*Acute leukemia*

Overexpression of the human gene BAALC (brain and acute leukemia, cytoplasmic), was shown to be associated with inferior outcome and chemotherapy resistance in adult patients with cytogenetically-normal acute myeloid leukemia (CN-AML), T cell-acute lymphoblastic leukemia (T-ALL) and B-precursor acute lymphoblastic leukemia (B-ALL)[123,124,125,126,127]. IGFBP7 was strongly correlated with BAALC-expression, implicating IGFBP7 in acute leukemia [128]. Aberrent expression of IGFBP7 in adult leukemia was correlated with chemotherapy resistance and inferior survival. Addition of IGFBP7 to leukemic cell lines inhibited cell growth without induction of apoptosis or senescence, suggesting a role of IGFBP7 in contributing to drug resistance through reduced sensitivity to cytostatic drugs [128]. Aberrently increased levels of IGFBP7 were found in CSF from children with acute lymphoblastic leukemia, implicating IGFBP7 with a more aggressive subtype of ALL [129]. IGFBP7 was also aberrantly overexpressed in the majority of AML at diagnosis and upon relapse, but not at remission stage [130]. Thus, IGFBP7 was shown to play a positive contributing role in the interaction between leukemia cells and the microenvironment, which may promote the leukemic cells' adhesion, invasion, and migration.

While the data observed in studies of leukemia and glioblastoma portray IGFBP7 in a negative role with respect to cancer, the vast majority of data from studies of solid tumors are in disagreement with these conclusions. It is possible that cell signaling pathways that result in senescence or apoptosis due to IGFBP7 are not present or functional in hematopoietic or glioma cells.
