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. 2007 Mar 19;104(12):5103–5108. doi: 10.1073/pnas.0701158104

Fig. 4.

Fig. 4.

Cooperative interaction between Shh and activated K-Ras. (A) Proliferation curves for Ink4a/Arf, Trp53 null PDECs expressing GFP, Shh, K-Ras, or both Shh and K-Ras. (B) Cystic ductal lesion induced after orthotopic transplantation of K-Ras- and Shh-expressing Trp53 null PDECs. Note abundant reactive stroma. (C) H&E-stained tissue section illustrating the histology of tumors induced after orthotopic transplantation of Ink4a/Arf, Trp53 null PDECs expressing both Shh and activated K-Ras. Tumors are mostly undifferentiated (D), with regions of ductal differentiation (box in C, and E). (F) RT-PCR analysis of Shh pathway components in tumors induced after orthotopic transplantation of RCAS-k-ras-infected PDECs (R1–R6) or RCAS-Shh- and RCAS-k-ras-infected PDECs (RS1–RS7). Tumors R1–R3 and RS1–RS3 lack Ink4a/Arf. Tumors R4–R6 and RS4–RS7 lack Trp53 and Ink4a/Arf. β-actin serves as a control.