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Conference Paper: Identification of discriminatory gene expression of EBV-associated primary lymphoepithelioma-like carcinoma of lung by oligonucleotide microarray analysis

TitleIdentification of discriminatory gene expression of EBV-associated primary lymphoepithelioma-like carcinoma of lung by oligonucleotide microarray analysis
Authors
Issue Date2005
PublisherAmerican Association for Cancer Research
Citation
The 96th Annual Meeting of the American Association for Cancer Research (AACR 2005), Anaheim CA, 16–20 April 2005. In Cancer Research, 2005, v. 65 n. 9 suppl., p. 18, abstract no. 75 How to Cite?
AbstractLymphoepithelioma-like carcinomas (LELC) of the lung is a distinct type of primary lung cancer constituting 5-9% of non-small cell lung cancers. LELC occurring in oriental ethnic groups are etiologically related to EBV infection and demonstrate clonal episomal EBV genomes as well as EBV marker expression in tumor cells. There is no relation with tobacco exposure but a close morphological resemblance to nasopharyngeal undifferentiated carcinomas, which is also a common EBV-related tumor in Chinese, is striking. The molecular pathways involved in lung LELC are incompletely understood. In order to identify signature molecules of LELC, we compared the expression profiles of 8 untreated, EBV-positive primary lung LELC with 9 normal lung tissues by oligonucleotide microarray analysis (HGU133A chips, Affymetrix). Verification of the differential expression of selective genes was performed using quantitative PCR (tagman probes) and immunohistochemical evaluation on a tissue microarray. The data were evaluated with the method of feature partitioning for single and pair-wise gene expression (Yap et al, 2004) which identified a discriminatory gene set of 1480 genes capable of distinguishing LELC from the normal lung tissue expression profiles with 100% accuracy. The identified gene set included a higher proportion of genes related to active cellular proliferation, mitosis, cell cycle, DNA replication and nuclear division compared to the arrayed probe set. Examples of tumor-related genes in the discriminatory gene set included those involved in EBV viral gene interaction (BS69, EBI3, EIF5A, KPNA2, MYB, p100, RECK, TAL1), cell proliferation or growth (EZH2, HMGA1, PTTG1, STK6), cell adhesion or extracellular matrix modification (EPHB2, GPI, HMMR, MMP9, MMP12, TIMP3, TNXB), apoptosis or cell survival (AVEN, BCL2, BIRC5, GG2-1), tumor suppression (DAPK1, GADD45B, PLAGL1, PPARG, RTN4), cell cycle checkpoint (CDKN1C, CGR19, WFDC1), anti-angiogenesis (ADAMTS1) and negative regulation of cell growth (CTNNAL1, DLC1, DUSP6, TGFBR2, TGFBR3, TU3A). A change of cytoskeletal expression profile was also observed with underexpression of KRT 7, SCEL and overexpression of the keratins KRT5, 6A and B, 8, 13, 15, 17, 19 as well as some basal cell or cell junction markers such as BPAG1 and KIND1. In addition, several genes related to potential resistance to drug treatment showed elevated expression (ABCE1, CTPS, RRM2, TYMS). The identified genes could contribute to a better understanding of EBV- induced carcinogenesis as well as signify new molecular targets of therapy for EBV-related tumors of the lung and other body regions. (Supported by HKSAR RGC grants 7486/03M, 7468/04M)
Persistent Identifierhttp://hdl.handle.net/10722/104786
ISSN
2015 Impact Factor: 8.556
2015 SCImago Journal Rankings: 5.372

 

DC FieldValueLanguage
dc.contributor.authorWong, MPen_HK
dc.contributor.authorLam, DCLen_HK
dc.contributor.authorYap, DYLen_HK
dc.contributor.authorGirard, Len_HK
dc.contributor.authorTam, IYSen_HK
dc.contributor.authorChung, LPen_HK
dc.contributor.authorChiu, SWen_HK
dc.contributor.authorLam, WKen_HK
dc.contributor.authorDanchin, Aen_HK
dc.contributor.authorMinna, JDen_HK
dc.date.accessioned2010-09-25T22:07:17Z-
dc.date.available2010-09-25T22:07:17Z-
dc.date.issued2005en_HK
dc.identifier.citationThe 96th Annual Meeting of the American Association for Cancer Research (AACR 2005), Anaheim CA, 16–20 April 2005. In Cancer Research, 2005, v. 65 n. 9 suppl., p. 18, abstract no. 75en_HK
dc.identifier.issn0008-5472-
dc.identifier.urihttp://hdl.handle.net/10722/104786-
dc.description.abstractLymphoepithelioma-like carcinomas (LELC) of the lung is a distinct type of primary lung cancer constituting 5-9% of non-small cell lung cancers. LELC occurring in oriental ethnic groups are etiologically related to EBV infection and demonstrate clonal episomal EBV genomes as well as EBV marker expression in tumor cells. There is no relation with tobacco exposure but a close morphological resemblance to nasopharyngeal undifferentiated carcinomas, which is also a common EBV-related tumor in Chinese, is striking. The molecular pathways involved in lung LELC are incompletely understood. In order to identify signature molecules of LELC, we compared the expression profiles of 8 untreated, EBV-positive primary lung LELC with 9 normal lung tissues by oligonucleotide microarray analysis (HGU133A chips, Affymetrix). Verification of the differential expression of selective genes was performed using quantitative PCR (tagman probes) and immunohistochemical evaluation on a tissue microarray. The data were evaluated with the method of feature partitioning for single and pair-wise gene expression (Yap et al, 2004) which identified a discriminatory gene set of 1480 genes capable of distinguishing LELC from the normal lung tissue expression profiles with 100% accuracy. The identified gene set included a higher proportion of genes related to active cellular proliferation, mitosis, cell cycle, DNA replication and nuclear division compared to the arrayed probe set. Examples of tumor-related genes in the discriminatory gene set included those involved in EBV viral gene interaction (BS69, EBI3, EIF5A, KPNA2, MYB, p100, RECK, TAL1), cell proliferation or growth (EZH2, HMGA1, PTTG1, STK6), cell adhesion or extracellular matrix modification (EPHB2, GPI, HMMR, MMP9, MMP12, TIMP3, TNXB), apoptosis or cell survival (AVEN, BCL2, BIRC5, GG2-1), tumor suppression (DAPK1, GADD45B, PLAGL1, PPARG, RTN4), cell cycle checkpoint (CDKN1C, CGR19, WFDC1), anti-angiogenesis (ADAMTS1) and negative regulation of cell growth (CTNNAL1, DLC1, DUSP6, TGFBR2, TGFBR3, TU3A). A change of cytoskeletal expression profile was also observed with underexpression of KRT 7, SCEL and overexpression of the keratins KRT5, 6A and B, 8, 13, 15, 17, 19 as well as some basal cell or cell junction markers such as BPAG1 and KIND1. In addition, several genes related to potential resistance to drug treatment showed elevated expression (ABCE1, CTPS, RRM2, TYMS). The identified genes could contribute to a better understanding of EBV- induced carcinogenesis as well as signify new molecular targets of therapy for EBV-related tumors of the lung and other body regions. (Supported by HKSAR RGC grants 7486/03M, 7468/04M)-
dc.languageengen_HK
dc.publisherAmerican Association for Cancer Research-
dc.relation.ispartofCancer Researchen_HK
dc.titleIdentification of discriminatory gene expression of EBV-associated primary lymphoepithelioma-like carcinoma of lung by oligonucleotide microarray analysisen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailWong, MP: mwpik@hkucc.hku.hken_HK
dc.identifier.emailTam, IYS: h9718676@graduate.hku.hken_HK
dc.identifier.emailChung, LP: lpchung@hkucc.hku.hken_HK
dc.identifier.emailLam, WK: lamwk@hku.hken_HK
dc.identifier.authorityWong, MP=rp00348en_HK
dc.identifier.authorityChung, LP=rp00249en_HK
dc.identifier.hkuros101787en_HK
dc.identifier.volume65en_HK
dc.identifier.spage18, abstract no. 75en_HK
dc.identifier.epage18, abstract no. 75-

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