B-Raf activation cooperates with PTEN loss to drive c-Myc expression in advanced prostate cancer. Mus musculus

Anaysis of the response to different therapeutic agents at the transcriptional level. The design of the experiment allows to determine how the comnination target therapy (Rapamycin + PD0325901) treatment shifted the transcriptome towards a less aggressive or even a wild type phenotype. It also allows exploring the molecular changes involved in the transition from a non metastatic to a metastatic prostate cancer mouse model. Overall design: Total RNA obtained form vehicle treated Nkx3.1CE2/+; Ptenf/f; BrafCA/+ (n=3), combinatorial Rapamycin and PD0325901 treated Nkx3.1CE2/+; Ptenf/f; BrafCA/+ (n=3) and vehicle treated intact Nkx3.1CE2/+; Ptenf/f (n = 6) prostate. Please contact Cory Abate-Shen ([e-mail]) and Jingqiang Wang ([e-mail]) for questions about the submission.

本数据集针对不同治疗药物在转录水平上的应答展开分析。本实验设计可明确联合靶向治疗（雷帕霉素（Rapamycin）+ PD0325901）如何将转录组向更低侵袭性甚至野生型表型转变，同时可探究非转移性前列腺癌小鼠模型向转移性前列腺癌小鼠模型转化过程中的分子变化。
实验整体设计如下：提取自经溶媒处理的Nkx3.1CE2/+; Ptenf/f; BrafCA/+小鼠前列腺组织总RNA（n=3）、经雷帕霉素联合PD0325901处理的Nkx3.1CE2/+; Ptenf/f; BrafCA/+小鼠前列腺组织总RNA（n=3），以及经溶媒处理的完整型Nkx3.1CE2/+; Ptenf/f小鼠前列腺组织总RNA（n=6）。
若对本数据集提交有任何疑问，请联系Cory Abate-Shen（[e-mail]）与Jingqiang Wang（[e-mail]）。