In This Issue
Cancer Discov March 1 2016 6 (3) 217-219; DOI:10.1158/2159-8290.CD-ITI6-3
B cells are recruited to the pancreas during PDAC initiation and support tumor growth through IL35-mediated signaling.
HIF1α prevents PDAC initiation by suppressing protumorigenic B cell recruitment to the pancreas, which is required for PDAC progression.
Inhibition of PI3Kγ/BTK signaling between B cells and FcRγ-positive macrophages reactivates T cell–dependent immune responses and suppresses PDAC tumor growth in mice.
Next-generation sequencing of circulating tumor DNA can be used to monitor response to therapy and identify potential treatment strategies, which can be validated in patient-derived or circulating tumor cell–derived xenografts.
Previously unidentified BRAF in-frame deletions promote the formation of homodimers, which activate MAPK signaling and are sensitive to LY3009120.
Mutant KRASG12C exhibits a dynamic nucleotide state that is responsive to upstream signaling, and its activation can be selectively and potently suppressed by small-molecule binding to the GDP-bound state.