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PTEN  is a novel tumour suppressor gene that encodes a dual-specificity phosphatase with homology to adhesion molecules tensin and auxillin. It recently has been suggested that  PTEN  dephosphorylates phosphatidylinositol 3,4,5-trisphosphate [PtdIns(3,4,5)P 3 ], which mediates growth factor-induced activation of intracellular signalling, in particular through the serine-threonine kinase Akt, a known cell survival-promoting factor.  PTEN  has been mapped to 10q23.3, a region disrupted in several human tumours including haematological malignancies. We have analysed  PTEN  in a series of primary acute leukaemias and non-Hodgkin's lymphomas (NHLs) as well as in cell lines. We have also examined whether a correlation could be found between PTEN and Akt levels in these samples. We show here that the majority of cell lines studied carries  PTEN  abnormalities. At the structural level, we found mutations and hemizygous deletions in 40% of these cell lines, while a smaller number of primary haematological malignancies, in particular NHLs, carries  PTEN  mutations. Moreover, one-third of the cell lines had low PTENtranscript levels, and 60% of these samples had low or absent PTEN protein, which could not be attributed to gene silencing by hypermethylation. In addition, we found that PTEN and phosphorylated Akt levels are inversely correlated in the large majority of the examined samples. These findings suggest that  PTEN  plays a role in the pathogenesis of haematological malignancies and that it might be inactivated through a wider range of mechanisms than initially considered. The finding that PTEN levels inversely correlate with phosphorylated Akt supports the hypothesis that PTEN regulates PtdIns(3,4,5)P 3  and suggests a role for PTEN in apoptosis.

PTEN Is Inversely Correlated With the Cell Survival Factor Akt/PKB and Is Inactivated Via Multiple Mechanisms in Haematological Malignancies