Short communication: Thermosensitive liposomal taxol formulation: heatmediated targeted drug delivery in murine melanoma

Sharma, Dipika; Chelvi, T. P.; Kaur, J; Ralhan, Ranju

doi:10.1097/00008390-199806000-00006

Cited by 44 publications

(25 citation statements)

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“…31,37,39,50,51 Both in vitro and in vivo studies proved that this combination induced a "thermal enhancement" for PTX cytotoxicity. 31,50,51 In current clinical trials, PTX is administered with hyperthermic perfusion for the treatment of ovarian and lung cancers and gastrointestinal neoplasms (http://www.clinicaltrial.gov).…”

Section: Discussionmentioning

confidence: 96%

Targeting mitotic exit with hyperthermia or APC/C inhibition to increase paclitaxel efficacy

et al. 2013

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Microtubule-poisoning drugs, such as Paclitaxel (or taxol, PtX), are powerful and commonly used anti-neoplastic agents for the treatment of several malignancies. PtX triggers cell death, mainly through a mitotic arrest following the activation of the spindle assembly checkpoint (SAC). Cells treated with PtX slowly slip from this mitotic block and die by mitotic catastrophe. However, cancer cells can acquire or are intrinsically resistant to this drug, posing one of the main obstacles for PtX clinical effectiveness. In order to override PtX resistance and increase its efficacy, we investigated both the enhancement of mitotic slippage and the block of mitotic exit.to test these opposing strategies, we used physiological hyperthermia (Ht) to force exit from PtX-induced mitotic block and the anaphase-promoting complex/cyclosome (APC/C) inhibitor, protAMe, to block mitotic exit. We observed that application of Ht on PtX-treated cells forced mitotic slippage, as shown by the rapid decline of cyclin B levels and by microscopy analysis. Similarly, Ht induced mitotic exit in cells blocked in mitosis by other antimitotic drugs, such as Nocodazole and the Aurora A inhibitor MLN8054, indicating a common effect of Ht on mitotic cells. On the other hand, protAMe prevented mitotic exit of PtX and MLN8054 arrested cells, prolonged mitosis, and induced apoptosis. In addition, we showed that protAMe prevented Ht-mediated mitotic exit, indicating that stress-induced APC/C activation is necessary for Ht-induced mitotic slippage.Finally, Ht significantly increased PtX cytotoxicity, regardless of cancer cells' sensitivity to PtX, and this activity was superior to the combination of PtX with pro-tAMe. Our data suggested that forced mitotic exit of cells arrested in mitosis by anti-mitotic drugs, such as PtX, can be a more successful anticancer strategy than blocking mitotic exit by inactivation of the APC/C.

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Section: Discussionmentioning

confidence: 96%

Targeting mitotic exit with hyperthermia or APC/C inhibition to increase paclitaxel efficacy

et al. 2013

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“…The in vivo efficacy of the thermosensitive PTX liposomes was determined in B16F10 murine melanoma transplanted into C57Bl/6 mice in combination with local hyperthermia. A significant reduction of tumor volume and an increase in survival time were observed in tumorbearing mice treated with a combination of hyperthermia and thermosensitive PTX liposomes compared with animals treated with an equivalent dose of Cr-P with or without hyperthermia [83]. Another approach was based on a thermosensitive pluronic acid (Pluronic® F127) hydrogel in which PTX-containing liposomes were embedded.…”

Section: Paclitaxel Encapsulated In Thermosensitive Liposomesmentioning

confidence: 99%

Liposomal paclitaxel formulations

Koudelka

Tuřánek

2012

Journal of Controlled Release

305

247

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“…To overcome this problem several drug delivery systems (Alkan et al,1994;Shrama et al, 1995;Burt et al, 1999;Kan et al, 1999;Das et al, 2001;Feng and Huang, 2001) and especially liposomes (Crosasso et al, 2000) have been used. Unfortunately, the amount of paclitaxel that can be incorporated into lipid bilayers is limited (Balasubramanian and Straubinger, 1994;Shieh et al, 1997;Sharma et al, 1998). A valid approach to overcome this problem is the use of lipophilic prodrug of paclitaxel which could be retained in a lipophilic carrier.…”

Section: Introductionmentioning

confidence: 99%

Lipophilic prodrug of paclitaxel: Interaction with a dimyristoylphosphatidylcholine monolayer

Giuffrida

Dosio

Castelli

et al. 2014

International Journal of Pharmaceutics

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Short communication: Thermosensitive liposomal taxol formulation: heatmediated targeted drug delivery in murine melanoma

Cited by 44 publications

References 0 publications

Targeting mitotic exit with hyperthermia or APC/C inhibition to increase paclitaxel efficacy

Targeting mitotic exit with hyperthermia or APC/C inhibition to increase paclitaxel efficacy

Liposomal paclitaxel formulations

Lipophilic prodrug of paclitaxel: Interaction with a dimyristoylphosphatidylcholine monolayer

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