In this issue of Blood, Sasca et al present intriguing data that the cell surface marker NCAM1 (neural cell adhesion molecule 1, also known as CD56), which is expressed in approximately 15% to 20% of acute myeloid leukemia (AML) cases, promotes chemotherapy resistance and leukemia stem cell (LSC, also referred to as a leukemia initiating cell) function, in part through activation of the MAPK signaling cascade (see figure). Notably, they provide data that pharmacologic inhibitors of the MAPK pathway synergistically cooperate with cytarabine (Ara-C) in eliminating NCAM1-expressing AML cells, suggesting that NCAM1 may represent both a potential targetable vulnerability and a biomarker for guiding treatment decisions in AML.

Original languageEnglish
Pages (from-to)2247-2248
Number of pages2
Issue number21
StatePublished - May 23 2019


Dive into the research topics of 'NCAM1 supports therapy resistance and LSC function in AML'. Together they form a unique fingerprint.

Cite this