Self-enforcing feedback activation between BCL6 and pre-B cell receptor signaling defines a distinct subtype of acute lymphoblastic leukemia.

نویسندگان

  • Huimin Geng
  • Christian Hurtz
  • Kyle B Lenz
  • Zhengshan Chen
  • Dirk Baumjohann
  • Sarah Thompson
  • Natalya A Goloviznina
  • Wei-Yi Chen
  • Jianya Huan
  • Dorian LaTocha
  • Erica Ballabio
  • Gang Xiao
  • Jae-Woong Lee
  • Anne Deucher
  • Zhongxia Qi
  • Eugene Park
  • Chuanxin Huang
  • Rahul Nahar
  • Soo-Mi Kweon
  • Seyedmehdi Shojaee
  • Lai N Chan
  • Jingwei Yu
  • Steven M Kornblau
  • Janetta J Bijl
  • B Hilda Ye
  • K Mark Ansel
  • Elisabeth Paietta
  • Ari Melnick
  • Stephen P Hunger
  • Peter Kurre
  • Jeffrey W Tyner
  • Mignon L Loh
  • Robert G Roeder
  • Brian J Druker
  • Jan A Burger
  • Thomas A Milne
  • Bill H Chang
  • Markus Müschen
چکیده

Studying 830 pre-B ALL cases from four clinical trials, we found that human ALL can be divided into two fundamentally distinct subtypes based on pre-BCR function. While absent in the majority of ALL cases, tonic pre-BCR signaling was found in 112 cases (13.5%). In these cases, tonic pre-BCR signaling induced activation of BCL6, which in turn increased pre-BCR signaling output at the transcriptional level. Interestingly, inhibition of pre-BCR-related tyrosine kinases reduced constitutive BCL6 expression and selectively killed patient-derived pre-BCR(+) ALL cells. These findings identify a genetically and phenotypically distinct subset of human ALL that critically depends on tonic pre-BCR signaling. In vivo treatment studies suggested that pre-BCR tyrosine kinase inhibitors are useful for the treatment of patients with pre-BCR(+) ALL.

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عنوان ژورنال:
  • Cancer cell

دوره 27 3  شماره 

صفحات  -

تاریخ انتشار 2015