In This Issue
Cancer Discov September 1 2017 7 (9) 920-923; DOI:10.1158/2159-8290.CD-ITI7-9
Parallel development of the first-generation TRK TKI larotrectinib with the next-generation TKI LOXO-195 allowed for rapid use of LOXO-195 to treat patients with acquired larotrectinib resistance.
Sequencing of an African-American prostate cancer cohort identified ERF as a tumor suppressor in prostate cancer and shows that increasing ethnic diversity enhances the discovery of potential cancer drivers.
In patients with high-grade ovarian carcinoma treated with the PARP inhibitor rucaparib, secondary reversion mutations in HR genes restore the open reading frame and HR activity to confer resistance.
Multiclonal BRCA2 reversion mutations were detected in circulating cell-free DNA from two patients with metastatic prostate cancer after PARP inhibitor treatment, suggesting a mechanism of resistance.
Sequencing cfDNA from patients with olaparib-treated prostate cancer reveals that reduced cfDNA is a biomarker of response and can harbor resistance mutations that may guide treatment.
The BTK inhibitor ibrutinib has activity in patients with relapsed or refractory B-cell lymphomas of the CNS, and dual treatment with PI3K/mTOR inhibitors may enhance ibrutinib efficacy in patients with CD79B-mutant tumors.
The CDH6-targeting antibody–drug conjugate HKT288 causes regression of patient-derived xenografts of CDH6-overexpressing ovarian and renal cancers.