Mitochondrial Inhibitor Atovaquone Increases Tumor Oxygenation and Inhibits Hypoxic Gene Expression in Patients with Non-Small Cell Lung Cancer.

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Authors

Skwarski, M
McGowan, DR
Belcher, E
Di Chiara, F
Stavroulias, D
McCole, M
Derham, JL
Chu, K-Y
Teoh, E
Chauhan, J
O'Reilly, D
Harris, BHL
Macklin, PS
Bull, JA
Green, M
Rodriguez-Berriguete, G
Prevo, R
Folkes, LK
Campo, L
Ferencz, P
Croal, PL
Flight, H
Qi, C
Holmes, J
O'Connor, JPB
Gleeson, FV
McKenna, WG
Harris, AL
Bulte, D
Buffa, FM
Macpherson, RE
Higgins, GS

Document Type

Journal Article

Date

2021-05-01

Date Accepted

2021-02-11

Date Available

2021-03-31T14:45:55Z

Abstract

PURPOSE: Tumor hypoxia fuels an aggressive tumor phenotype and confers resistance to anticancer treatments. We conducted a clinical trial to determine whether the antimalarial drug atovaquone, a known mitochondrial inhibitor, reduces hypoxia in non-small cell lung cancer (NSCLC). PATIENTS AND METHODS: Patients with NSCLC scheduled for surgery were recruited sequentially into two cohorts: cohort 1 received oral atovaquone at the standard clinical dose of 750 mg twice daily, while cohort 2 did not. Primary imaging endpoint was change in tumor hypoxic volume (HV) measured by hypoxia PET-CT. Intercohort comparison of hypoxia gene expression signatures using RNA sequencing from resected tumors was performed. RESULTS: Thirty patients were evaluable for hypoxia PET-CT analysis, 15 per cohort. Median treatment duration was 12 days. Eleven (73.3%) atovaquone-treated patients had meaningful HV reduction, with median change -28% [95% confidence interval (CI), -58.2 to -4.4]. In contrast, median change in untreated patients was +15.5% (95% CI, -6.5 to 35.5). Linear regression estimated the expected mean HV was 55% (95% CI, 24%-74%) lower in cohort 1 compared with cohort 2 (P = 0.004), adjusting for cohort, tumor volume, and baseline HV. A key pharmacodynamics endpoint was reduction in hypoxia-regulated genes, which were significantly downregulated in atovaquone-treated tumors. Data from multiple additional measures of tumor hypoxia and perfusion are presented. No atovaquone-related adverse events were reported. CONCLUSIONS: This is the first clinical evidence that targeting tumor mitochondrial metabolism can reduce hypoxia and produce relevant antitumor effects at the mRNA level. Repurposing atovaquone for this purpose may improve treatment outcomes for NSCLC.

Citation

Clinical cancer research : an official journal of the American Association for Cancer Research, 2021

Source Title

Publisher

AMER ASSOC CANCER RESEARCH

ISSN

1078-0432

eISSN

1557-3265

Research Team

Quantitative Biomedical Imaging
Quantitative Biomedical Imaging

Notes