PTCL
In addition, we describe new and recurrent, albeit less frequent, genetic defects including mutations in FYN, ATM, B2M and CD58 implicating SRC signaling, impaired DNA damage response and escape from immune surveillance mechanisms in the pathogenesis of PTCL.
In addition, we describe new and recurrent, albeit less frequent, genetic defects including mutations in FYN, <span class="gene" id="24413734-5-110-113">ATM</span>, B2M and CD58 implicating SRC signaling, impaired DNA damage response and escape from immune surveillance mechanisms in the pathogenesis of <span class="disease" id="24413734-5-254-258">PTCL</span>.