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Article: The CXCL12-CXCR4 chemotactic pathway as a target of adjuvant breast cancer therapies

TitleThe CXCL12-CXCR4 chemotactic pathway as a target of adjuvant breast cancer therapies
Authors
Issue Date2004
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/cancer/
Citation
Nature Reviews Cancer, 2004, v. 4 n. 11, p. 901-909 How to Cite?
AbstractDose-dense adjuvant breast cancer chemotherapy is a new treatment strategy that aims to improve tumour control by using more frequent cytotoxic dosing together with continuous granulocyte colony-stimulating factor (G-CSF) to minimize neutropaenia. In addition to stimulating neutrophil proliferation, G-CSF mobilizes neutrophils from the bone marrow through proteolytic disruption of the chemokine receptor CXCR4 and its chemotactic ligand CXCL12. As breast cancers also express CXCR4 and oestrogen induces CXCL12, the success of dose-dense treatment could partly reflect inhibition of CXCR4-dependent micrometastatic homing and/or paracrine survival, and suggests a benefit of adjuvant oestrogen suppression for patients with oestrogen-receptor-negative, CXCR4-positive disease.
Persistent Identifierhttp://hdl.handle.net/10722/77814
ISSN
2015 Impact Factor: 34.244
2015 SCImago Journal Rankings: 25.467
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorEpstein, RJen_HK
dc.date.accessioned2010-09-06T07:36:01Z-
dc.date.available2010-09-06T07:36:01Z-
dc.date.issued2004en_HK
dc.identifier.citationNature Reviews Cancer, 2004, v. 4 n. 11, p. 901-909en_HK
dc.identifier.issn1474-175Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/77814-
dc.description.abstractDose-dense adjuvant breast cancer chemotherapy is a new treatment strategy that aims to improve tumour control by using more frequent cytotoxic dosing together with continuous granulocyte colony-stimulating factor (G-CSF) to minimize neutropaenia. In addition to stimulating neutrophil proliferation, G-CSF mobilizes neutrophils from the bone marrow through proteolytic disruption of the chemokine receptor CXCR4 and its chemotactic ligand CXCL12. As breast cancers also express CXCR4 and oestrogen induces CXCL12, the success of dose-dense treatment could partly reflect inhibition of CXCR4-dependent micrometastatic homing and/or paracrine survival, and suggests a benefit of adjuvant oestrogen suppression for patients with oestrogen-receptor-negative, CXCR4-positive disease.en_HK
dc.languageengen_HK
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/cancer/en_HK
dc.relation.ispartofNature Reviews Canceren_HK
dc.titleThe CXCL12-CXCR4 chemotactic pathway as a target of adjuvant breast cancer therapiesen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1474-175X&volume=4 &issue=11&spage=901&epage=909&date=2004&atitle=The+CXCL12-CXCR4+chemotactic+pathway+as+a+target+of+adjuvant+breast+cancer+therapiesen_HK
dc.identifier.emailEpstein, RJ: repstein@hku.hken_HK
dc.identifier.authorityEpstein, RJ=rp00501en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1038/nrc1473en_HK
dc.identifier.pmid15516962-
dc.identifier.scopuseid_2-s2.0-8144225469en_HK
dc.identifier.hkuros96353en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-8144225469&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume4en_HK
dc.identifier.issue11en_HK
dc.identifier.spage901en_HK
dc.identifier.epage909en_HK
dc.identifier.isiWOS:000224815700016-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridEpstein, RJ=34975074500en_HK
dc.identifier.citeulike9790052-

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