The Phosphatidylinositol 3-kinase/Akt Signaling Pathway in Neuroendocrine Tumors
- PMID: 27990410
- PMCID: PMC5157925
The Phosphatidylinositol 3-kinase/Akt Signaling Pathway in Neuroendocrine Tumors
Abstract
The phosphatidylinositol 3-kinase (PI3K)-Akt pathway is often aberrantly activated in neuroendocrine-derived cancers. Therefore, selectively targeting this pathway using small-molecule inhibitors may reduce neuroendocrine tumor burden, potentiate adjunct therapies, and achieve symptomatic control for patients with hormonally active and inoperable disease. Here, we discuss the role of the PI3K-Akt pathway in the malignant transformation of neuroendocrine tumors, specifically carcinoids and small cell lung cancers. The collective findings presented in this review propose that selective targeting of the PI3K-Akt pathway may mitigate neuroendocrine tumor progression, thus offering a viable therapeutic approach for managing systemic disease.
Keywords: ASCL1; Akt; Carcinoids; Chromogranin A; NE Tumors; Notch pathway; Raf-1 pathway; SCLC.
References
-
- Sippel R, Carpenter J, Kunnimalaiyaan M, Chen H. The role of human achaete-scute homolog-1 in medullary thyroid cancer cells. Surgery. 2003;134:866–871. discussion 871-863. [PubMed: 14668716] - PubMed
-
- Van Gompel J, Sippel R, Warner T, Chen H. Gastrointestinal carcinoid tumors: factors that predict outcome. World J Surg. 2004;28:387–392. [PubMed: 14994141] - PubMed
-
- Sippel R, Carpenter J, Kunnimalaiyaan M, Lagerholm S, Chen H. Raf-1 activation suppresses neuroendocrine marker and hormone levels in human gastrointestinal carcinoid cells. Am J Physiol Gastrointest Liver Physiol. 2003;285:G245–G254. [PubMed: 12851216] - PubMed
-
- Kunnimalaiyaan M, Ndiaye M, Chen H. Apoptosis-mediated medullary thyroid cancer growth suppression by the PI3K inhibitor LY294002. Surgery. 2006;140:1009–1014. discussion 1014-1005. [PubMed: 17188151] - PubMed
-
- Lal A, Chen H. Treatment of advanced carcinoid tumors. Curr Opin Oncol. 2006;18:9–15. [PubMed: 16357558] - PubMed
Publication types
Grants and funding
LinkOut - more resources
Full Text Sources
Research Materials
Miscellaneous