Faculty Collaboration Database

Potential Molecular Targeted Therapeutics: Role of PI3-K/Akt/mTOR Inhibition in Cancer. Anticancer Agents Med Chem 2016;16(1):29-37

Date

07/17/2015

Pubmed ID

26179270

DOI

10.2174/1871520615666150716104408

Scopus ID

2-s2.0-84947937697 (requires institutional sign-in at Scopus site)   18 Citations

Abstract

Primary liver cancer is one of the most commonly occurring cancers worldwide. Hepatocellular carcinoma (HCC) represents the majority of primary liver cancer and is the 3rd most common cause of cancer-related deaths globally. Survival rates of patients with HCC are dependent upon early detection as concomitant liver dysfunction and advanced disease limits traditional therapeutic options such as resection or ablation. Unfortunately, at the time of diagnosis, most patients are not eligible for curative surgery and have a five-year relative survival rate less than 20%, leading to systemic therapy as the only option. Currently, sorafenib is the only approved systemic therapy; however, it has a limited survival advantage and low efficacy prompting alternative strategies. The inception of sorafenib for HCC systemic therapy and the understanding involved of cancer therapy have led to an enhanced focus of the PI3-k/Akt/mTOR pathway as a potential area of targeting including pan and isoform-specific PI3-K inhibitors, Akt blockade, and mTOR suppression. The multitude, expanding roles, and varying clinical trials of these inhibitors have led to an increase in knowledge and availability for current and future studies. In this review, we provide a review of the literature with the aim to focus on potential targets for HCC therapies as well as an in depth focus on Akt inhibition.

Author List

Sokolowski KM, Koprowski S, Kunnimalaiyaan S, Balamurugan M, Gamblin TC, Kunnimalaiyaan M

MESH terms used to index this publication - Major topics in bold

Antineoplastic Agents
Carcinoma, Hepatocellular
Humans
Liver Neoplasms
Molecular Targeted Therapy
Phosphatidylinositol 3-Kinases
Protein Kinase Inhibitors
Proto-Oncogene Proteins c-akt
TOR Serine-Threonine Kinases