ArticleAmerican journal of nuclear medicine and molecular imaging2014
Targeting histone deacetylase in lung cancer for early diagnosis: (18)F-FAHA PET/CT imaging of NNK-treated A/J mice model.
Article in American journal of nuclear medicine and molecular imaging, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- Introducing HDAC-Targeting Radiopharmaceuticals for Glioblastoma Imaging and Therapy.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Advances in the Development of PET Ligands Targeting Histone Deacetylases for the Assessment of Neurodegenerative Diseases.Molecules (Basel, Switzerland) · 2018Review
- Article
- PET/MR Imaging: New Frontier in Alzheimer's Disease and Other Dementias.Frontiers in molecular neuroscience · 2017Review
- Pharmacological Modulation of Lung Carcinogenesis in Smokers: Preclinical and Clinical Evidence.Trends in pharmacological sciences · 2016Review
- Novel Histone Deacetylase Class IIa Selective Substrate Radiotracers for PET Imaging of Epigenetic Regulation in the Brain.PloS one · 2015Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Elevated levels of histone deacetylases (HDACs) have been indicated in the development of some cancers. HDAC has been imaged using (18)F-FAHA and may serve as a marker to study epigenetics. We report evaluation of (18)F-FAHA as a probe in the early diagnosis of lung cancer using (18)F-FAHA PET/CT studies of A/J mice treated with NNK. (18)F-FAHA radiosynthesis was carried out in specific activity of ~2 Ci/μmol. A/J mice were divided into 2 groups: 1. Controls; 2. NNK treatment group with NNK (100 mg/kg, ip, weekly for 4 wks). Mice were injected 100-200 μCi i.v. (18)F-FAHA and then scanned in Inveon PET/CT under anesthesia using 2.0% isoflurane. Midbrain, cerebellum and brainstem uptake of (18)F-FAHA was displaced by the known HDAC inhibitor, suberanilohydroxamic acid (SAHA) with less than 10% activity remaining. CT revealed presence of lung nodules in 8 to 10-month old NNK mice while control mice were free of tumors. Little uptake of (18)F-FAHA was observed in the control mice lungs while significant (18)F-FAHA uptake occurred in the lungs of NNK-treated mice with tumor/nontumor >2.0. Ex vivo scans of the excised NNK and control mice lungs confirmed presence of extensive amounts of lung nodules seen by CT and confirmed by (18)F-FAHA in the NNK mice with tumor/nontumor >6.0. Our preliminary imaging studies with A/J mice lung cancer model suggest (18)F-FAHA PET may allow the study of epigenetic mechanisms involved in NNK-induced tumorigenesis in the lungs.
Indexed as
Identifiers
24982818PMC4074498W245217128What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.