Tideman, H

Wong, NS

Xia, Y

Journal of Dental Research

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Title The biological effect of fenretinide in nasopharyngeal carcinomacellsAuthor(s) Xia, Y; Wong, NS; Tideman, HCitation15th Annual Scientific Meeting of the International Associationfor Dental Research (Southeast Asian Division), Taiwan, 2-4October 2000, v. 80 n. 4, p. 1386Issued Date 2001URL http://hdl.handle.net/10722/53919Rights Creative Commons: Attribution 3.0 Hong Kong License1386 Divisional Abstracts: Southeast Asian Division J Dent Res 80 (4) 2001P-48 The Biological Effect Of Fenretinide In Nasopharyngeal Carcinoma Cells Y. XIA!, P-52 Norcantharidin induced post G2/M arrest apoptosis is dependent with wild type p53NS.WN ,H. TIDEMAN (Dept. of OMFS, Faculty of Dentistry & Dept. of Hongt- CY. Huangt SC. Kok' SH. Lin' SK. Lee2 J.J.. Lees MS, Hsioa2M and Kuot MYPBiochemistry, Faculty of Medicine, University of Hong Kong, Hong Kong)DeamnofDnity1DcnenofVeray dci2As a member of the retinoids family, fenretinide (N-(4-hydroxyphenyl)retinamide) is a promising ,Ntoa awnUiest.Tiachemopreventive agents under intensive inveatigation. It has demonstrated potent efficacy and Norcantharidin, a synthetic analogue of phosphatase type 2A (PP2A) inhibitors - cantharidin, has bern reported toreduced toxicity against a variety of tumors including some head and neck caricers. To study its have effect on treatment of human and animnal tumors. The tamor cell kitling mechanisms hy norcantharidin,biological activity on nasopharyngeal carcinoma (NPC), the CNE3 cells originated from a NPC however, remain unclear. In this experiment, the investigation was made to anderstand the mechanisms ofwere treated W'Ith fenretinide. The cell morphological changes were observed by fluorescent norcantharidin mediated cytotoxicity. Effort was made to investigate if norcantharidin exerts its cytotoxicitymicroscopy, and cellular DNA alterations were detected with biochemical approaches inclsding spsthoug orcantdapintin.OT imdepcoasd usent-mcancism eK,CeLl2 sowtin p5AC) analyss2sowe(ua that3 bige usdtosegel electrophoresis and flow cytometry. The obvious cell shrinkcage, chromatin condensation and of norcantharidin arrested the cells at the G2/H phase and post G2/M apoptosis in KB. CAL27 cell tines. Therenuclear fragmentation after treatment of fenretinide indicated the occurrence of apoptosis, which was, however, little apoptosis found in mutant p53 cell line exposed to norcantharidin. The resalts showed thatwas stipportedby the characeristic DNA 'adder' formaton on agarosegelnnrcthetsa-Gdipekillsratumoridcellsleftucientlyls cofiespondytortheirdpo3tstatus.s Theuresultsesultsshowrdartanehdidin,atthighwaesecsporte blwythmethracteristicamDNT'ader'eformationroindns augars gelttatfndethnieisubG pn dosage, kills tumor cells efficiently correspond to their p53 status. Western blot was used to further investigatepresene onow-ctometic hitogra. Theefore our inding sgesthtfntide5a whether p53 plays a role in the induction of G2/M arrest as well as apoptosis after espose to norcanthafidin.effective aetoptotis inducer in NPC cells at clinically relevant doses.. It is interesting and Induction of p53 expression was found in wild type p53 cell tine bat not in mulnat p53 cell line exposed tomeaningful to explore further the cellular pathways activated by feniretinide which might give norcantharidin using westemn blot analysis. p53 downstream genes were also detected afternoecanthardin esposureinsight to the crcinogenesis of PC and help withnovel therapeuwithtwesterns blot andtimmblnthastomm emohstrycatminrvivai tumoromnderlmo The.resultsulshowedwthathnanocaantariddiinsight o thecrcinogeesisfNPC andhelp wih noveltherapetic strtegies.induced apoptosis through p53 and hax dependent mechanisms. The delivery of p53 into the mutant p53 cell lineswould enhance norcantharidine act on cells. T'he results implied thatnorcantharidin induced apoptosis through p53dependent mechanisms. Addition of p53 may increase the chemo-sensitization effect of Norcantharidin.The Association of Areca Quid Chewing and Oral Precancerous Lesions 53 Molecular Typintg by Randomin Amnplification of Polymorphic DNA (RA.PD), andP4 K LIN*, YH YANG, Cl- CHENG, CC LKN and TY SHIEH (Graduate Institute of P- 3 Biotyping of Sequential Oral Isolates of Candida albicaans in HIV infection L. P.Oral ealt Scinces Kaosiun Medcal nivesity Kaosiun, Tawan)SAMARANAYAKE*. Y. H. SAMARANAYAKE, P. C. S. TSANG, S. ANIL Oral Bio-Origii altHocaltho Sciwenes, Kaohsiungd redcal qunivertity,gKhossiung Taiwaedn) Sciences. Faculty of Dentistry, University of Hong Kong, SAR ChinaHIinetdpinsThe sigifican assocationetweenoral cncer ad arecaquid cewing as bee repoeedainieveralinvestiatorssusingannarrarof geeticnadtphentypichtols,yhvecnhonothatHhavinechednatientmany southeast Asia countries. However, the relationship of Chewing habit with oral are frequently infected with the identical sub-type of C albicanu over multiple episodes of infection whileprecancerous lesions has not been conclusive. The purpose of this research is to investigate the others have found the opposite. Aims: Hence the purpose of this study was to evaluate the genetic andassociation between oral precancerous lesiont and different types of areca quid chewing (Lao- pheniotypic diversity of oral C. albicansn isolates on single and sequential visits in HIV-infected ethnichwa quid and betel quid) in Taiwan. A matched case-control study was conducted in Kaohsiung Chinese. Materials: A total of 16 ambulatory, community dwelling HIV-infected individuals were examinedMedical University Hospital. There were three groups of cases: 127 patients of oral cancer, gg over a period of one year. At each visit the oral cavity was sampled using the oral rinsc techniquepatients of oral submucous fibrosis and 129 patients of other oral precancerous lesions. The (Sanmaranayake et al J Oral Pathol. 1986; 15:251-4) and cultured on Sabourauds dextrose agar to obtain thecontrol matchcdbysex, ageand occupatin variablesforyeast growth. TUp tostfivewcolonytoformingoo unitsr(CnU) i ofC.FUlbfiC.nalweren selectedeand identintfiedatteachcnornatrolgoup weasvmache bysrex,aganid occupatsmoiongvariableskfor each pbatinent The visit, yielding a total of 441 isolates from 16 patients. To obtain the genotypic profile all isolates were typedinforatio of ehavorofa ec qui cheing, mokig an driking as otaindbyby RAPD analysis using two custom synthesised primers (Gibco BR, Hong Kong; Nucleic Acid Res 1992;questionnaires. The odds ratio of chewing areca quid was 23,7g for having oral cancer, 164.96 20 513742). The organisms were biotyped using a combination of the API 20C, APIZym and boric acidfor having oral submucous fibrosis and 23.68 for having other oral precancerous lesions, while resistance test IXu anbd Samaranayake Arch Oral Biol 1995; 40: 577.579). Conclusions: I) multiple clonesadjusted by smoking and drinking. Among oral cancer patients, the percentage of chewing both of C. albicans exist intra-orally in HIV disease 2) hence, it is essential to select and evaluate more than aLao-hwa quid and betel quid was higher than chewing only betel quid (39.37% vs. 20.47%). sinjee CPU at each visit to decipoher their complete oathogenic profile. 3) in general, most patients anocgar toThe same feature was also seen among patients of oral submucous fibrosis (38.64% vs. 22.73%). carry the same strain throug_hout, 45 as there is little congruenice between the RAPD ezenotvyes and theAmong patients of other oral precancerous lesions, the percentage of chewing only Lao-hwa quid biolvoes it is impeKrative to use multiple tveing tools to ascertain the 'true seguential carriaiee. 5) althouehwas higher than chewing only betel quid (31.01% vs. 15.50%/). We concluded that areca-quid the RAPD technigue is simple, versatile and reRroducible for evaluatineg seguential carriage of yeasts,chewing was highly associated withoral precancerouxlesions, and Lao-hwa quid migh be-more judicial selection of Rrimers and their combined use aooeSar essential to obtain reliable data.risky thanbetel quid. The risk of ha-ving oral cancer or.precancerous lesions was also affected (Supported by the Research Grants Council of Hong Kong)by longer chewing history and larger daily consumption.50 Growth Inhibition -of an Oral Squamnoun Cell line by an Antlsenne PD54 Sequential isolates of Casndida albicains in HIV infection exhibits progressiveF JV Oligodeoxynncleotlde Complementary to Human CCNDI mRNA. CHEN, QIANMINGn, F D resistance to human lactoferrin. 'Y. H. SAMARANAYAKE' L. P.LUG, GANG, LI, BINGQI, L. P. SAMARANAYAKE. (oral BioSciencem, Faculty of Dentistry, The SAMARANAYAKE, V. T. BEENA and K. W. S. YEUNG , Oral Bio-Sciences,Univessity ofHongKong,HongK g)~~~~~~~~Facultyof Dentistry, The University of Hong Kong, Hong Kong, SAR.A variety of innate defense factors in saliva such as lactoferrin contribute to mucosal protection,Background and Purpose: Cyclin Dl1, the product of proto-oncogene CCNDJ, has been identified as an and changes in the salivary concentrations of lactoferrin (HLF) have been observed in HIV-limportant positive cell cycle regulator, Oar recent studies have demonstrated that aberrant Cyclin DI ifcin i:Teamo hssuywst eemn h nsir ucpiiiyo 9gntpdwe .aimed to observe the growth inhibition of an oral squamous cell line by an anises oral C. albicans isolates from six HIV-infected individuals during sequential visits, to HLF using aoligodeoxyniucleotidle to human CCND) mRNA. Maetrial A Methods: A humnan oral squamous cell blastoospore viability assay. Methodt: The organisms were genotyped using a RAPD assaycarcinoma cell line, BcaCD885, was evaluated for the amplification of CCNDI using a differential accotding to Bostak et al. (3. Gen. Microbiol.. 1993; 139: 2179-84), The HLF viability assay waspolymnerase chain reaction (PCR; CHEN, et al. Oral Oncology, 2000,36:, 95 - 99), A direct PCR- DNA conducted according to the method of Soukka et al. (FEMS Microbiol Letts., 1992; 90; 223-28) bysequencing methsod was used to confirm the accuracy of the PCR amplification. Then, an anti-sense exposing a standard suspension of the organisms to 20 pg/ml human lactoferrin (Sigma) for 60 min.oligodeoxynucleotides complementary to human CCNDI mRNA was transducted into BcaCD885 cell and estimating the yield of colony forming units on Sabourauds' dextrose agar. Results: Exposuretine using leptofectin as a vector (Zhou P. et al. Oncogene, 1995; 11(3,1; 571 - 803. The yield of colony to HLF caused a rapid loss of viability among all isolates to varying degrees. None of the sequential,forming units of this cell line before and after the transduction were compared, as well as with an 59 C. albicans isolates demonstrated significant differences in sensitivity so HLF from one visit sooligodeoxynucleotide-free, blank transdluction, Results: Based on the differential PCR results, the next. The ten genotypes demonstrated no significant differences in susceptibility to HLF andBcaCD88S demonstrated the amplification of CCNDI, whilst DNA sequencing confirmed the accuatacy were uniformly sensitive to the enzyme. On regression analysis of a sequentially isolated genotypeof the PCR products. The number of colony forming units from the squamous cell line in cultttre of one patient, a significant negative correlation (r--0.78) between the HLF resistance and the HIVdecreased significantly in the group treated with the anti- sense oligodeoxynucleotides, when compared disease progression was seen. Conclusion: These results indicate that a minority of C. albicanswith alt the control giroups, Conclusion: T'he results suggest that the antisense oliatodeoxynucleotides ta trititaoal nHVdsaemydvlnoorsierssac ohmnlcoerna(with overexoression of CCND1). Hence, CCNDI may be a target for gtene theraov in oral cancers. (Ti an adaptlive resoonse. while the maiority are unaffected.work was supported in part by a grant from the University Researe Committee Grants of the University (Supported by a grant from the Research Grants Council and the CRCG of the University of Hongof Hong Kong, Hong Kong, No.10203005 / 30713 / 08011 / 302 / 01). Kong, Hong Kong SAR).p2lw'AF'ctpl alterations in relation to the expression of p53 and Ki-67 5 The Association of Areca Quid Chewing and Radiographic Alveolar Bone Loss.,P-51 inoalsumoscllcrinms CN HSIAO*, GL HOU, YH YANG, CC LIN, and TY SHIEH (Graduate InstituteN. SAOWX-APA, L.. CHAREONKITKAJORN, P. AMOIRNPHIM0NTHA.\I, of Oral Health Sciences, Kaohsiung Medical University, Kaohsiung, Taiwan)1K. AXRYATA\WONG AiND S. KOONTONGKAEW' (Prince of SongkldaUniverorv,Fsulrv o Dentsry sndHat Ya ReinlHoia,Taln) Areca quid chewing is a common masticatory drug used in South East Asia, India, and the SouthTo anaIN-zerelevantfctors of noplastic tansformatin in Pacific.caIttishusedcdailyItbys600e millionypeoplell worldwide,woandid isanpublicpu healthalproblem.m.InntheToanlrerelesnt A1;Ctoso cpl r s mto i h rl aiy h past fifteen years, many investigations about areca quid chewing have focused on exploringexrelsqumuselcriononp321mattIs n3) Ih poivertsfp5,I2and Ki-67waim uostcmcllineigtdn epidemiology, premalignant changes, genetic factors and components of areca quid, butoral quamus cllcacinoas (oo34) Theposiive rtes f p5~ P21and i-67 investigations conceming periodontitis have been quite few. The purpose of this study is toexpression wvere 59, 82 sod 91%, respectivelyl. Generally, p53 was mostly observed in evaluate the relationship between areca quid chewing and periodontitis. One hundred and seventybasal lavers wvhile p2) wsva consistentlv elevated in the ouperficial, differentiated cells seven subjects were recruited in the sample with which 117 areca quid chewers and 60 subjects

The biological effect of fenretinide in nasopharyngeal carcinoma cells

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The biological effect of fenretinide in nasopharyngeal carcinoma cells

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