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Space-filling model of the PTEN protein (blue) complexed with tartaric acid (brown) [5] Phosphatase and tensin homolog (PTEN) is a phosphatase in humans and is encoded by the PTEN gene. [6] Mutations of this gene are a step in the development of many cancers, specifically
PTEN inhibitors, such as bisperoxovanadium, [35] can enhance the PI3K/AKT pathway to promote cell migration, [36] survival [37] and proliferation. [7] While there are some concerns over possible cell cycle dysregulation and tumorigenesis, temporary and moderate PTEN inhibition may confer neuroprotection against traumatic brain injury [ 38 ] and ...
The 5-year event free survival, disease-free survival, and overall survival rate in the phase 3 clinical study in DS-AMKL were 79, 89, 84 percent, respectively. [13] Other studies that use a treatment regimen similar to that used in the phase 3 clinical study report overall survival rates of ~80% [7] and long-term survivals of 74-91%. [9]
The 5-year survival rate for children with leukemia is 83.6% in the USA. This means that 83.6% of children diagnosed with leukemia live for 5 years or more after their diagnosis. This is greatly improved from a 5-year survival rate of 36.5% in 1975. The improvement is largely attributed to advances in therapy, particularly therapy for ALL.
Phosphatase and tensin homolog (PTEN) antagonises PI3K by converting PI(3,4,5)P 3 into PI(4,5)P 2. Loss of PTEN function leads to over-activation of Akt and is common in cancer cells (PTEN is a tumour suppressor). SH2-containing Inositol Phosphatase (SHIP) also dephosphorylates PI(3,4,5)P 3, at the 5' position of the inositol ring. [22]
Under this model, cancer arises as the result of a single, isolated event, rather than the slow accumulation of multiple mutations. [4] The exact function of some tumor suppressor genes is not currently known (e.g. MEN1, WT1), [5] but based on these genes following the Knudson "two-hit" hypothesis, they are strongly presumed to be suppressor genes.
Some examples of genetic mutations and their prognoses are: mutations in the IGHV region are associated with a median overall survival (OS) of more than 20–25 years, while no mutations in this region is associated with a median OS of 8–10 years; deletion of chromosome 13q is associated with a median OS of 17 years; and trisomy of chromosome ...
The mechanism of BAL is related to several mutations. The most common abnormalities are t(9;22) and MLL gene rearrangement at 11q23. T(9;22) affect the ABL gene at 9q34 and BCR at 22q11. The hybrid gene product ABL/BCR is an oncogene which could lead several types of leukemia including BAL. ABL/BCR could active several molecular pathways: