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- Publisher Website: 10.2174/1566524033479401
- Scopus: eid_2-s2.0-0346146997
- PMID: 14682494
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Article: TRAIL: A potential agent for cancer therapy
Title | TRAIL: A potential agent for cancer therapy |
---|---|
Authors | |
Issue Date | 2003 |
Publisher | Bentham 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? |
Abstract | Induction 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 Identifier | http://hdl.handle.net/10722/84353 |
ISSN | 2023 Impact Factor: 2.2 2023 SCImago Journal Rankings: 0.531 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Shi, J | en_HK |
dc.contributor.author | Zheng, D | en_HK |
dc.contributor.author | Man, K | en_HK |
dc.contributor.author | Fan, ST | en_HK |
dc.contributor.author | Xu, R | en_HK |
dc.date.accessioned | 2010-09-06T08:51:57Z | - |
dc.date.available | 2010-09-06T08:51:57Z | - |
dc.date.issued | 2003 | en_HK |
dc.identifier.citation | Current Molecular Medicine, 2003, v. 3 n. 8, p. 727-736 | en_HK |
dc.identifier.issn | 1566-5240 | en_HK |
dc.identifier.uri | http://hdl.handle.net/10722/84353 | - |
dc.description.abstract | Induction 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.language | eng | en_HK |
dc.publisher | Bentham Science Publishers Ltd. The Journal's web site is located at http://www.bentham.org/cmm/index.htm | en_HK |
dc.relation.ispartof | Current Molecular Medicine | en_HK |
dc.title | TRAIL: A potential agent for cancer therapy | en_HK |
dc.type | Article | en_HK |
dc.identifier.openurl | http://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+therapy | en_HK |
dc.identifier.email | Man, K: kwanman@hkucc.hku.hk | en_HK |
dc.identifier.email | Fan, ST: stfan@hku.hk | en_HK |
dc.identifier.authority | Man, K=rp00417 | en_HK |
dc.identifier.authority | Fan, ST=rp00355 | en_HK |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.2174/1566524033479401 | en_HK |
dc.identifier.pmid | 14682494 | - |
dc.identifier.scopus | eid_2-s2.0-0346146997 | en_HK |
dc.identifier.hkuros | 87858 | en_HK |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-0346146997&selection=ref&src=s&origin=recordpage | en_HK |
dc.identifier.volume | 3 | en_HK |
dc.identifier.issue | 8 | en_HK |
dc.identifier.spage | 727 | en_HK |
dc.identifier.epage | 736 | en_HK |
dc.identifier.isi | WOS:000187158400005 | - |
dc.publisher.place | Netherlands | en_HK |
dc.identifier.scopusauthorid | Shi, J=7404495444 | en_HK |
dc.identifier.scopusauthorid | Zheng, D=7202567084 | en_HK |
dc.identifier.scopusauthorid | Man, K=7101754072 | en_HK |
dc.identifier.scopusauthorid | Fan, ST=7402678224 | en_HK |
dc.identifier.scopusauthorid | Xu, R=7402813857 | en_HK |
dc.identifier.issnl | 1566-5240 | - |