2018 June

Chromosomal rearrangements involving the gene that encodes the RET tyrosine kinase are known oncogenic drivers in 1% to 2% of patients with non–small cell lung cancer. These RET rearrangements occur with characteristic partners, most commonly KIF5B, but also CCDC6, NCOA, TRIM33, CUX1, KIAA1217, FRMD4A, and KIAA1468.

Myelofibrosis is a myeloproliferative neoplasm characterized by splenomegaly, progressive cytopenias, and transformation to acute myeloid leukemia. This review will describe mutations detected in myelofibrosis and discuss how to incorporate mutation information into risk stratification and therapeutic decision making for patients with myelofibrosis.

In an ideal world, researchers conduct preclinical studies that generate a targeted therapy, which eventually makes its way through early, middle, and late-stage trial development and FDA approval. That smooth transition does not happen often, but early results involving an agent that affects 2 endogenous inhibitors of p53 look promising.

Robert L. Ferris, MD, PhD, Physician Editor-In-Chief of the Journal of Targeted Therapies, discusses genomic rearrangements and the allelic fraction of that genomic rearrangement as a major component of an individual’s cancer.