Therapeutic efficacy and apoptosis and necrosis kinetics of doxorubicin compared with cisplatin, combined with whole-body hyperthermia in a rat mammary adenocarcinoma

Toyota, Nobuhiko; Strebel, F. R.; Stephens, L. Clifton; Matsuda, Hiroyuki; Oshiro, Tatuso; Jenkins, Gaye; Bull, Joan M C

doi:10.1002/(sici)1097-0215(19980518)76:4<499::aid-ijc10>3.0.co;2-3

Cited by 19 publications

(7 citation statements)

References 13 publications

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“…These effects are likely related to DOXO-induced DNA damages also previously characterized in this rat breast tumor model (Evans et al, 1986). The apoptotic effects correlate with the antitumor activity of DOXO, as evidenced in the corresponding MTLn3 in vivo model (Toyota et al, 1998). DOXO-induced apoptosis in MTLn3 cells is known to cause mitochondrial perturbations.…”

Section: Discussionsupporting

confidence: 66%

Mitochondrial proliferation during apoptosis induced by anticancer agents: effects of doxorubicin and mitoxantrone on cancer and cardiac cells

et al. 2004

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Section: Discussionsupporting

confidence: 66%

Mitochondrial proliferation during apoptosis induced by anticancer agents: effects of doxorubicin and mitoxantrone on cancer and cardiac cells

et al. 2004

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“…We used the rat mammary adenocarcinoma cell line MTLn3, which is often used as a model to study molecular mechanisms of metastasis formation (Kiley et al, 1999b) and responses to drug therapy both in vitro and in vivo (Toyota et al, 1998;Huigsloot et al, 2001Huigsloot et al, , 2002 To inhibit apoptosis we also used MTLn3 cells that overexpress Bcl-2. The soft agar colony formation assay estimates the ability of single tumor cells to survive and proliferate in an anchorage-independent manner (both required for tumor growth and metastasis).…”

mentioning

confidence: 99%

Inhibition of Protein Kinase Cα Enhances Anticancer Agent-Induced Loss of Anchorage-Independent Growth Regardless of Protection against Apoptosis by Bcl-2

Huigsloot

Tijdens²,

Water³

2003

Molecular Pharmacology

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“…When cells die by apoptosis, they die singly and are rapidly eliminated by neighboring healthy parenchymal cells and macrophages (20). Thus, if tissue is examined for apoptosis shortly after the application of cytotoxic damage, cells undergoing apoptosis will be more likely to be present in the tissue and detectable by apoptosis detection methods.…”

Section: Discussionmentioning

confidence: 99%

The Role of Hyperthermia in Regional Alkylating Agent Chemotherapy

Abdel‐Wahab¹,

Grubbs²,

Viglianti

et al. 2004

Clinical Cancer Research

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The role of hyperthermia during regional alkylating agent chemotherapy is controversial. The aim of this study was to determine the exact contribution of hyperthermia to tumor response during isolated limb infusion with L-phenylalanine mustard. Rats bearing rodent fibrosarcoma on the hindlimb underwent isolated limb infusion with saline, saline plus heat, L-phenylalanine mustard, L-phenylalanine mustard under conditions of normothermia, or L-phenylalanine mustard plus hyperthermia. Heat was administered locally using an in-line hot water circulation loop. Treatment with L-phenylalanine mustard at a concentration of 15 or 50 g/mL was ineffective at producing tumor growth delay (P ‫؍‬ 0.24 and 0.41, respectively). Furthermore, thermal enhancement of L-phenylalanine mustard activity was not seen at 15 g/mL. However, administration of high-dose L-phenylalanine mustard, 50 g/mL, with increasing amounts of heat yielded increasing tumor growth delay, increased regressions, and decreased proliferative index. Although L-phenylalanine mustard infusion under normothermia yielded a tumor growth delay of 7.1 days, combination L-phenylalanine mustard ؉ hyperthermia treatment produced tumor growth delay of 27.0 days (P < 0.01; with two of five animals showing a complete response). Four hours after isolated limb infusion, 50.9% of cells in tumor treated with L-phenylalanine mustard ؉ hyperthermia experienced apoptosis, whereas only 18.1, 16, and 4.4% of cells underwent apoptosis after treatment with L-phenylalanine mustard, saline ؉ hyperthermia, or saline. The mean concentration of L-phenylalanine mustard within tumor relative to perfusate following isolated limb infusion was found to be similar among all groups at 0.023, 0.025, and 0.032 in animals undergoing isolated limb infusion with L-phenylalanine mustard, L-phenylalanine mustard ؉ normothermia, and L-phenylalanine mustard ؉ hyperthermia, respectively. These data indicate a synergistic cytotoxic effect of Lphenylalanine mustard ؉ hyperthermia in isolated limb infusion, which is not attributable to enhanced tumor drug uptake.

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Therapeutic efficacy and apoptosis and necrosis kinetics of doxorubicin compared with cisplatin, combined with whole-body hyperthermia in a rat mammary adenocarcinoma

Cited by 19 publications

References 13 publications

Mitochondrial proliferation during apoptosis induced by anticancer agents: effects of doxorubicin and mitoxantrone on cancer and cardiac cells

Mitochondrial proliferation during apoptosis induced by anticancer agents: effects of doxorubicin and mitoxantrone on cancer and cardiac cells

Inhibition of Protein Kinase Cα Enhances Anticancer Agent-Induced Loss of Anchorage-Independent Growth Regardless of Protection against Apoptosis by Bcl-2

The Role of Hyperthermia in Regional Alkylating Agent Chemotherapy

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