Publications by authors named "Asserewou Etekpo"
Background: The mechanistic target of rapamycin complex 1 (mTORC1) is a nutrient-sensing pathway and a key regulator of amino acid and glucose metabolism. Dysregulation of the mTOR pathways is implicated in the pathogenesis of metabolic syndrome, obesity, type 2 diabetes, and pancreatic cancer.
Objectives: We investigated the impact of inhibition of mTORC1/mTORC2 and synergism with metformin on pancreatic tumor growth and metabolomics.
Pancreatic cancer is the fourth cause of cancer deaths in the U.S. with most patients diagnosed at advanced stages followed by short survival.
View Article and Find Full Text PDFArticle Synopsis
- Imetelstat (GRN163L) is a powerful inhibitor of telomerase that has been shown to shorten telomeres and limit the life of certain pancreatic cancer cell lines.
- In studies with AsPC1 and L3.6pl pancreatic cancer cells, GRN163L caused initial telomere shortening, with AsPC1 cells eventually entering a crisis phase and dying off, while L3.6pl cells developed resistance after a temporary crisis.
- Combining GRN163L with 3-aminobenzamide (3AB), which inhibits a related process, further shortened telomeres in resistant L3.6pl cells and suggests a potential combined therapeutic strategy for pancreatic cancer.
Pancreatic Cancer (PC) is a devastating lethal disease. Therefore, there is an urgent need to develop new intervention strategies. The mammalian Target of Rapamycin (mTOR) is a conserved kinase and master regulator of metabolism and cell growth.
View Article and Find Full Text PDFRadiation therapy is a staple treatment for pancreatic cancer. However, owing to the intrinsic radioresistance of pancreatic cancer cells, radiation therapy often fails to increase survival of pancreatic cancer patients. Radiation impedes cancer cells by inducing DNA damage, which can activate cell cycle checkpoints.
View Article and Find Full Text PDF