H
Helene Pelicano
Researcher at University of Texas MD Anderson Cancer Center
Publications - 54
Citations - 11035
Helene Pelicano is an academic researcher from University of Texas MD Anderson Cancer Center. The author has contributed to research in topics: Cancer cell & Mitochondrion. The author has an hindex of 34, co-authored 53 publications receiving 10005 citations. Previous affiliations of Helene Pelicano include University of Texas at Austin.
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Journal ArticleDOI
ROS stress in cancer cells and therapeutic implications.
TL;DR: ROS stress in cancer cells is reviewed, its underlying mechanisms and relationship with mitochondrial malfunction and alteration in drug sensitivity are reviewed, and new therapeutic strategies that take advantage of increased ROS in cancer Cells to enhance therapeutic activity and selectivity are suggested.
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Glycolysis inhibition for anticancer treatment
TL;DR: The increased dependence of cancer cells on glycolytic pathway for ATP generation provides a biochemical basis for the design of therapeutic strategies to preferentially kill cancer cells by pharmacological inhibition of Glycolysis.
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The circadian gene Period2 plays an important role in tumor suppression and DNA damage response in vivo.
TL;DR: It is reported here that mice deficient in the mPer2 gene are cancer prone and suggested that the m per2 gene functions in tumor suppression by regulating DNA damage-responsive pathways.
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Selective killing of oncogenically transformed cells through a ROS-mediated mechanism by β-phenylethyl isothiocyanate
Dunyaporn Trachootham,Yan Zhou,Hui Zhang,Hui Zhang,Y. Demizu,Zhao Chen,Zhao Chen,Helene Pelicano,Paul J. Chiao,Paul J. Chiao,Geetha Achanta,Ralph B. Arlinghaus,Ralph B. Arlinghaus,Jinsong Liu,Jinsong Liu,Peng Huang,Peng Huang +16 more
TL;DR: It is shown that abnormal increases in ROS can be exploited to selectively kill cancer cells using beta-phenylethyl isothiocyanate (PEITC), which exhibits therapeutic activity and prolongs animal survival in vivo.
Journal Article
Inhibition of glycolysis in cancer cells: a novel strategy to overcome drug resistance associated with mitochondrial respiratory defect and hypoxia.
Rui-Hua Xu,Helene Pelicano,Yan Zhou,Jennifer S. Carew,Li Feng,Kapil N. Bhalla,Michael J. Keating,Peng Huang +7 more
TL;DR: This study reports that inhibition of glycolysis severely depletes ATP in cancer cells, especially in clones of cancer cells with mitochondrial respiration defects, and leads to rapid dephosphorylation of the gly colysis-apoptosis integrating molecule BAD at Ser(112), relocalization of BAX to mitochondria, and massive cell death.