Table 1.

The SP/NK-1R system in acute myeloid leukemia (AML) cells.

Leukemia cells express SP but not neurokinin A: related to leukemia and bone marrow fibrosis

SP increases the proliferation of bone marrow progenitors; neurokinin A exerts an opposite effect

AML cells express the NK-1R which mediates the antileukemic action of NK-1R antagonists

SP induces the proliferation of AML cells

Two NK-1R isoforms in AML cells: the truncated form is higher expressed than the full-length

AML cells: full-length expression is higher than in healthy cells, in which is not expressed

Compared with lymphocytes, AML cells overexpress the truncated splice variant

AML patients/cells: a high NK-1R expression is found in white blood cells

AML patients show an up-regulation of the NK-1R mRNA expression

SP, via the NK-1R, promotes a weak mitochondrial and intracellular Ca++ flux

All AML patients express the NK-1R. Healthy subjects: expression observed in 8% of population

AML cells express SP and NK-1R. Healthy subjects: no immunoreactivity