In This Issue
Cancer Discov September 1 2013 3 (9) 953-957; DOI:10.1158/2159-8290.CD-ITI13-09
Increased expression of mutant Nras, not loss of wild-type Nras, drives transformation in the hematopoietic lineage.
Treatment with DNA methyltransferase inhibitors overcomes chemoresistance in high-risk DLBCL via demethylation and reactivation of SMAD1.
An ARF876L mutation confers ligand-specific resistance and is found in the circulating tumor DNA of ARN-509–treated patients with progressive castration-resistant prostate cancer.
A recurring androgen receptor (AR) mutation identified in enzalutamide-resistant prostate cancer cells converts enzalutamide from an AR antagonist to an AR agonist.
The coamplified genes TLOC1 and SKIL cooperate to induce transformation via regulation of distinct tumor phenotypes.
Activation of EGFR signaling specifically limits the sensitivity of FGFR3-activated bladder cancer cells to FGFR inhibitors.
The cytostatic effects of α-difluoromethylornithine (DFMO) are attributable to reduced cellular thymidine levels caused by depletion of an essential cofactor of thymidine synthase.