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Article: EGFR array: Uses in the detection of plasma EGFR mutations in non-small cell lung cancer patients

TitleEGFR array: Uses in the detection of plasma EGFR mutations in non-small cell lung cancer patients
Authors
KeywordsEGFR array
Follow-up
Non-small-cell lung cancer
Plasma EGFR mutations
Tyrosine kinase inhibitor therapy
Issue Date2012
PublisherLippincott Williams & Wilkins.
Citation
Journal Of Thoracic Oncology, 2012, v. 7 n. 7, p. 1131-1140 How to Cite?
AbstractINTRODUCTION: We aim to develop a simple and sensitive array-based method for the detection of epidermal growth factor receptor (EGFR) gene mutations in the plasma of non-small-cell lung cancer patients and determine its use in the follow-up of those on tyrosine-kinase inhibitor (TKI) therapy. METHOD: DNA from 100 μl of plasma was amplified in the presence of peptide nucleic acid clamp to provide single-stranded template for the allele-specific arrayed primer extension reaction, incorporating cyanine-5-deoxycytidine triphosphate in the newly synthesized strands. The fluorescent product was visualized by laser at 670 nm. RESULTS: Eleven different types of EGFR TKI drug-sensitive mutants (SM) were identified in plasma-DNA from 46 of 51 patients. Five patients carried only wild-type sequence. Plasma-DNA finding was concordant in 36 of 37 cases with tumor-sequencing data. This method could detect as little as 62.5 copies of mutant L858R; 125 copies of E709K + G719A or 625 copies of del 746-750 in the presence of 100,000 copies of wild-type EGFR. In 21 patients on longitudinal follow-up for up to 18 months, SM was found in all initial plasma samples, except for three samples collected after recent chemotherapy. Nine of 16 patients (56%) who responded to TKI had undetectable plasma EGFR mutant. SM was present concurrently with drug-resistant mutant in 44% of patients with disease progression while on TKI, the remaining 56% might have other mechanisms of resistance. CONCLUSION: The EGFR array provides a sensitive, inexpensive, and robust method for monitoring non-small-cell lung cancer patients' response to TKI, and obviates the need of repeated lung biopsy. Copyright © 2012 by the International Association for the Study of Lung Cancer.
Persistent Identifierhttp://hdl.handle.net/10722/159617
ISSN
2014 Impact Factor: 5.282
2014 SCImago Journal Rankings: 2.436
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYam, Ien_HK
dc.contributor.authorLam, DCLen_HK
dc.contributor.authorChan, Ken_HK
dc.contributor.authorHo, JCMen_HK
dc.contributor.authorIp, Men_HK
dc.contributor.authorLam, WKen_HK
dc.contributor.authorChan, TKen_HK
dc.contributor.authorChan, Ven_HK
dc.date.accessioned2012-08-16T05:53:26Z-
dc.date.available2012-08-16T05:53:26Z-
dc.date.issued2012en_HK
dc.identifier.citationJournal Of Thoracic Oncology, 2012, v. 7 n. 7, p. 1131-1140en_HK
dc.identifier.issn1556-0864en_HK
dc.identifier.urihttp://hdl.handle.net/10722/159617-
dc.description.abstractINTRODUCTION: We aim to develop a simple and sensitive array-based method for the detection of epidermal growth factor receptor (EGFR) gene mutations in the plasma of non-small-cell lung cancer patients and determine its use in the follow-up of those on tyrosine-kinase inhibitor (TKI) therapy. METHOD: DNA from 100 μl of plasma was amplified in the presence of peptide nucleic acid clamp to provide single-stranded template for the allele-specific arrayed primer extension reaction, incorporating cyanine-5-deoxycytidine triphosphate in the newly synthesized strands. The fluorescent product was visualized by laser at 670 nm. RESULTS: Eleven different types of EGFR TKI drug-sensitive mutants (SM) were identified in plasma-DNA from 46 of 51 patients. Five patients carried only wild-type sequence. Plasma-DNA finding was concordant in 36 of 37 cases with tumor-sequencing data. This method could detect as little as 62.5 copies of mutant L858R; 125 copies of E709K + G719A or 625 copies of del 746-750 in the presence of 100,000 copies of wild-type EGFR. In 21 patients on longitudinal follow-up for up to 18 months, SM was found in all initial plasma samples, except for three samples collected after recent chemotherapy. Nine of 16 patients (56%) who responded to TKI had undetectable plasma EGFR mutant. SM was present concurrently with drug-resistant mutant in 44% of patients with disease progression while on TKI, the remaining 56% might have other mechanisms of resistance. CONCLUSION: The EGFR array provides a sensitive, inexpensive, and robust method for monitoring non-small-cell lung cancer patients' response to TKI, and obviates the need of repeated lung biopsy. Copyright © 2012 by the International Association for the Study of Lung Cancer.en_HK
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins.-
dc.relation.ispartofJournal of Thoracic Oncologyen_HK
dc.subjectEGFR arrayen_HK
dc.subjectFollow-upen_HK
dc.subjectNon-small-cell lung canceren_HK
dc.subjectPlasma EGFR mutationsen_HK
dc.subjectTyrosine kinase inhibitor therapyen_HK
dc.subject.meshCarcinoma, Non-Small-Cell Lung - blood - genetics - pathology-
dc.subject.meshDNA, Neoplasm - blood - genetics-
dc.subject.meshMutation - genetics-
dc.subject.meshReceptor, Epidermal Growth Factor - genetics-
dc.subject.meshTumor Markers, Biological - blood - genetics-
dc.titleEGFR array: Uses in the detection of plasma EGFR mutations in non-small cell lung cancer patientsen_HK
dc.typeArticleen_HK
dc.identifier.emailChan, K: kaimin@hkucc.hku.hken_HK
dc.identifier.emailIp, M: msmip@hku.hken_HK
dc.identifier.emailChan, V: vnychana@hkucc.hku.hken_HK
dc.identifier.emailLam, DCL: dcllam@hku.hk-
dc.identifier.emailHo, JCM: jhocm@hku.hk-
dc.identifier.authorityChan, K=rp00489en_HK
dc.identifier.authorityIp, M=rp00347en_HK
dc.identifier.authorityChan, V=rp00320en_HK
dc.identifier.authorityLam, DCL=rp01345-
dc.identifier.authorityHo, JCM=rp00258-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1097/JTO.0b013e3182558198en_HK
dc.identifier.pmid22610259en_HK
dc.identifier.scopuseid_2-s2.0-84862893803en_HK
dc.identifier.hkuros202205en_US
dc.identifier.hkuros218566-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-84862893803&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume7en_HK
dc.identifier.issue7en_HK
dc.identifier.spage1131en_HK
dc.identifier.epage1140en_HK
dc.identifier.isiWOS:000306458700113-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridYam, I=6603358817en_HK
dc.identifier.scopusauthoridLam, DCL=54896046800en_HK
dc.identifier.scopusauthoridChan, K=7406032228en_HK
dc.identifier.scopusauthoridHo, JCM=55217696400en_HK
dc.identifier.scopusauthoridIp, M=7102423259en_HK
dc.identifier.scopusauthoridLam, WK=35934675100en_HK
dc.identifier.scopusauthoridChan, TK=7402687762en_HK
dc.identifier.scopusauthoridChan, V=7202654865en_HK

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