Format

Send to

Choose Destination
Cancer Cell. 2014 Dec 8;26(6):788-795. doi: 10.1016/j.ccell.2014.10.001.

Is reliance on mitochondrial respiration a "chink in the armor" of therapy-resistant cancer?

Author information

1
Tumor Initiation & Maintenance Program, Degenerative Disease Program, Sanford-Burnham Medical Research Institute, La Jolla, CA 92037, USA. Electronic address: dwolf@sanfordburnham.org.

Abstract

A series of recent reports has suggested PGC1α-driven upregulation of mitochondrial oxidative phosphorylation as a selective vulnerability of drug-resistant cancers. Accordingly, chemical inhibitors of respiration led to selective eradication of such cancer cells due to their preferential sensitivity to mitochondrial production of reactive oxygen species. These insights create a timely opportunity for a biomarker guided application of already existing and newly emerging mitochondrial inhibitors in recurrent drug-resistant cancer, including lymphomas, melanomas, and other malignant diseases marked by increased mitochondrial respiration.

PMID:
25490445
PMCID:
PMC4761590
DOI:
10.1016/j.ccell.2014.10.001
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Elsevier Science Icon for PubMed Central
Loading ...
Support Center