/ΔβRII–transgenic SCCs. (B) Results of TGF-β1–specific ELISA. Each group contained 4–6 samples.

Gangwen Han, et al. J Clin Invest. 2005 July 1;115(7):1714-1723.
3.
Figure 9

Figure 9. From: Distinct mechanisms of TGF-?1-mediated epithelial-to-mesenchymal transition and metastasis during skin carcinogenesis.

Schematic depicting the potential mechanisms of uncoupling TGF-β1–mediated EMT and tumor invasion by ΔβRII expression. The dotted lines indicate potential mechanisms of the cooperative effects between TGF-β1 overexpression and ΔβRII expression on tumor invasion and metastasis.

Gangwen Han, et al. J Clin Invest. 2005 July 1;115(7):1714-1723.
4.
Figure 1

Figure 1. From: Distinct mechanisms of TGF-?1-mediated epithelial-to-mesenchymal transition and metastasis during skin carcinogenesis.

Immunostaining for TGF-β1, TGF-βRII, and pSmad2 in human skin cancer samples revealed a patchy increase in TGF-β1 and decrease in TGF-βRII staining in AK and CIS, and the same alterations were uniform in SCC. pSmad2-positive cells were detected in AK and CIS. Scale bar: 40 μm for all panels.

Gangwen Han, et al. J Clin Invest. 2005 July 1;115(7):1714-1723.
5.
Figure 4

Figure 4. From: Distinct mechanisms of TGF-?1-mediated epithelial-to-mesenchymal transition and metastasis during skin carcinogenesis.

BrdU labeling in skin and papillomas 21 weeks after DMBA initiation and 1 week with (TGF-β1) or without (Control) TGF-β1 transgene induction. (A) Control skin adjacent to a papilloma. (B) TGF-β1–transgenic skin adjacent to a papilloma. (C) Control papilloma. (D) TGF-β1–transgenic papilloma. Scale bar in A: 20 μm for A and B; 40 μm for C and D.

Gangwen Han, et al. J Clin Invest. 2005 July 1;115(7):1714-1723.
6.
Figure 6

Figure 6. From: Distinct mechanisms of TGF-?1-mediated epithelial-to-mesenchymal transition and metastasis during skin carcinogenesis.

Immunohistochemical staining for E-cadherin and β- and γ-catenins in primary SCCs from ΔβRII-, TGF-β1–, and TGF-β1/ΔβRII–transgenic mice 25 weeks after DMBA initiation and in a lymph node metastasis from TGF-β1/ΔβRII–transgenic SCCs. Note that all ΔβRII- and TGF-β1/ΔβRII–transgenic SCCs and TGF-β1/ΔβRII metastatic cells demonstrated staining for membrane-associated E-cadherin and β- and γ-catenins. Lung metastatic cells from TGF-β1/ΔβRII–transgenic SCCs revealed a similar staining pattern (data not shown). However, these molecules appeared in the cytoplasm of cells in TGF-β1–transgenic SCCs. Scale bar: 40 μm for all panels.

Gangwen Han, et al. J Clin Invest. 2005 July 1;115(7):1714-1723.
7.
Figure 2

Figure 2. From: Distinct mechanisms of TGF-?1-mediated epithelial-to-mesenchymal transition and metastasis during skin carcinogenesis.

Skin tumor formation and tumor types in transgenic mice. (A) Schematic of the skin chemical carcinogenesis and TGF-β1 transgene induction protocol. (B) Kinetics of tumor formation. Each point represents the average number of tumors per mouse. (C) H&E staining of TGF-β1/ΔβRII–transgenic SCC. (D) TGF-β1–transgenic SPCC. (E) Metastatic lesion in lymph node showing SCC cells surrounded by lymphocytes. (F) Lung metastasis that originated from TGF-β1/ΔβRII–transgenic SCCs. The dotted line delineates lung tissue adjacent to the metastatic lesion. Scale bar in C: 40 μm for CF.

Gangwen Han, et al. J Clin Invest. 2005 July 1;115(7):1714-1723.
8.
Figure 8

Figure 8. From: Distinct mechanisms of TGF-?1-mediated epithelial-to-mesenchymal transition and metastasis during skin carcinogenesis.

Analysis of Notch, Rho/Rac, and MAPK signaling components in SCC samples with different genotypes. Data were averaged from 5 SCCs from each group. One control SCC with the lowest expression level of individual molecules was assigned the value of 1 arbitrary unit as determined by quantitative RT-PCR in A and B. *P < 0.05 compared with control SCCs; P < 0.05 compared with TGF-β1–transgenic SCCs. (C) Western blot analysis of MAPK components. A pair of samples from each group is presented. Four to six samples in each group were examined and exhibited patterns similar to the representative samples shown here. p-Erk1, phosphorylated Erk1.

Gangwen Han, et al. J Clin Invest. 2005 July 1;115(7):1714-1723.
9.
Figure 7

Figure 7. From: Distinct mechanisms of TGF-?1-mediated epithelial-to-mesenchymal transition and metastasis during skin carcinogenesis.

Angiogenesis and proteinase expression. (A) CD31 immunofluorescence. CD31 (green) highlights vessels. K14 (red) highlights the epithelial portion of tumors. Scale bar: 75 μm for all panels. (B) Percentage of the stromal area covered by vessels in TGF-β1/ΔβRII–, TGF-β1–, and ΔβRII-transgenic and control SCCs. The numbers in parentheses represents the number of tumors examined from each group. *P < 0.05. (C and D) Expression levels of VEGFR1 and VEGF (C) and MMP-2 and MMP-9 (D) detected by RPA in SCCs from TGF-β1–, ΔβRII-, and TGF-β1/ΔβRII–transgenic and control mice 25 weeks after DMBA initiation. L32 (C) or cyclophilin (Cyc.; D) was used to normalize the amount of RNA loaded in each lane.

Gangwen Han, et al. J Clin Invest. 2005 July 1;115(7):1714-1723.

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