ArticleEuropean journal of nuclear medicine and molecular imaging2011
Early assessment of tumor response to JAC106, an anti-tubulin agent, by 3'-deoxy-3'-[¹⁸F]fluorothymidine in preclinical tumor models.
Article in European journal of nuclear medicine and molecular imaging, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 10 citations in OpenAlex.
- FLT-PET for early response evaluation of colorectal cancer patients with liver metastases: a prospective study.EJNMMI research · 2017Article
- Monitoring of anti-cancer treatment with (18)F-FDG and (18)F-FLT PET: a comprehensive review of pre-clinical studies.American journal of nuclear medicine and molecular imaging · 2015Review
- [18F]-FLT positron emission tomography can be used to image the response of sensitive tumors to PI3-kinase inhibition with the novel agent GDC-0941.Molecular cancer therapeutics · 2013Article
- Reproducibility of static and dynamic (18)F-FDG, (18)F-FLT, and (18)F-FMISO MicroPET studies in a murine model of HER2+ breast cancer.Molecular imaging and biology · 2013Article
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Authors and funding
12 authors at 5 institutions in 1 country.
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Abstract
purposeWe determined whether [(18)F]fluorothymidine (FLT) positron emission tomography (PET) can detect early effects on tumor proliferation of JAC106, a new anti-tubulin agent.
methodsInhibition of tubulin polymerization and [(3)H]colchicine binding were assessed in vitro. The effects of JAC106 on cytotoxicity, mitotic arrest, [(18)F]FLT uptake, and thymidine kinase 1 (TK1) activity were examined in SW620 and KB-V1 cells. Dose-dependent antitumor effects of JAC106 were monitored by measuring tumor growth and by dynamic [(18)F]FLT PET imaging in mice bearing SW620 and KB-V1 tumors. The proliferation status of tumors was examined.
resultsJAC106 potently inhibited tubulin polymerization and decreased the viability of SW620 (p < 0.001, half maximal inhibitory concentration, IC(50) = 3.15 ± 1.4) and KB-V1 (p < 0.01, IC(50) = 21.84 ± 24.59) cells. Exposure to JAC106 induced mitotic arrest starting at 18 h and dose-dependently increased [(18)F]FLT uptake/1 × 10(5) cells (p < 0.05) and TK1 activity and expression in vitro. Administration of 30 mg/kg JAC106 to mice inhibited the growth of SW620 and KB-VI tumors (%T/C 3.34 and 20.6%, respectively). The baseline standardized uptake values (SUV) of SW620 and KB-V1 tumors were 0.96 ± 0.31 and 2.29 ± 0.70, respectively, with a significant difference (p < 0.01). After 3 days of treatment with 30 mg/kg JAC106, the [(18)F]FLT SUVs of SW620 and KB-V1 tumors, normalized to those before treatment, were 77.9 ± 22.4% (p = 0.059) and 43.2 ± 14.0% (p < 0.01), respectively. JAC106 significantly decreased the number of Ki-67-positive cells, TK1 activity, cell fraction in G(0)G(1) phase, and tumor expression of cyclins E, A, and B1 on day 3.
conclusion[(18)F]FLT PET can be used to monitor JAC106 inhibition of tumor growth, beginning 3 days after treatment. Incorporation of [(18)F]FLT PET may be useful in the early clinical development of JAC106.
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