AKT1 belongs to a family of serine-threonine protein
kinases which also includes AKT2 and AKT3.
AKT1 plays a key role in multiple cell processes, including growth, proliferation, survival,
and angiogenesis. AKT1 acts as a downstream mediator of phosphatidylinositol 3-kinase (PI3K; Figure
Figure 1. Schematic of the MAPK and PI3K
pathways. Growth factor binding to receptor
tyrosine kinase results in activation of
the MAPK signaling pathway
(RAS-RAF-MEK-ERK) and the PI3K pathway (PI3K-AKT-mTOR). The letter "K" within the schema
denotes the tyrosine kinase domain.
Suggested Citation: Lovly, C., L. Horn, W. Pao. 2015. AKT1. My Cancer
(Updated December 7).
Last Updated: December 7, 2015
AKT1 in Colorectal Cancer
Somatic mutations in AKT1 have been found
in <1–6% of all colorectal cancer (Carpten et al.
2007; COSMIC; Fumagalli et al.
2008; Kim et
al. 2008). In colorectal cancer, the only AKT1 mutation observed up to this time is
the E17K mutation, which has also been observed in other types of cancer. This mutation in
the Pleckstrin homology domain alters the ligand binding site and leads to constitutive
kinase activity. Preclinical data have shown that the presence of this activating
mutation results in cellular transformation in vitro and in vivo (Carpten et al.
2007). Specific clinical characteristics of colorectal cancer patients harboring
AKT1 mutations have yet to be described. AKT1 mutations and PTEN mutations appear to be
mutually exclusive. Likewise, AKT1 mutations and PI3K mutations appear to be mutually
Suggested Citation: Chan, E. 2015. AKT1 in Colorectal Cancer. My Cancer
(Updated June 18).
Last Updated: June 18, 2015
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