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Article: TRAIL: A potential agent for cancer therapy

TitleTRAIL: A potential agent for cancer therapy
Authors
Issue Date2003
PublisherBentham Science Publishers Ltd. The Journal's web site is located at http://www.bentham.org/cmm/index.htm
Citation
Current Molecular Medicine, 2003, v. 3 n. 8, p. 727-736 How to Cite?
AbstractInduction of apoptosis in cancer cells with chemotherapy and radiation treatment is a major strategy in cancer therapy at present. Nevertheless, innate or acquired resistance has been an obstacle for conventional clinical therapy. TNF-related apoptosis inducing ligand (TRAIL/Apo-2L) is a typical member of the TNF ligand family that induces apoptosis through activating the death receptors. In recent years, considerable attention has been focused on the potential benefits of TRAIL in cancer therapy, as the majority of cancer cells are sensitive to TRAIL-induced apoptosis, while most normal cells are TRAIL-resistant. Furthermore, the use of TRAIL in combination with chemotherapeutic agents or irradiation strengthens its apoptotic effects. In this review, we will discuss the regulation mechanism of TRAIL-induced apoptosis and the molecular basis of the synergies created by its use in combination with chemotherapeutic agents and irradiation. We also analyze in detail that TRAIL may be cytotoxic, as this is a potential obstacle to its development for being used in cancer therapy.
Persistent Identifierhttp://hdl.handle.net/10722/84353
ISSN
2023 Impact Factor: 2.2
2023 SCImago Journal Rankings: 0.531
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorShi, Jen_HK
dc.contributor.authorZheng, Den_HK
dc.contributor.authorMan, Ken_HK
dc.contributor.authorFan, STen_HK
dc.contributor.authorXu, Ren_HK
dc.date.accessioned2010-09-06T08:51:57Z-
dc.date.available2010-09-06T08:51:57Z-
dc.date.issued2003en_HK
dc.identifier.citationCurrent Molecular Medicine, 2003, v. 3 n. 8, p. 727-736en_HK
dc.identifier.issn1566-5240en_HK
dc.identifier.urihttp://hdl.handle.net/10722/84353-
dc.description.abstractInduction of apoptosis in cancer cells with chemotherapy and radiation treatment is a major strategy in cancer therapy at present. Nevertheless, innate or acquired resistance has been an obstacle for conventional clinical therapy. TNF-related apoptosis inducing ligand (TRAIL/Apo-2L) is a typical member of the TNF ligand family that induces apoptosis through activating the death receptors. In recent years, considerable attention has been focused on the potential benefits of TRAIL in cancer therapy, as the majority of cancer cells are sensitive to TRAIL-induced apoptosis, while most normal cells are TRAIL-resistant. Furthermore, the use of TRAIL in combination with chemotherapeutic agents or irradiation strengthens its apoptotic effects. In this review, we will discuss the regulation mechanism of TRAIL-induced apoptosis and the molecular basis of the synergies created by its use in combination with chemotherapeutic agents and irradiation. We also analyze in detail that TRAIL may be cytotoxic, as this is a potential obstacle to its development for being used in cancer therapy.en_HK
dc.languageengen_HK
dc.publisherBentham Science Publishers Ltd. The Journal's web site is located at http://www.bentham.org/cmm/index.htmen_HK
dc.relation.ispartofCurrent Molecular Medicineen_HK
dc.titleTRAIL: A potential agent for cancer therapyen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1566-5240&volume=3&issue=8&spage=727&epage=736&date=2003&atitle=TRAIL:+a+potential+agent+for+cancer+therapyen_HK
dc.identifier.emailMan, K: kwanman@hkucc.hku.hken_HK
dc.identifier.emailFan, ST: stfan@hku.hken_HK
dc.identifier.authorityMan, K=rp00417en_HK
dc.identifier.authorityFan, ST=rp00355en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.2174/1566524033479401en_HK
dc.identifier.pmid14682494-
dc.identifier.scopuseid_2-s2.0-0346146997en_HK
dc.identifier.hkuros87858en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0346146997&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume3en_HK
dc.identifier.issue8en_HK
dc.identifier.spage727en_HK
dc.identifier.epage736en_HK
dc.identifier.isiWOS:000187158400005-
dc.publisher.placeNetherlandsen_HK
dc.identifier.scopusauthoridShi, J=7404495444en_HK
dc.identifier.scopusauthoridZheng, D=7202567084en_HK
dc.identifier.scopusauthoridMan, K=7101754072en_HK
dc.identifier.scopusauthoridFan, ST=7402678224en_HK
dc.identifier.scopusauthoridXu, R=7402813857en_HK
dc.identifier.issnl1566-5240-

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