• What is AKT1?
  • AKT1 in Colorectal Cancer
  • Clinical Trials


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 1).


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.

Related Pathways


Contributors: Christine M. Lovly, M.D., Ph.D., Leora Horn, M.D., M.Sc., William Pao, M.D., Ph.D. (through April 2014)

Suggested Citation: Lovly, C., L. Horn, W. Pao. 2015. AKT1. My Cancer Genome https://www.padiracinnovation.org/content/disease/colorectal-cancer/akt1/?tab=0 (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 exclusive.​

Contributors: Emily Chan, M.D., Ph.D.

Suggested Citation: Chan, E. 2015. AKT1 in Colorectal Cancer. My Cancer Genome https://www.padiracinnovation.org/content/disease/colorectal-cancer/akt1/ (Updated June 18).

Last Updated: June 18, 2015

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