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Title:
Beyond PTEN mutations: the PI3K pathway as an integrator of multiple inputs during tumorigenesis | Nature Reviews Cancer
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Nature Reviews Cancer - Mutation or deletion of PTEN is found in many cancers — however, in others, deregulation of the PI3K–PTEN network occurs in the absence of PTEN mutation. This...
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- Does the ribosome translate cancer?
- How does the PI3K pathway integrate signals from numerous sources, and how can this information be used in the rational design of cancer therapies?
- Selecting patients for epidermal growth factor receptor inhibitor treatment: a FISH story or a tale of mutations?
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Mutation or deletion of PTEN is found in many cancers â however, in others, deregulation of the PI3KâPTEN network occurs in the absence of PTEN mutation. This review examines whether 'crosstalk' with other tumorigenic signalling pathways contributes to PI3KâPTEN deregulation. The tumour-suppressor phosphatase with tensin homology (PTEN) is the most important negative regulator of the cell-survival signalling pathway initiated by phosphatidylinositol 3-kinase (PI3K). Although PTEN is mutated or deleted in many tumours, deregulation of the PI3KâPTEN network also occurs through other mechanisms. Crosstalk between the PI3K pathways and other tumorigenic signalling pathways, such as those that involve Ras, p53, TOR (target of rapamycin) or DJ1, can contribute to this deregulation. How does the PI3K pathway integrate signals from numerous sources, and how can this information be used in the rational design of cancer therapies?
datePublished:2006-02-02T00:00:00Z
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Mutation or deletion of PTEN is found in many cancers â however, in others, deregulation of the PI3KâPTEN network occurs in the absence of PTEN mutation. This review examines whether 'crosstalk' with other tumorigenic signalling pathways contributes to PI3KâPTEN deregulation. The tumour-suppressor phosphatase with tensin homology (PTEN) is the most important negative regulator of the cell-survival signalling pathway initiated by phosphatidylinositol 3-kinase (PI3K). Although PTEN is mutated or deleted in many tumours, deregulation of the PI3KâPTEN network also occurs through other mechanisms. Crosstalk between the PI3K pathways and other tumorigenic signalling pathways, such as those that involve Ras, p53, TOR (target of rapamycin) or DJ1, can contribute to this deregulation. How does the PI3K pathway integrate signals from numerous sources, and how can this information be used in the rational design of cancer therapies?
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