Identification of unique and common low abundance tumour-specific transcripts by suppression subtractive hybridization and oligonucleotide probe array analysis
Most human cancers are characterized by genetic aberrations accompanied by altered expression and function of numerous genes. Applying genome-wide, microarray gene expression analysis to identify deregulated genes in different tumour types can provide potential gene candidates as diagnostic and prog...
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| Published in: | Oncogene Vol. 27; no. 29; pp. 4128 - 4136 |
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| Main Authors: | , , , |
| Format: | Journal Article |
| Language: | English |
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London
Nature Publishing Group UK
03.07.2008
Nature Publishing Nature Publishing Group |
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| ISSN: | 0950-9232, 1476-5594, 1476-5594 |
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| Abstract | Most human cancers are characterized by genetic aberrations accompanied by altered expression and function of numerous genes. Applying genome-wide, microarray gene expression analysis to identify deregulated genes in different tumour types can provide potential gene candidates as diagnostic and prognostic tools and promising targets for drug development. However, the detection of deregulated genes with low levels of expression remains a major challenge. In this study, we have designed a strategy, termed modified suppression subtractive hybridization (mSSH), to identify genes encoding rare transcripts. The strategy entails incorporating the T
7
-promoter sequence at the 5′ end of the noncoding cDNA strand during first strand cDNA synthesis to generate unidirectional antisense RNA from the resultant cDNA following conventional SSH. These transcripts are subsequently analysed by Affymetrix oligonucleotide gene arrays. Here, we have used five hepatocellular carcinoma (HCC), five breast carcinoma and four nasopharyngeal carcinoma (NPC) biopsies separately as testers and their corresponding normal biopsies as drivers to enrich for low abundance tumour type-specific transcripts. The total detectable number of probe sets following mSSH was reduced almost 10-fold in comparison to those detected for the same resected tumour tissues without undergoing subtraction, thus yielding a subtraction efficacy of over 90%. Using this experimental approach, we have identified 48 HCC-specific, 45 breast carcinoma-specific, and 83 NPC-specific genes. In addition, 115 genes were upregulated in all the three cancer types. When compared to gene-profiling data obtained without mSSH, the majority of these identified transcripts were of low abundance in the original cancer tissues. mSSH can therefore serve as a comprehensive molecular strategy for pursuing functional genomic studies of human cancers. |
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| AbstractList | Most human cancers are characterized by genetic aberrations accompanied by altered expression and function of numerous genes. Applying genome-wide, microarray gene expression analysis to identify deregulated genes in different tumour types can provide potential gene candidates as diagnostic and prognostic tools and promising targets for drug development. However, the detection of deregulated genes with low levels of expression remains a major challenge. In this study, we have designed a strategy, termed modified suppression subtractive hybridization (mSSH), to identify genes encoding rare transcripts. The strategy entails incorporating the T sub(7)-promoter sequence at the 5' end of the noncoding cDNA strand during first strand cDNA synthesis to generate unidirectional antisense RNA from the resultant cDNA following conventional SSH. These transcripts are subsequently analysed by Affymetrix oligonucleotide gene arrays. Here, we have used five hepatocellular carcinoma (HCC), five breast carcinoma and four nasopharyngeal carcinoma (NPC) biopsies separately as testers and their corresponding normal biopsies as drivers to enrich for low abundance tumour type-specific transcripts. The total detectable number of probe sets following mSSH was reduced almost 10-fold in comparison to those detected for the same resected tumour tissues without undergoing subtraction, thus yielding a subtraction efficacy of over 90%. Using this experimental approach, we have identified 48 HCC-specific, 45 breast carcinoma-specific, and 83 NPC-specific genes. In addition, 115 genes were upregulated in all the three cancer types. When compared to gene-profiling data obtained without mSSH, the majority of these identified transcripts were of low abundance in the original cancer tissues. mSSH can therefore serve as a comprehensive molecular strategy for pursuing functional genomic studies of human cancers.Oncogene (2008) 27, 4128-4136; doi:10.1038/onc.2008.50; published online 10 March 2008 Most human cancers are characterized by genetic aberrations accompanied by altered expression and function of numerous genes. Applying genome-wide, microarray gene expression analysis to identify deregulated genes in different tumour types can provide potential gene candidates as diagnostic and prognostic tools and promising targets for drug development. However, the detection of deregulated genes with low levels of expression remains a major challenge. In this study, we have designed a strategy, termed modified suppression subtractive hybridization (mSSH), to identify genes encoding rare transcripts. The strategy entails incorporating the T sub(7)-promoter sequence at the 5' end of the noncoding cDNA strand during first strand cDNA synthesis to generate unidirectional antisense RNA from the resultant cDNA following conventional SSH. These transcripts are subsequently analysed by Affymetrix oligonucleotide gene arrays. Here, we have used five hepatocellular carcinoma (HCC), five breast carcinoma and four nasopharyngeal carcinoma (NPC) biopsies separately as testers and their corresponding normal biopsies as drivers to enrich for low abundance tumour type-specific transcripts. The total detectable number of probe sets following mSSH was reduced almost 10-fold in comparison to those detected for the same resected tumour tissues without undergoing subtraction, thus yielding a subtraction efficacy of over 90%. Using this experimental approach, we have identified 48 HCC-specific, 45 breast carcinoma-specific, and 83 NPC-specific genes. In addition, 115 genes were upregulated in all the three cancer types. When compared to gene- profiling data obtained without mSSH, the majority of these identified transcripts were of low abundance in the original cancer tissues. mSSH can therefore serve as a comprehensive molecular strategy for pursuing functional genomic studies of human cancers. Most human cancers are characterized by genetic aberrations accompanied by altered expression and function of numerous genes. Applying genome-wide, microarray gene expression analysis to identify deregulated genes in different tumour types can provide potential gene candidates as diagnostic and prognostic tools and promising targets for drug development. However, the detection of deregulated genes with low levels of expression remains a major challenge. In this study, we have designed a strategy, termed modified suppression subtractive hybridization (mSSH), to identify genes encoding rare transcripts. The strategy entails incorporating the T(7)-promoter sequence at the 5' end of the noncoding cDNA strand during first strand cDNA synthesis to generate unidirectional antisense RNA from the resultant cDNA following conventional SSH. These transcripts are subsequently analysed by Affymetrix oligonucleotide gene arrays. Here, we have used five hepatocellular carcinoma (HCC), five breast carcinoma and four nasopharyngeal carcinoma (NPC) biopsies separately as testers and their corresponding normal biopsies as drivers to enrich for low abundance tumour type-specific transcripts. The total detectable number of probe sets following mSSH was reduced almost 10-fold in comparison to those detected for the same resected tumour tissues without undergoing subtraction, thus yielding a subtraction efficacy of over 90%. Using this experimental approach, we have identified 48 HCC-specific, 45 breast carcinoma-specific, and 83 NPC-specific genes. In addition, 115 genes were upregulated in all the three cancer types. When compared to gene-profiling data obtained without mSSH, the majority of these identified transcripts were of low abundance in the original cancer tissues. mSSH can therefore serve as a comprehensive molecular strategy for pursuing functional genomic studies of human cancers.Most human cancers are characterized by genetic aberrations accompanied by altered expression and function of numerous genes. Applying genome-wide, microarray gene expression analysis to identify deregulated genes in different tumour types can provide potential gene candidates as diagnostic and prognostic tools and promising targets for drug development. However, the detection of deregulated genes with low levels of expression remains a major challenge. In this study, we have designed a strategy, termed modified suppression subtractive hybridization (mSSH), to identify genes encoding rare transcripts. The strategy entails incorporating the T(7)-promoter sequence at the 5' end of the noncoding cDNA strand during first strand cDNA synthesis to generate unidirectional antisense RNA from the resultant cDNA following conventional SSH. These transcripts are subsequently analysed by Affymetrix oligonucleotide gene arrays. Here, we have used five hepatocellular carcinoma (HCC), five breast carcinoma and four nasopharyngeal carcinoma (NPC) biopsies separately as testers and their corresponding normal biopsies as drivers to enrich for low abundance tumour type-specific transcripts. The total detectable number of probe sets following mSSH was reduced almost 10-fold in comparison to those detected for the same resected tumour tissues without undergoing subtraction, thus yielding a subtraction efficacy of over 90%. Using this experimental approach, we have identified 48 HCC-specific, 45 breast carcinoma-specific, and 83 NPC-specific genes. In addition, 115 genes were upregulated in all the three cancer types. When compared to gene-profiling data obtained without mSSH, the majority of these identified transcripts were of low abundance in the original cancer tissues. mSSH can therefore serve as a comprehensive molecular strategy for pursuing functional genomic studies of human cancers. Most human cancers are characterized by genetic aberrations accompanied by altered expression and function of numerous genes. Applying genome-wide, microarray gene expression analysis to identify deregulated genes in different tumour types can provide potential gene candidates as diagnostic and prognostic tools and promising targets for drug development. However, the detection of deregulated genes with low levels of expression remains a major challenge. In this study, we have designed a strategy, termed modified suppression subtractive hybridization (mSSH), to identify genes encoding rare transcripts. The strategy entails incorporating the T 7 -promoter sequence at the 5′ end of the noncoding cDNA strand during first strand cDNA synthesis to generate unidirectional antisense RNA from the resultant cDNA following conventional SSH. These transcripts are subsequently analysed by Affymetrix oligonucleotide gene arrays. Here, we have used five hepatocellular carcinoma (HCC), five breast carcinoma and four nasopharyngeal carcinoma (NPC) biopsies separately as testers and their corresponding normal biopsies as drivers to enrich for low abundance tumour type-specific transcripts. The total detectable number of probe sets following mSSH was reduced almost 10-fold in comparison to those detected for the same resected tumour tissues without undergoing subtraction, thus yielding a subtraction efficacy of over 90%. Using this experimental approach, we have identified 48 HCC-specific, 45 breast carcinoma-specific, and 83 NPC-specific genes. In addition, 115 genes were upregulated in all the three cancer types. When compared to gene-profiling data obtained without mSSH, the majority of these identified transcripts were of low abundance in the original cancer tissues. mSSH can therefore serve as a comprehensive molecular strategy for pursuing functional genomic studies of human cancers. Most human cancers are characterized by genetic aberrations accompanied by altered expression and function of numerous genes. Applying genome-wide, microarray gene expression analysis to identify deregulated genes in different tumour types can provide potential gene candidates as diagnostic and prognostic tools and promising targets for drug development. However, the detection of deregulated genes with low levels of expression remains a major challenge. In this study, we have designed a strategy, termed modified suppression subtractive hybridization (mSSH), to identify genes encoding rare transcripts. The strategy entails incorporating the T(7)-promoter sequence at the 5' end of the noncoding cDNA strand during first strand cDNA synthesis to generate unidirectional antisense RNA from the resultant cDNA following conventional SSH. These transcripts are subsequently analysed by Affymetrix oligonucleotide gene arrays. Here, we have used five hepatocellular carcinoma (HCC), five breast carcinoma and four nasopharyngeal carcinoma (NPC) biopsies separately as testers and their corresponding normal biopsies as drivers to enrich for low abundance tumour type-specific transcripts. The total detectable number of probe sets following mSSH was reduced almost 10-fold in comparison to those detected for the same resected tumour tissues without undergoing subtraction, thus yielding a subtraction efficacy of over 90%. Using this experimental approach, we have identified 48 HCC-specific, 45 breast carcinoma-specific, and 83 NPC-specific genes. In addition, 115 genes were upregulated in all the three cancer types. When compared to gene-profiling data obtained without mSSH, the majority of these identified transcripts were of low abundance in the original cancer tissues. mSSH can therefore serve as a comprehensive molecular strategy for pursuing functional genomic studies of human cancers. [PUBLICATION ABSTRACT] Most human cancers are characterized by genetic aberrations accompanied by altered expression and function of numerous genes. Applying genome-wide, microarray gene expression analysis to identify deregulated genes in different tumour types can provide potential gene candidates as diagnostic and prognostic tools and promising targets for drug development. However, the detection of deregulated genes with low levels of expression remains a major challenge. In this study, we have designed a strategy, termed modified suppression subtractive hybridization (mSSH), to identify genes encoding rare transcripts. The strategy entails incorporating the T(7)-promoter sequence at the 5' end of the noncoding cDNA strand during first strand cDNA synthesis to generate unidirectional antisense RNA from the resultant cDNA following conventional SSH. These transcripts are subsequently analysed by Affymetrix oligonucleotide gene arrays. Here, we have used five hepatocellular carcinoma (HCC), five breast carcinoma and four nasopharyngeal carcinoma (NPC) biopsies separately as testers and their corresponding normal biopsies as drivers to enrich for low abundance tumour type-specific transcripts. The total detectable number of probe sets following mSSH was reduced almost 10-fold in comparison to those detected for the same resected tumour tissues without undergoing subtraction, thus yielding a subtraction efficacy of over 90%. Using this experimental approach, we have identified 48 HCC-specific, 45 breast carcinoma-specific, and 83 NPC-specific genes. In addition, 115 genes were upregulated in all the three cancer types. When compared to gene-profiling data obtained without mSSH, the majority of these identified transcripts were of low abundance in the original cancer tissues. mSSH can therefore serve as a comprehensive molecular strategy for pursuing functional genomic studies of human cancers. Most human cancers are characterized by genetic aberrations accompanied by altered expression and function of numerous genes. Applying genome-wide, microarray gene expression analysis to identify deregulated genes in different tumour types can provide potential gene candidates as diagnostic and prognostic tools and promising targets for drug development. However, the detection of deregulated genes with low levels of expression remains a major challenge. In this study, we have designed a strategy, termed modified suppression subtractive hybridization (mSSH), to identify genes encoding rare transcripts. The strategy entails incorporating the T7-promoter sequence at the 5′ end of the noncoding cDNA strand during first strand cDNA synthesis to generate unidirectional antisense RNA from the resultant cDNA following conventional SSH. These transcripts are subsequently analysed by Affymetrix oligonucleotide gene arrays. Here, we have used five hepatocellular carcinoma (HCC), five breast carcinoma and four nasopharyngeal carcinoma (NPC) biopsies separately as testers and their corresponding normal biopsies as drivers to enrich for low abundance tumour type-specific transcripts. The total detectable number of probe sets following mSSH was reduced almost 10-fold in comparison to those detected for the same resected tumour tissues without undergoing subtraction, thus yielding a subtraction efficacy of over 90%. Using this experimental approach, we have identified 48 HCC-specific, 45 breast carcinoma-specific, and 83 NPC-specific genes. In addition, 115 genes were upregulated in all the three cancer types. When compared to gene-profiling data obtained without mSSH, the majority of these identified transcripts were of low abundance in the original cancer tissues. mSSH can therefore serve as a comprehensive molecular strategy for pursuing functional genomic studies of human cancers. |
| Audience | Academic |
| Author | Ooi, L L P J Goh, C H K Liu, B H Hui, K M |
| Author_xml | – sequence: 1 givenname: B H surname: Liu fullname: Liu, B H organization: Division of Cellular and Molecular Research, Bek Chai Heah Laboratory of Cancer Genomics, Humphrey Oei Institute of Cancer Research, National Cancer Centre – sequence: 2 givenname: C H K surname: Goh fullname: Goh, C H K organization: Department of Otolaryngology, Singapore General Hospital – sequence: 3 givenname: L L P J surname: Ooi fullname: Ooi, L L P J organization: Division of Surgical Oncology, National Cancer Centre – sequence: 4 givenname: K M surname: Hui fullname: Hui, K M email: cmrhkm@nccs.com.sg organization: Division of Cellular and Molecular Research, Bek Chai Heah Laboratory of Cancer Genomics, Humphrey Oei Institute of Cancer Research, National Cancer Centre |
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| CitedBy_id | crossref_primary_10_1016_j_canlet_2008_11_005 crossref_primary_10_1016_j_tig_2014_07_006 crossref_primary_10_1002_ijc_28405 crossref_primary_10_1111_iju_12183 crossref_primary_10_3390_ijms18030235 crossref_primary_10_1007_s00436_009_1470_5 crossref_primary_10_1186_s12943_017_0647_2 crossref_primary_10_1038_s41417_021_00311_x |
| Cites_doi | 10.1038/sj.onc.1210365 10.1158/1078-0432.CCR-06-2236 10.1073/pnas.1233632100 10.1111/j.1478-3231.1999.tb00054.x 10.1200/JCO.2006.07.4187 10.1038/sj.onc.1206865 10.1158/1078-0432.CCR-05-1530 10.1073/pnas.93.12.6025 10.1038/sj.onc.1208732 10.1073/pnas.88.7.2825 10.1038/nrc1452 10.1126/science.287.5460.1977 10.1016/S1097-2765(01)00260-X 10.1038/sj.onc.1210405 10.1038/35000501 10.1126/science.1089769 10.1016/S0168-8278(97)80083-9 10.1038/sj.onc.1209023 10.1200/JCO.2005.04.7019 10.1158/0008-5472.CAN-03-2361 10.1038/nm733 10.1038/4447 10.1056/NEJMoa060096 10.1016/j.tig.2005.12.005 10.1186/1471-2105-7-23 10.1038/sj.onc.1206556 |
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| Copyright | Springer Nature Limited 2008 2008 INIST-CNRS COPYRIGHT 2008 Nature Publishing Group Copyright Nature Publishing Group Jul 3, 2008 Nature Publishing Group 2008. |
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| Keywords | breast cancer affymetrix GeneChip arrays nasopharyngeal carcinoma suppression subtractive hybridization hepatocellular carcinoma low abundance transcripts Breast disease Suppression Hepatic disease Hepatocellular carcinoma Breast cancer Identification Malignant tumor Nasopharynx carcinoma Gene expression Carcinogenesis Mammary gland diseases ENT disease Digestive diseases Pharynx disease Oligonucleotide Cancer |
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| References | Lau, Ho, Hui (CR13) 2007; 26 Young, Rickinson (CR26) 2004; 4 Chen, Yu, Chen, Chang, Chen, Yuan (CR6) 2007; 356 Beer, Kardia, Huang, Giordano, Levin, Misek (CR3) 2002; 8 Lah, Cercek, Blejee, Kos, Gorodetsky, Somers (CR12) 2000; 6 Draghici, Khatri, Eklund, Szallasi (CR10) 2006; 22 Qin, Beyer, Hudson, Linford, Morris, Kerr (CR17) 2006; 7 Diatchenko, Lau, Campbell, Chenchik, Moqadam, Huang (CR9) 1996; 93 Thornburg, Kulwichit, Edwards, Shair, Bendt, Raab-Traub (CR21) 2006; 25 Yu, Kumaresan, Miller, Tan (CR27) 2006; 12 Amatscheck, Koenig, Auer, Steinlein, Pacher, Gruenfelder (CR2) 2004; 64 Brentani, Caballero, Camargo, Silva, Silva, Neto (CR5) 2003; 100 Wang, Ooi, Hui (CR24) 2007; 13 Lee, Tomasetto, Sager (CR14) 1991; 88 Thuerigen, Schneeweiss, Toedt, Warnat, Hahn, Kramer (CR22) 2006; 20 Sander (CR19) 2000; 287 Russo, Zegar, Goirdano (CR18) 2003; 22 Shiota, Kishimoto, Suyama, Okubo, Katayama, Harada (CR20) 1997; 27 Kirk, Lesi, Mendy, Szymanska, Whittle, Goedert (CR11) 2005; 24 Tsopanomichalou, Kouroumalis, Ergazaki, Spandidos (CR23) 1999; 19 Comijn, Berx, Vermassen, Verschueren, Grunsven, Bruyneel (CR7) 2001; 7 Alizadeh, Eisen, Davis, Ma, Lossos, Rosenwald (CR1) 2000; 403 Lipshutz, Fodor, Gingeras, Lockhart (CR15) 1999; 21 Del Rio, Molina, Bascoul-Mollevi, Copois, Bibeau, Chalbos (CR8) 2007; 25 Bonavida (CR4) 2007; 26 Young, Murray (CR25) 2003; 22 Odom, Zizlsperger, Gordon, Bell, Rinaldi, Murray (CR16) 2004; 303 S Amatscheck (BFonc200850_CR2) 2004; 64 J Comijn (BFonc200850_CR7) 2001; 7 LX Qin (BFonc200850_CR17) 2006; 7 DT Odom (BFonc200850_CR16) 2004; 303 GD Kirk (BFonc200850_CR11) 2005; 24 M Del Rio (BFonc200850_CR8) 2007; 25 H Brentani (BFonc200850_CR5) 2003; 100 O Thuerigen (BFonc200850_CR22) 2006; 20 RJ Lipshutz (BFonc200850_CR15) 1999; 21 AA Alizadeh (BFonc200850_CR1) 2000; 403 B Bonavida (BFonc200850_CR4) 2007; 26 G Shiota (BFonc200850_CR20) 1997; 27 WM Lau (BFonc200850_CR13) 2007; 26 C Sander (BFonc200850_CR19) 2000; 287 S Wang (BFonc200850_CR24) 2007; 13 L Diatchenko (BFonc200850_CR9) 1996; 93 TT Lah (BFonc200850_CR12) 2000; 6 DG Beer (BFonc200850_CR3) 2002; 8 LS Young (BFonc200850_CR26) 2004; 4 G Russo (BFonc200850_CR18) 2003; 22 NJ Thornburg (BFonc200850_CR21) 2006; 25 LS Young (BFonc200850_CR25) 2003; 22 K Yu (BFonc200850_CR27) 2006; 12 HY Chen (BFonc200850_CR6) 2007; 356 M Tsopanomichalou (BFonc200850_CR23) 1999; 19 SW Lee (BFonc200850_CR14) 1991; 88 S Draghici (BFonc200850_CR10) 2006; 22 |
| References_xml | – volume: 26 start-page: 3629 year: 2007 end-page: 3636 ident: CR4 article-title: Rituximab-induced inhibition of antiapoptotic cell survival pathways: impolications in chemo/immunoresistance, rituximab unresponsiveness, prognostic and novel therapeutic interventions publication-title: Oncogene doi: 10.1038/sj.onc.1210365 – volume: 13 start-page: 6275 year: 2007 end-page: 6283 ident: CR24 article-title: Identification and validation of a novel gene signature associated with the recurrence of human hepatocellular carcinoma publication-title: Clin Cancer Res doi: 10.1158/1078-0432.CCR-06-2236 – volume: 100 start-page: 13418 year: 2003 end-page: 13423 ident: CR5 article-title: The generation and utilization of a cancer-oriented representation of the human transcriptome by using expressed sequence tags publication-title: Proc Natl Acad Sci USA doi: 10.1073/pnas.1233632100 – volume: 19 start-page: 305 year: 1999 end-page: 311 ident: CR23 article-title: Loss of heterozygosity and microsatellite instability in human non-neoplastic hepatic lesions publication-title: Liver doi: 10.1111/j.1478-3231.1999.tb00054.x – volume: 25 start-page: 773 year: 2007 end-page: 780 ident: CR8 article-title: Gene expression signature in advanced colorectal cancer patients select drugs and response for the use of leucovorin, fluorouracil, and irinotecan publication-title: J Clin Oncol doi: 10.1200/JCO.2006.07.4187 – volume: 22 start-page: 6497 year: 2003 end-page: 6507 ident: CR18 article-title: Advantages and limitations of micoarray technology in human cancer publication-title: Oncogene doi: 10.1038/sj.onc.1206865 – volume: 12 start-page: 3288 year: 2006 end-page: 3296 ident: CR27 article-title: A modular analysis of breast cancer reveals a novel low-grade molecular signature in estrogen receptor-positive tumors publication-title: Clin Cancer Res doi: 10.1158/1078-0432.CCR-05-1530 – volume: 93 start-page: 6025 year: 1996 end-page: 6030 ident: CR9 article-title: Suppresion subtractive hybridization: a method for generating differentially regulated or tissue-specific cDNA probes and libralies publication-title: Proc Natl Acad Sci USA doi: 10.1073/pnas.93.12.6025 – volume: 24 start-page: 5858 year: 2005 end-page: 5867 ident: CR11 article-title: 249(ser) TP53 mutation in plasma DNA, hepatitis B viral infection, and risk of hepatocellular carcinoma publication-title: Oncogene doi: 10.1038/sj.onc.1208732 – volume: 88 start-page: 2825 year: 1991 end-page: 2829 ident: CR14 article-title: Positive selection of candidate tumor-suppressor genes by subtractive hybridization publication-title: Proc Natl Acad Sci USA doi: 10.1073/pnas.88.7.2825 – volume: 4 start-page: 757 year: 2004 end-page: 768 ident: CR26 article-title: Epstein-Barr virus: 40 years on publication-title: Nat Rev Cancer doi: 10.1038/nrc1452 – volume: 287 start-page: 1977 year: 2000 end-page: 1978 ident: CR19 article-title: Genomic medicine and the future of health care publication-title: Science doi: 10.1126/science.287.5460.1977 – volume: 7 start-page: 1267 year: 2001 end-page: 1278 ident: CR7 article-title: The two-handed E box binding zinc finger protein SIP1 downregulates E-cadherin and induces invasions publication-title: Mol Cell doi: 10.1016/S1097-2765(01)00260-X – volume: 26 start-page: 6050 year: 2007 end-page: 6060 ident: CR13 article-title: p16(INK4A)-silencing augments DNA damage-induced apoptosis in cervical cancer cells publication-title: Oncogene doi: 10.1038/sj.onc.1210405 – volume: 403 start-page: 503 year: 2000 end-page: 511 ident: CR1 article-title: Distinct types of diffuse large B-cell lymphoma identified by gene expression profiling publication-title: Nature doi: 10.1038/35000501 – volume: 303 start-page: 1378 year: 2004 end-page: 1381 ident: CR16 article-title: Control of pancreas and liver gene expression by HNF transcription factors publication-title: Science doi: 10.1126/science.1089769 – volume: 27 start-page: 661 year: 1997 end-page: 668 ident: CR20 article-title: Prognostic significance of serum anti-p53 antibody in patients with hepatocellular carcinoma publication-title: J Hepatol doi: 10.1016/S0168-8278(97)80083-9 – volume: 25 start-page: 288 year: 2006 end-page: 297 ident: CR21 article-title: LMP1 signalling and activation of NF-kB in LMP1 transgenic mice publication-title: Oncogene doi: 10.1038/sj.onc.1209023 – volume: 20 start-page: 1839 year: 2006 end-page: 1845 ident: CR22 article-title: Gene expression signature predicting pathologic complete response with gemcitabine, epirubicin, and docetaxel in primary breast cancer publication-title: J Clin Oncol doi: 10.1200/JCO.2005.04.7019 – volume: 64 start-page: 844 year: 2004 end-page: 856 ident: CR2 article-title: Tissue-wide expression profiling using cDNA subtraction and microarrays to identify tumor-specific genes publication-title: Cancer Res doi: 10.1158/0008-5472.CAN-03-2361 – volume: 8 start-page: 816 year: 2002 end-page: 824 ident: CR3 article-title: Gene-expression profiles predict survival of patients with lung adenocarcinoma publication-title: Nat Med doi: 10.1038/nm733 – volume: 6 start-page: 578 year: 2000 end-page: 584 ident: CR12 article-title: Cathepsin B, a prognostic indicator in lymp node-negative breast carcinoma patients: comparison with Cathepsin D, Cathepsin L, and other clinical indicators publication-title: Clin Cancer Res – volume: 21 start-page: 20 year: 1999 end-page: 24 ident: CR15 article-title: High density synthetic oligonucleotide arrays publication-title: Nat Genet doi: 10.1038/4447 – volume: 356 start-page: 11 year: 2007 end-page: 20 ident: CR6 article-title: A five-gene signature and clinical outcome in non-small-cell lung cancer publication-title: N Engl J Med doi: 10.1056/NEJMoa060096 – volume: 22 start-page: 101 year: 2006 end-page: 109 ident: CR10 article-title: Reliability and reproducibility issues in DNA microarray measurements publication-title: Trends Genet doi: 10.1016/j.tig.2005.12.005 – volume: 7 start-page: 23 year: 2006 ident: CR17 article-title: Evaluation of methods for oligonucleotide array data via quantitative real-time PCR publication-title: BMC Bioinformatics doi: 10.1186/1471-2105-7-23 – volume: 22 start-page: 5108 year: 2003 end-page: 5121 ident: CR25 article-title: Epstein-Barr virus and oncogenesis: from latent genes to tumours publication-title: Oncogene doi: 10.1038/sj.onc.1206556 – volume: 24 start-page: 5858 year: 2005 ident: BFonc200850_CR11 publication-title: Oncogene doi: 10.1038/sj.onc.1208732 – volume: 4 start-page: 757 year: 2004 ident: BFonc200850_CR26 publication-title: Nat Rev Cancer doi: 10.1038/nrc1452 – volume: 287 start-page: 1977 year: 2000 ident: BFonc200850_CR19 publication-title: Science doi: 10.1126/science.287.5460.1977 – volume: 356 start-page: 11 year: 2007 ident: BFonc200850_CR6 publication-title: N Engl J Med doi: 10.1056/NEJMoa060096 – volume: 22 start-page: 6497 year: 2003 ident: BFonc200850_CR18 publication-title: Oncogene doi: 10.1038/sj.onc.1206865 – volume: 93 start-page: 6025 year: 1996 ident: BFonc200850_CR9 publication-title: Proc Natl Acad Sci USA doi: 10.1073/pnas.93.12.6025 – volume: 20 start-page: 1839 year: 2006 ident: BFonc200850_CR22 publication-title: J Clin Oncol doi: 10.1200/JCO.2005.04.7019 – volume: 27 start-page: 661 year: 1997 ident: BFonc200850_CR20 publication-title: J Hepatol doi: 10.1016/S0168-8278(97)80083-9 – volume: 6 start-page: 578 year: 2000 ident: BFonc200850_CR12 publication-title: Clin Cancer Res – volume: 26 start-page: 3629 year: 2007 ident: BFonc200850_CR4 publication-title: Oncogene doi: 10.1038/sj.onc.1210365 – volume: 88 start-page: 2825 year: 1991 ident: BFonc200850_CR14 publication-title: Proc Natl Acad Sci USA doi: 10.1073/pnas.88.7.2825 – volume: 7 start-page: 23 year: 2006 ident: BFonc200850_CR17 publication-title: BMC Bioinformatics doi: 10.1186/1471-2105-7-23 – volume: 22 start-page: 5108 year: 2003 ident: BFonc200850_CR25 publication-title: Oncogene doi: 10.1038/sj.onc.1206556 – volume: 8 start-page: 816 year: 2002 ident: BFonc200850_CR3 publication-title: Nat Med doi: 10.1038/nm733 – volume: 22 start-page: 101 year: 2006 ident: BFonc200850_CR10 publication-title: Trends Genet doi: 10.1016/j.tig.2005.12.005 – volume: 100 start-page: 13418 year: 2003 ident: BFonc200850_CR5 publication-title: Proc Natl Acad Sci USA doi: 10.1073/pnas.1233632100 – volume: 26 start-page: 6050 year: 2007 ident: BFonc200850_CR13 publication-title: Oncogene doi: 10.1038/sj.onc.1210405 – volume: 13 start-page: 6275 year: 2007 ident: BFonc200850_CR24 publication-title: Clin Cancer Res doi: 10.1158/1078-0432.CCR-06-2236 – volume: 403 start-page: 503 year: 2000 ident: BFonc200850_CR1 publication-title: Nature doi: 10.1038/35000501 – volume: 25 start-page: 773 year: 2007 ident: BFonc200850_CR8 publication-title: J Clin Oncol doi: 10.1200/JCO.2006.07.4187 – volume: 25 start-page: 288 year: 2006 ident: BFonc200850_CR21 publication-title: Oncogene doi: 10.1038/sj.onc.1209023 – volume: 12 start-page: 3288 year: 2006 ident: BFonc200850_CR27 publication-title: Clin Cancer Res doi: 10.1158/1078-0432.CCR-05-1530 – volume: 303 start-page: 1378 year: 2004 ident: BFonc200850_CR16 publication-title: Science doi: 10.1126/science.1089769 – volume: 64 start-page: 844 year: 2004 ident: BFonc200850_CR2 publication-title: Cancer Res doi: 10.1158/0008-5472.CAN-03-2361 – volume: 19 start-page: 305 year: 1999 ident: BFonc200850_CR23 publication-title: Liver doi: 10.1111/j.1478-3231.1999.tb00054.x – volume: 7 start-page: 1267 year: 2001 ident: BFonc200850_CR7 publication-title: Mol Cell doi: 10.1016/S1097-2765(01)00260-X – volume: 21 start-page: 20 year: 1999 ident: BFonc200850_CR15 publication-title: Nat Genet doi: 10.1038/4447 |
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| SubjectTerms | Abundance Antisense RNA Antisense therapy Apoptosis Biological and medical sciences Biopsy Breast cancer Breast carcinoma Cancer Care and treatment Cell Biology Cell physiology Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes Deoxyribonucleic acid DNA DNA microarrays DNA Probes - genetics DNA, Complementary DNA, Neoplasm - genetics DNA, Neoplasm - metabolism Drug development Fundamental and applied biological sciences. Psychology Gastroenterology. Liver. Pancreas. Abdomen Gene expression Gene Expression Profiling - methods Genes, Neoplasm Genetic aspects Genomics Genomics - methods Gynecology. Andrology. Obstetrics Hepatocellular carcinoma Human Genetics Humans Hybridization Internal Medicine Liver cancer Liver. Biliary tract. Portal circulation. Exocrine pancreas Mammary gland diseases Medical diagnosis Medical sciences Medicine Medicine & Public Health Methods Molecular and cellular biology Nasopharyngeal carcinoma Neoplasms - genetics Neoplasms - metabolism Neoplasms - pathology Nucleic acid hybridization Oligonucleotide Array Sequence Analysis - methods Oligonucleotides oncogenomics Oncology Research methodology Ribonucleic acid Risk factors RNA RNA, Neoplasm - biosynthesis RNA, Neoplasm - genetics Throat cancer Transcription, Genetic Tumors |
| Title | Identification of unique and common low abundance tumour-specific transcripts by suppression subtractive hybridization and oligonucleotide probe array analysis |
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