Jeffrey L. Kutok

TL;DR: The acquisition of a T674I resistance mutation at the time of relapse demonstrates that FIP1L1-PDGFRalpha is the target of imatinib, and data indicate that the deletion of genetic material may result in gain-of-function fusion proteins.

TL;DR: The genomic region encoding the miR-17-92 microRNA (miRNA) cluster is often amplified in lymphoma and other cancers, and cancer cells carrying this amplification have higher expression of miRNA in this cluster, and this mechanism probably contributed to the lymphoproliferative disease and autoimmunity ofmiR- 17-92-transgenic mice and contributes to lymphoma development in patients with amplifications of this coding region.

TL;DR: Evidence is provided that the survival of BCR deficient mature B cells can be rescued by a single signaling pathway downstream of the BCR, namely PI3K signaling, with the FOXO1 transcription factor playing a central role.

TL;DR: It is demonstrated that FLT3-ITD mutant proteins are sufficient to induce a myeloproliferative disorder, but are insufficient to recapitulate the AML phenotype observed in humans.

TL;DR: The effects of respiratory hyperoxia are entirely T cell– and natural killer cell–dependent, thereby justifying the testing of supplemental oxygen as an immunological coadjuvant to combine with existing immunotherapies for cancer.