aCGH from mouse gPAK testicular teratocarcinomas

Testicular germ cell tumors are among the most responsive solid cancers to conventional chemotherapy. To elucidate the underlying mechanisms, we developed a mouse testicular germ cell tumor model in which germ cell-specific oncogenic Kras activation and tumor suppressor Pten inactivation was driven by CRE-mediated recombination. The resulting mice rapidly developed malignant, metastatic testicular cancers composed of both teratoma and embryonal carcinoma, the latter of which exhibited stem cell characteristics, including expression of the pluripotency factor OCT4. As part of our analysis of mouse gPAK testicular tumors, as well as comparison to benign 129-Dnd1Ter/Ter testicular teratomas, we used NimbleGen Mouse CGH 3x720k Whole-Genome Tiling Arrays to assess copy number variations in this novel genetically engineered mouse model of malignant, metastatic testicular cancer. DNA from six mouse gPAK testicular teratocarcinomas and six mouse 129-Dnd1Ter/Ter testicular teratomas was analyzed relative to DNA from normal mouse spleen.