Publications by authors named "Millie Fox"

Activated Cdc42-associated kinase (ACK), a non-receptor tyrosine kinase, is an effector for the small GTPase Cdc42. ACK is emerging as an important component of the cancer landscape and thus, a promising target for the treatment of many malignancies. ACK is also being increasingly recognized as a potentially influential player in the regulation of protein homoeostasis.

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Article Synopsis
  • - The PI3K-AKT pathway is often active in breast cancer, and inhibitors targeting this pathway, like capivasertib and AZD8186, are used in treatments, but the reasons for resistance to these therapies aren't well understood on a broad scale.
  • - CRISPR screenings identified key genes that lead to treatment resistance, revealing that reactivation of PI3K-AKT-mTOR signaling is the primary mechanism, while deletion of certain genes can either confer resistance or increase sensitivity to these drugs.
  • - Loss of Mcl-1 enhances the effectiveness of PI3K-AKT inhibitors by promoting faster cell death, and combining Mcl-1 inhibitors with PI3K-AKT inhibitors shows promise for overcoming resistance in various breast
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Activated Cdc42-associated kinase (ACK) is an oncogenic nonreceptor tyrosine kinase associated with poor prognosis in several human cancers. ACK promotes proliferation, in part by contributing to the activation of Akt, the major effector of class 1A phosphoinositide 3-kinases (PI3Ks), which transduce signals via membrane phosphoinositol lipids. We now show that ACK also interacts with other key components of class 1A PI3K signaling, the PI3K regulatory subunits.

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The phosphatidylinositol 3-kinase (PI3K) pathway is a critical regulator of many cellular processes including cell survival, growth, proliferation and motility. Not surprisingly therefore, the PI3K pathway is one of the most frequently mutated pathways in human cancers. In addition to their canonical role as part of the PI3K holoenzyme, the class IA PI3K regulatory subunits undertake critical functions independent of PI3K.

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Activated Cdc42-associated kinase or ACK, is a non-receptor tyrosine kinase and an effector protein for the small G protein Cdc42. A substantial body of evidence has accumulated in the past few years heavily implicating ACK as a driver of oncogenic processes. Concomitantly, more is also being revealed regarding the signalling pathways involving ACK and molecular details of its modes of action.

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