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dc.contributor.authorRalph, Stephen J
dc.contributor.authorLow, Pauline
dc.contributor.authorDong, Langfeng
dc.contributor.authorLawen, Alfons
dc.contributor.authorNeuzil, Jiri
dc.contributor.editorAtta-ur-Rahman
dc.date.accessioned2017-05-03T14:15:00Z
dc.date.available2017-05-03T14:15:00Z
dc.date.issued2006
dc.date.modified2009-08-26T07:03:51Z
dc.identifier.issn1574-8928
dc.identifier.urihttp://hdl.handle.net/10072/22671
dc.description.abstractMitochondria are proving to be worthy targets for activating specific killing of cancer cells in tumors and a diverse range of mitochondrial targeted drugs are currently in clinical trial to determine their effectiveness as anti-cancer therapies. The mechanism of action of mitochondrial targeted anti-cancer drugs relies on their ability to disrupt the energy producing systems of cancer cell mitochondria, leading to increased reactive oxygen species and activation of the mitochondrial dependent cell death signaling pathways inside cancer cells. We propose that this emerging class of drugs be called "mitocans", a term that reflects their mitochondrial targeting and anti-cancer roles. They are discussed in this review in the context of their mode of action whereby they target the functional differences and altered properties of the mitochondria inside cancerous but not normal cells. Hence, mitocans include drugs affecting the following mitochondrial associated activities: hexokinase inhibitors; electron transport/respiratory chain blockers; activators of the mitochondrial membrane permeability transition pore targeting constituent protein subunits, either the voltage dependent anion-selective channel (VDAC) or adenine nucleotide transporter (ANT); inhibitors of Bcl-2 anti-apoptotic family proteins and Bax/Bid pro-apoptotic mimetics. In particular, a recent surge has occurred in the number of patent documents describing small molecule inhibitors and BH3 mimetic blockers of Bcl-2/Bcl-xL function as obvious and important targets for promoting mitochondrial induced cancer cell death and for enhancing the actions of other chemotherapeutic agents. One of the other highly significant results to emerge from clinical applications of mitochondrial targeted drugs as cancer therapies to date is that they have shown limited side-effects on the normal "healthy" cell populations in vivo. It is still too early to judge the clinical impact that mitocans will make in treating cancer. Further clinical studies will be required before these novel drugs become established as single modality anti-cancer therapies or are used in conjunction with existing chemotherapies. However, it is clear from the present studies that mitocans offer great potential as effective and exciting new developments in cancer therapy, providing direct activation of cancer cell death by mitochondrial mediated apoptosis and that this complements the other pathways by which existing treatments kill cancer cells. Undoubtedly, mitocans will become an integral part of modern weaponry in the fight to eliminate cancer.
dc.description.peerreviewedYes
dc.description.publicationstatusYes
dc.languageEnglish
dc.language.isoeng
dc.publisherBentham Science Publishers Ltd
dc.publisher.placeSaif Zone, Sharjah, U.A.E.
dc.publisher.urihttp://www.bentham.org/pra/index.htm
dc.publisher.urihttp://www.benthamdirect.org/pages/b_viewarticle.php
dc.relation.ispartofstudentpublicationN
dc.relation.ispartofpagefrom327
dc.relation.ispartofpageto346
dc.relation.ispartofissue3
dc.relation.ispartofjournalRecent Patents on Anti-Cancer Drug Discovery
dc.relation.ispartofvolume1
dc.rights.retentionY
dc.subject.fieldofresearchBiochemistry and cell biology
dc.subject.fieldofresearchOncology and carcinogenesis
dc.subject.fieldofresearchcode3101
dc.subject.fieldofresearchcode3211
dc.titleMitocans: Mitochondrial Targeted Anti-Cancer Drugs as Improved Therapies and Related Patent Documents
dc.typeJournal article
dc.type.descriptionC1 - Articles
dc.type.codeC - Journal Articles
gro.rights.copyright© 2006 Bentham Science Publishers. Please refer to the journal's website for access to the definitive, published version.
gro.date.issued2006
gro.hasfulltextNo Full Text
gro.griffith.authorNeuzil, Jiri
gro.griffith.authorRalph, Stephen J.


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