Tumour tissue selectivity in the uptake and retention of SN 28049, a new topoisomerase II-directed anticancer agent

Lukka, Pradeep B.; Chen, Ying Yi; Finlay, Graeme J.; Joseph, Wayne R.; Richardson, Emma; Paxton, James W.; Baguley, Bruce C.

doi:10.1007/s00280-013-2280-0

Cited by 4 publications

References 26 publications

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Regioselective Synthesis of Benzo[h][1,6]‐naphthyridines and Chromenopyrazinones through Alkyne Cyclization

2017

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A regioselective approach to the synthesis of benzo[h][1,6]‐naphthyridine and chromenopyrazinone derivatives was developed. The synthetic route to benzo[h][1,6]‐naphthyridines involves the N‐propargylation of aromatic aminobenzaldehydes, followed by reaction with propargylamine in the presence of DBU (1,8‐diazabicyclo[5.4.0]undec‐7‐ene). For the synthesis of chromenopyrazine and chromenopyrazinone derivatives, the acetonitrile group was introduced to salicylaldehyde derivatives, and a DBU‐promoted cyclization reaction between aldehydes and propargylamine gave the chromenopyrazines. The intramolecular heterocycloaddition reaction between the triple bond and the azadiene, which is formed as an intermediate, gave the desired structures.

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Regioselective Synthesis of Benzo[h][1,6]‐naphthyridines and Chromenopyrazinones through Alkyne Cyclization

2017

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Classical and Targeted Anticancer Drugs: An Appraisal of Mechanisms of Multidrug Resistance

Baguley

2016

Methods in Molecular Biology

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The mechanisms by which tumor cells resist the action of multiple anticancer drugs, often with widely different chemical structures, have been pursued for more than 30 years. The identification of P-glycoprotein (P-gp), a drug efflux transporter protein with affinity for multiple therapeutic drugs, provided an important potential mechanism and further work, which identified other members of ATP-binding cassette (ABC) family that act as drug transporters. Several observations, including results of clinical trials with pharmacological inhibitors of P-gp, have suggested that mechanisms other than efflux transporters should be considered as contributors to resistance, and in this review mechanisms of anticancer drug resistance are considered more broadly. Cells in human tumors exist is a state of continuous turnover, allowing ongoing selection and "survival of the fittest." Tumor cells die not only as a consequence of drug therapy but also by apoptosis induced by their microenvironment. Cell death can be mediated by host immune mechanisms and by nonimmune cells acting on so-called death receptors. The tumor cell proliferation rate is also important because it controls tumor regeneration. Resistance to therapy might therefore be considered to arise from a reduction of several distinct cell death mechanisms, as well as from an increased ability to regenerate. This review provides a perspective on these mechanisms, together with brief descriptions of some of the methods that can be used to investigate them in a clinical situation.

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Selective cellular uptake and retention of SN 28049, a new DNA-binding topoisomerase II-directed antitumor agent

Chen

Lukka

Joseph

et al. 2014

Cancer Chemother Pharmacol

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Tumour tissue selectivity in the uptake and retention of SN 28049, a new topoisomerase II-directed anticancer agent

Abstract: SN 28049 shows dramatic differences in both tumour AUC and antitumour activity against different tumours. These differences point to the presence of a tumour-specific uptake and retention mechanism.

Cited by 4 publications

References 26 publications

Regioselective Synthesis of Benzo[h][1,6]‐naphthyridines and Chromenopyrazinones through Alkyne Cyclization

Regioselective Synthesis of Benzo[h][1,6]‐naphthyridines and Chromenopyrazinones through Alkyne Cyclization

Classical and Targeted Anticancer Drugs: An Appraisal of Mechanisms of Multidrug Resistance

Selective cellular uptake and retention of SN 28049, a new DNA-binding topoisomerase II-directed antitumor agent

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