Quantitative Analysis of the Concentration of Trifluridine in Tumor Hypoxic Regions Using a Novel Platform Combining Functional Endoscopy and Mass Spectrometry.


Journal

Clinical pharmacology and therapeutics
ISSN: 1532-6535
Titre abrégé: Clin Pharmacol Ther
Pays: United States
ID NLM: 0372741

Informations de publication

Date de publication:
06 Oct 2023
Historique:
received: 12 04 2023
accepted: 22 09 2023
pubmed: 7 10 2023
medline: 7 10 2023
entrez: 7 10 2023
Statut: aheadofprint

Résumé

Hypoxic regions in solid tumors are highly resistant to drugs and thus represents an obstacle in drug discovery. Currently, however, there are technical barriers in sampling human hypoxic tumors and examining drug delivery with high sensitivity and accuracy. Herein, we present a new platform combining functional endoscopy and highly sensitive liquid chromatography-mass spectrometry (LC-MS) to assess drug delivery to hypoxic regions. Because oxygen saturation endoscopic imaging (OXEI), a functional endoscopy, can evaluate lesions and hypoxia in real-time by simultaneously acquiring a pseudocolor map of oxygen saturation and conventional endoscopic images, this platform can be used to evaluate drug delivery with human samples from hypoxic regions. As the first clinical application of this platform, the relationship between hypoxic regions and the concentration of trifluridine (FTD) incorporated into DNA was evaluated in patients with advanced gastric cancer treated with FTD/tipiracil (FTD/TPI; n = 13) by obtaining and analysis of tissue samples by OXEI and LC-MS and vascular maturity index by CD31/α-SMA staining ex vivo. The results showed that the concentration of FTD was significantly higher in the normoxic region than in the hypoxic region (P < 0.05) and there were significantly more immature vessels in hypoxic regions than in normoxic regions (P < 0.05). These results indicate that the platform was sufficiently sensitive to evaluate differences in drug anabolism in different oxygenic regions of human tumor tissue. This new platform allows quantitative drug analysis in hypoxic regions and is expected to initiate a new era of drug discovery and development.

Identifiants

pubmed: 37803526
doi: 10.1002/cpt.3066
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : Taiho Pharmaceutical Co., Ltd.
Organisme : Japan Research Foundation for Clinical Pharmacology

Informations de copyright

© 2023 The Authors. Clinical Pharmacology & Therapeutics published by Wiley Periodicals LLC on behalf of American Society for Clinical Pharmacology and Therapeutics.

Références

Vaupel, P., Thews, O. & Hoeckel, M. Treatment resistance of solid tumors: role of hypoxia and anemia. Med. Oncol. 18, 243-259 (2001).
Brown, J.M. & Wilson, W.R. Exploiting tumour hypoxia in cancer treatment. Nat. Rev. Cancer 4, 437-447 (2004).
Pouyssegur, J., Dayan, F. & Mazure, N.M. Hypoxia signalling in cancer and approaches to enforce tumour regression. Nature 441, 437-443 (2006).
Dhani, N., Fyles, A., Hedley, D. & Milosevic, M. The clinical significance of hypoxia in human cancers. Semin. Nucl. Med. 45, 110-121 (2015).
Cosse, J.P. & Michiels, C. Tumour hypoxia affects the responsiveness of cancer cells to chemotherapy and promotes cancer progression. Anticancer Agents Med Chem. 8, 790-797 (2008).
Brizel, D.M., Dodge, R.K., Clough, R.W. & Dewhirst, M.W. Oxygenation of head and neck cancer: changes during radiotherapy and impact on treatment outcome. Radiother. Oncol. 53, 113-117 (1999).
Peeters, S.G. et al. A comparative study of the hypoxia PET tracers [(1)(8)F]HX4, [(1)(8)F]FAZA, and [(1)(8)F]FMISO in a preclinical tumor model. Int. J. Radiat. Oncol. Biol. Phys. 91, 351-359 (2015).
Huang, Y., Fan, J., Li, Y., Fu, S., Chen, Y. & Wu, J. Imaging of tumor hypoxia with radionuclide-labeled tracers for PET. Front. Oncol. 11, 731503 (2021).
Reeves, K.M. et al. (18)F-FMISO PET imaging identifies hypoxia and immunosuppressive tumor microenvironments and guides targeted Evofosfamide therapy in tumors refractory to PD-1 and CTLA-4 inhibition. Clin. Cancer Res. 28, 327-337 (2022).
Eriksson, C., Masaki, N., Yao, I., Hayasaka, T. & Setou, M. MALDI imaging mass spectrometry - a mini review of methods and recent developments. Mass Spectrom. 2, S0022 (2013).
Nishidate, M. et al. Applications of MALDI mass spectrometry imaging for pharmacokinetic studies during drug development. Drug Metab. Pharmacokinet. 34, 209-216 (2019).
Jiang, L. et al. MALDI-mass spectrometric imaging revealing hypoxia-driven lipids and proteins in a breast tumor model. Anal. Chem. 87, 5947-5956 (2015).
Kaneko, K. et al. Hypoxia imaging endoscopy equipped with laser light source from preclinical live animal study to first-in-human subject research. PLoS One 9, e99055 (2014).
Temmink, O.H., Emura, T., de Bruin, M., Fukushima, M. & Peters, G.J. Therapeutic potential of the dual-targeted TAS-102 formulation in the treatment of gastrointestinal malignancies. Cancer Sci. 98, 779-789 (2007).
Mayer, R.J. et al. Randomized trial of TAS-102 for refractory metastatic colorectal cancer. N. Engl. J. Med. 372, 1909-1919 (2015).
Shitara, K. et al. Trifluridine/tipiracil versus placebo in patients with heavily pretreated metastatic gastric cancer (TAGS): a randomised, double-blind, placebo-controlled, phase 3 trial. Lancet Oncol. 19, 1437-1448 (2018).
Matsuoka, K., Nakagawa, F., Kobunai, T. & Takechi, T. Trifluridine/tipiracil overcomes the resistance of human gastric 5-fluorouracil-refractory cells with high thymidylate synthase expression. Oncotarget 9, 13438-13450 (2018).
Nishihara, K. et al. A study of evaluating specific tissue oxygen saturation values of gastrointestinal tumors by removing adherent substances in oxygen saturation imaging. PLoS One 16, e0243165 (2021).
Bhandari, V. et al. Molecular landmarks of tumor hypoxia across cancer types. Nat. Genet. 51, 308-318 (2019).
Ye, Y. et al. Characterization of hypoxia-associated molecular features to aid hypoxia-targeted therapy. Nat. Metab. 1, 431-444 (2019).
Lee, P., Chandel, N.S. & Simon, M.C. Cellular adaptation to hypoxia through hypoxia inducible factors and beyond. Nat. Rev. Mol. Cell Biol. 21, 268-283 (2020).
Barsoum, I.B., Smallwood, C.A., Siemens, D.R. & Graham, C.H. A mechanism of hypoxia-mediated escape from adaptive immunity in cancer cells. Cancer Res. 74, 665-674 (2014).
Jayaprakash, P. et al. Targeted hypoxia reduction restores T cell infiltration and sensitizes prostate cancer to immunotherapy. J. Clin. Invest. 128, 5137-5149 (2018).
Ni, J. et al. Single-cell RNA sequencing of tumor-infiltrating NK cells reveals that inhibition of transcription factor HIF-1alpha unleashes NK cell activity. Immunity 52, 1075-1087.e1078 (2020).
Valable, S. et al. Imaging of brain oxygenation with magnetic resonance imaging: a validation with positron emission tomography in the healthy and tumoural brain. J. Cereb. Blood Flow Metab. 37, 2584-2597 (2017).
Colliez, F., Gallez, B. & Jordan, B.F. Assessing tumor oxygenation for predicting outcome in radiation oncology: a review of studies correlating tumor hypoxic status and outcome in the preclinical and clinical settings. Front. Oncol. 7, 10 (2017).
Hockel, M. et al. Intratumoral pO2 predicts survival in advanced cancer of the uterine cervix. Radiother. Oncol. 26, 45-50 (1993).
Nordsmark, M., Bentzen, S.M. & Overgaard, J. Measurement of human tumour oxygenation status by a polarographic needle electrode. An analysis of inter- and intratumour heterogeneity. Acta Oncol. 33, 383-389 (1994).
Sharma, A. et al. Hypoxia-targeted drug delivery. Chem. Soc. Rev. 48, 771-813 (2019).
Taylor, A.J., Dexter, A. & Bunch, J. Exploring ion suppression in mass spectrometry imaging of a heterogeneous tissue. Anal. Chem. 90, 5637-5645 (2018).
Koganemaru, S. et al. Quantitative analysis of drug distribution in heterogeneous tissues using dual-stacking capillary electrophoresis-mass spectrometry. Br. J. Pharmacol. 180, 762-774 (2023).
Ramakrishnan, S., Anand, V. & Roy, S. Vascular endothelial growth factor signaling in hypoxia and inflammation. J. Neuroimmune Pharmacol. 9, 142-160 (2014).
Miller, K. et al. Paclitaxel plus bevacizumab versus paclitaxel alone for metastatic breast cancer. N. Engl. J. Med. 357, 2666-2676 (2007).
Cassidy, J. et al. Randomized phase III study of capecitabine plus oxaliplatin compared with fluorouracil/folinic acid plus oxaliplatin as first-line therapy for metastatic colorectal cancer. J. Clin. Oncol. 26, 2006-2012 (2008).
Finn, R.S. et al. Atezolizumab plus bevacizumab in unresectable hepatocellular carcinoma. N. Engl. J. Med. 382, 1894-1905 (2020).
Tsukihara, H. et al. Efficacy of combination chemotherapy using a novel oral chemotherapeutic agent, TAS-102, together with bevacizumab, cetuximab, or panitumumab on human colorectal cancer xenografts. Oncol. Rep. 33, 2135-2142 (2015).
Suzuki, N., Nakagawa, F., Matsuoka, K. & Takechi, T. Effect of a novel oral chemotherapeutic agent containing a combination of trifluridine, tipiracil and the novel triple angiokinase inhibitor nintedanib, on human colorectal cancer xenografts. Oncol. Rep. 36, 3123-3130 (2016).
Kuboki, Y. et al. TAS-102 plus bevacizumab for patients with metastatic colorectal cancer refractory to standard therapies (C-TASK FORCE): an investigator-initiated, open-label, single-arm, multicentre, phase 1/2 study. Lancet Oncol. 18, 1172-1181 (2017).
Kawazoe, A. et al. Safety and activity of trifluridine/tipiracil and ramucirumab in previously treated advanced gastric cancer: an open-label, single-arm, phase 2 trial. Lancet Gastroenterol. Hepatol. 6, 209-217 (2021).

Auteurs

Shigehiro Koganemaru (S)

Department of Experimental Therapeutics, National Cancer Center Hospital East, Kashiwa, Japan.

Hirobumi Fuchigami (H)

Division of Developmental Therapeutics, Exploratory Oncology Research and Clinical Trial Center, National Cancer Center, Kashiwa, Japan.

Hiroki Yamashita (H)

Department of Gastroenterology and Endoscopy, National Cancer Center Hospital East, Kashiwa, Japan.

Chihiro Morizono (C)

Department of Experimental Therapeutics, National Cancer Center Hospital East, Kashiwa, Japan.
Division of Developmental Therapeutics, Exploratory Oncology Research and Clinical Trial Center, National Cancer Center, Kashiwa, Japan.

Hironori Sunakawa (H)

Department of Gastroenterology and Endoscopy, National Cancer Center Hospital East, Kashiwa, Japan.

Akihito Kawazoe (A)

Department of Gastroenterology and Gastrointestinal Oncology, National Cancer Center Hospital East, Kashiwa, Japan.

Yoshiaki Nakamura (Y)

Department of Gastroenterology and Gastrointestinal Oncology, National Cancer Center Hospital East, Kashiwa, Japan.

Yasutoshi Kuboki (Y)

Department of Experimental Therapeutics, National Cancer Center Hospital East, Kashiwa, Japan.

Kohei Shitara (K)

Department of Gastroenterology and Gastrointestinal Oncology, National Cancer Center Hospital East, Kashiwa, Japan.

Tomonori Yano (T)

Department of Gastroenterology and Endoscopy, National Cancer Center Hospital East, Kashiwa, Japan.

Toshihiko Doi (T)

Department of Experimental Therapeutics, National Cancer Center Hospital East, Kashiwa, Japan.

Masahiro Yasunaga (M)

Division of Developmental Therapeutics, Exploratory Oncology Research and Clinical Trial Center, National Cancer Center, Kashiwa, Japan.

Classifications MeSH