File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: In vitro study examining the effect of sub-lethal QS 755 nm lasers on the expression of p16INK4a on melanoma cell lines

TitleIn vitro study examining the effect of sub-lethal QS 755 nm lasers on the expression of p16INK4a on melanoma cell lines
Authors
KeywordsGene
Lasers
Melanoma
Sub-lethal damage
Issue Date2003
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/34073
Citation
Lasers In Surgery And Medicine, 2003, v. 32 n. 2, p. 88-93 How to Cite?
AbstractBackground and Objectives: Q-switched lasers had been used in the treatment of lentigo maligna but their role remains controversial. While previous studies have addressed the change in adhesion molecule expression after sub-lethal laser damage, no study has addressed the impact of sub-lethal laser damage at a molecular level. The p16 gene has been proposed as the candidate gene for melanoma. Our objective is to examine the effect of sub-lethal laser damage on p16 expression in melanoma cell lines. Study Design/Materials and Methods: Three human melanoma cell lines - HTB 66, Sk-mel-24 (HTB 71), and G361 - were irradiated by a Q-switched 755 nm Alexandrite laser at fluencies that ranged from 0.85 to 2.0 J/cm2. HTB 66 was the only cell line with significant expression of p16INK4a while the other two cells lines were p16INK4a negative and served as negative control. Protein and mRNA expression for p16 were assessed by flow cytometry and RT-PCR, respectively. Results: The level of p16INK4a protein in cell line HTB 66 increased significantly after laser irradiation as compared with non-irradiated cells. The level of p16INK4a protein did not change in p16INK4a-negative cell lines (Sk-mel-24 and G361). However, there was only a slight increase in the percentage of G0/G1 phase cells. Conclusions: Sub-lethal laser damage could increase DNA damage leading to an increase in p16 expression, and such effect would be particularly undesirable for patients with p16 mutation. Further studies are warranted to examine the role of sub-lethal laser damage in inducing p16 mutation. © 2003 Wiley-Liss, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/77333
ISSN
2015 Impact Factor: 2.135
2015 SCImago Journal Rankings: 0.977
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChan, HHLen_HK
dc.contributor.authorXiang, Len_HK
dc.contributor.authorLeung, JCKen_HK
dc.contributor.authorTsang, KWTen_HK
dc.contributor.authorLai, KNen_HK
dc.date.accessioned2010-09-06T07:30:46Z-
dc.date.available2010-09-06T07:30:46Z-
dc.date.issued2003en_HK
dc.identifier.citationLasers In Surgery And Medicine, 2003, v. 32 n. 2, p. 88-93en_HK
dc.identifier.issn0196-8092en_HK
dc.identifier.urihttp://hdl.handle.net/10722/77333-
dc.description.abstractBackground and Objectives: Q-switched lasers had been used in the treatment of lentigo maligna but their role remains controversial. While previous studies have addressed the change in adhesion molecule expression after sub-lethal laser damage, no study has addressed the impact of sub-lethal laser damage at a molecular level. The p16 gene has been proposed as the candidate gene for melanoma. Our objective is to examine the effect of sub-lethal laser damage on p16 expression in melanoma cell lines. Study Design/Materials and Methods: Three human melanoma cell lines - HTB 66, Sk-mel-24 (HTB 71), and G361 - were irradiated by a Q-switched 755 nm Alexandrite laser at fluencies that ranged from 0.85 to 2.0 J/cm2. HTB 66 was the only cell line with significant expression of p16INK4a while the other two cells lines were p16INK4a negative and served as negative control. Protein and mRNA expression for p16 were assessed by flow cytometry and RT-PCR, respectively. Results: The level of p16INK4a protein in cell line HTB 66 increased significantly after laser irradiation as compared with non-irradiated cells. The level of p16INK4a protein did not change in p16INK4a-negative cell lines (Sk-mel-24 and G361). However, there was only a slight increase in the percentage of G0/G1 phase cells. Conclusions: Sub-lethal laser damage could increase DNA damage leading to an increase in p16 expression, and such effect would be particularly undesirable for patients with p16 mutation. Further studies are warranted to examine the role of sub-lethal laser damage in inducing p16 mutation. © 2003 Wiley-Liss, Inc.en_HK
dc.languageengen_HK
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/34073en_HK
dc.relation.ispartofLasers in Surgery and Medicineen_HK
dc.rightsLasers in Surgery and Medicine. Copyright © John Wiley & Sons, Inc.en_HK
dc.subjectGeneen_HK
dc.subjectLasersen_HK
dc.subjectMelanomaen_HK
dc.subjectSub-lethal damageen_HK
dc.subject.meshAnalysis of Varianceen_HK
dc.subject.meshCyclin-Dependent Kinase Inhibitor p16 - genetics - radiation effectsen_HK
dc.subject.meshDose-Response Relationship, Radiationen_HK
dc.subject.meshFlow Cytometryen_HK
dc.subject.meshGene Expression Regulation, Neoplastic - radiation effectsen_HK
dc.subject.meshHumansen_HK
dc.subject.meshLaser Therapy, Low-Levelen_HK
dc.subject.meshMelanoma - genetics - pathology - radiotherapyen_HK
dc.subject.meshRNA, Messenger - geneticsen_HK
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_HK
dc.subject.meshSkin Neoplasms - genetics - pathology - radiotherapyen_HK
dc.subject.meshTumor Cells, Cultured - radiation effectsen_HK
dc.titleIn vitro study examining the effect of sub-lethal QS 755 nm lasers on the expression of p16INK4a on melanoma cell linesen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0196-8092&volume=32&spage=88&epage=93&date=2003&atitle=In+Vitro+Study+Examining+the+Effect+of+Sub-lethal+QS+755+nm+Lasers+on+the+Expression+of+p16INK4a+on+Melanoma+Cell+Linesen_HK
dc.identifier.emailLeung, JCK: jckleung@hku.hken_HK
dc.identifier.emailLai, KN: knlai@hku.hken_HK
dc.identifier.authorityLeung, JCK=rp00448en_HK
dc.identifier.authorityLai, KN=rp00324en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/lsm.10118en_HK
dc.identifier.pmid12561040en_HK
dc.identifier.scopuseid_2-s2.0-0037281760en_HK
dc.identifier.hkuros81132en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0037281760&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume32en_HK
dc.identifier.issue2en_HK
dc.identifier.spage88en_HK
dc.identifier.epage93en_HK
dc.identifier.isiWOS:000181181500003-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridChan, HHL=24555248900en_HK
dc.identifier.scopusauthoridXiang, L=7102911506en_HK
dc.identifier.scopusauthoridLeung, JCK=7202180349en_HK
dc.identifier.scopusauthoridTsang, KWT=7201555024en_HK
dc.identifier.scopusauthoridLai, KN=7402135706en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats