Identification of differentially expressed genes in oral squamous cell carcinoma
Identifieur interne : 002F86 ( Main/Exploration ); précédent : 002F85; suivant : 002F87Identification of differentially expressed genes in oral squamous cell carcinoma
Auteurs : Shilpi Arora [Inde] ; Ajay Matta [Inde] ; Nootan Kumar Shukla [Inde] ; S. V. S. Deo [Inde] ; Ranju Ralhan [Inde]Source :
- Molecular Carcinogenesis [ 0899-1987 ] ; 2005-02.
English descriptors
- Teeft :
- Ansari nagar, Antibody light chain, Arora, Biological implications, Biological targets, Buccal mucosa, Cancer cell lines, Cancer figure, Cancer hospital, Capillary action, Carcinoma, Cdna, Cdna fragments, Cdna microarrays, Cdna probes, Cell adhesion molecule, Cell carcinoma, Cell carcinomas, Cell line, Cell lines, Cell survival, Chemiluminescence method, Clone, Denaturing polyacrylamide, Detectable expression, Differential display, Differential display analysis, Differential expression, Differentially, Equal amount, Esophageal, Formaldehyde agarose, Further characterization, Gene, Gene expression, Genes differentially, Genetic alterations, Genomic dissection, Hep2, Histopathological analysis, Hsc2, Hsc2 cells, Human cancer cell lines, Hunter corp, Immunoblot analysis, Immunoglobulin kappa light chain, Immunohistochemical, Immunohistochemical analysis, Independent pathway, India institute, Initial approach, Leukocyte cell adhesion molecule, Malignant, Medical sciences, Melanoma metastasizing clone, Memd, Microarray analysis, Molecular mechanisms, Molecular targets, Molecular therapeutics, Mrna, Multimodality therapy, Murine moloney leukemia virus, Neck cancer, Nonmalignant, Nonmalignant tissues, Normal tissue, Normal tissues, Northern analysis, Northern blot analysis, Novel genes, Nylon membrane, Nylon membranes, Oral cancer, Oral cancer cell lines, Oral cancer patients, Oral carcinogenesis, Oral carcinoma, Oral carcinomas, Oral cavity, Oral tissues, Oral tumorigenesis, Oral tumors, Oscc, Oscc tissues, Osccs, Ovarian carcinoma, Overall survival, Pathway, Polymerase, Polymerase chain reaction, Positive control, Primary antibody, Primer, Product bands, Rabbit polyclonal antibody, Rapid advances, Representative differentially, Room temperature, Santa cruz biotechnology, Sequence tags, Show homology, Single base, Sodium dodecyl sulphate, Sperm, Sperm protein, Squamous cell carcinoma, Squamous cell carcinomas, Surgical resections, Target protein, Tissue sections, Tissue specimens, Transcription, Transcription chain reaction, Transcription polymerase, Tumor tissues, Tumorigenesis, Unknown genes, Variable region, Wdscc.
Abstract
Rapid advances in multimodality therapy have not significantly improved the overall 5‐yr survival of oral cancer patients in the past two decades, thereby underscoring the need for molecular therapeutics. The development of new treatment strategies for more effective management of oral cancer requires identification of novel biological targets. Therefore, the aim of this study was to identify novel genes associated with oral tumorigenesis by comparing gene expression profile of oral squamous cell carcinomas (OSCCs) and matched nonmalignant oral epithelial tissues with differential display. Of the 180 differentially expressed cDNAs isolated, reamplified, and cloned into pGEMT‐Easy Vector, 26 cDNAs were confirmed to be upregulated in OSCCs by reverse Northern blot analysis. The differentially expressed genes included components of immune system, signaling pathways, angiogenesis, cell structure, proliferation, apoptosis, cell‐adhesion, and cellular metabolism. Reverse transcription (RT)‐polymerase chain reaction (PCR) analysis of 15 OSCCs and matched nonmalignant oral tissues provided the first evidence that 14‐3‐3‐zeta, melanoma metastasizing clone D (MEMD), KIAA0471, sperm protein 17 (SP17), TC21, and anti‐TNF α antibody are upregulated in OSCCs. Immunohistochemical analysis confirmed overexpression of 14‐3‐3‐zeta and TC21 protein, a member of the Ras family, in OSCCs as compared to histologically normal oral tissues validating the differential display analysis. Identification of six novel differentially expressed genes in oral tumors adds to the repertoire of genes associated with oral carcinogenesis and provides candidate potential biological targets for diagnosis and/or therapy. Further characterization of the 14 unknown differentially expressed cDNAs identified in this study may provide significant clues for understanding the molecular mechanisms underlying oral tumorigenesis. © 2004 Wiley‐Liss, Inc.
Url:
DOI: 10.1002/mc.20048
Affiliations:
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110029</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Molecular Carcinogenesis</title><title level="j" type="alt">MOLECULAR CARCINOGENESIS</title><idno type="ISSN">0899-1987</idno><idno type="eISSN">1098-2744</idno><imprint><biblScope unit="vol">42</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="97">97</biblScope><biblScope unit="page" to="108">108</biblScope><biblScope unit="page-count">12</biblScope><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2005-02">2005-02</date></imprint><idno type="ISSN">0899-1987</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0899-1987</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Ansari nagar</term><term>Antibody light chain</term><term>Arora</term><term>Biological implications</term><term>Biological targets</term><term>Buccal mucosa</term><term>Cancer cell lines</term><term>Cancer figure</term><term>Cancer hospital</term><term>Capillary action</term><term>Carcinoma</term><term>Cdna</term><term>Cdna fragments</term><term>Cdna microarrays</term><term>Cdna probes</term><term>Cell adhesion molecule</term><term>Cell carcinoma</term><term>Cell carcinomas</term><term>Cell line</term><term>Cell lines</term><term>Cell survival</term><term>Chemiluminescence method</term><term>Clone</term><term>Denaturing polyacrylamide</term><term>Detectable expression</term><term>Differential display</term><term>Differential display analysis</term><term>Differential expression</term><term>Differentially</term><term>Equal amount</term><term>Esophageal</term><term>Formaldehyde agarose</term><term>Further characterization</term><term>Gene</term><term>Gene expression</term><term>Genes differentially</term><term>Genetic alterations</term><term>Genomic dissection</term><term>Hep2</term><term>Histopathological analysis</term><term>Hsc2</term><term>Hsc2 cells</term><term>Human cancer cell lines</term><term>Hunter corp</term><term>Immunoblot analysis</term><term>Immunoglobulin kappa light chain</term><term>Immunohistochemical</term><term>Immunohistochemical analysis</term><term>Independent pathway</term><term>India institute</term><term>Initial approach</term><term>Leukocyte cell adhesion molecule</term><term>Malignant</term><term>Medical sciences</term><term>Melanoma metastasizing clone</term><term>Memd</term><term>Microarray analysis</term><term>Molecular mechanisms</term><term>Molecular targets</term><term>Molecular therapeutics</term><term>Mrna</term><term>Multimodality therapy</term><term>Murine moloney leukemia virus</term><term>Neck cancer</term><term>Nonmalignant</term><term>Nonmalignant tissues</term><term>Normal tissue</term><term>Normal tissues</term><term>Northern analysis</term><term>Northern blot analysis</term><term>Novel genes</term><term>Nylon membrane</term><term>Nylon membranes</term><term>Oral cancer</term><term>Oral cancer cell lines</term><term>Oral cancer patients</term><term>Oral carcinogenesis</term><term>Oral carcinoma</term><term>Oral carcinomas</term><term>Oral cavity</term><term>Oral tissues</term><term>Oral tumorigenesis</term><term>Oral tumors</term><term>Oscc</term><term>Oscc tissues</term><term>Osccs</term><term>Ovarian carcinoma</term><term>Overall survival</term><term>Pathway</term><term>Polymerase</term><term>Polymerase chain reaction</term><term>Positive control</term><term>Primary antibody</term><term>Primer</term><term>Product bands</term><term>Rabbit polyclonal antibody</term><term>Rapid advances</term><term>Representative differentially</term><term>Room temperature</term><term>Santa cruz biotechnology</term><term>Sequence tags</term><term>Show homology</term><term>Single base</term><term>Sodium dodecyl sulphate</term><term>Sperm</term><term>Sperm protein</term><term>Squamous cell carcinoma</term><term>Squamous cell 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The development of new treatment strategies for more effective management of oral cancer requires identification of novel biological targets. Therefore, the aim of this study was to identify novel genes associated with oral tumorigenesis by comparing gene expression profile of oral squamous cell carcinomas (OSCCs) and matched nonmalignant oral epithelial tissues with differential display. Of the 180 differentially expressed cDNAs isolated, reamplified, and cloned into pGEMT‐Easy Vector, 26 cDNAs were confirmed to be upregulated in OSCCs by reverse Northern blot analysis. The differentially expressed genes included components of immune system, signaling pathways, angiogenesis, cell structure, proliferation, apoptosis, cell‐adhesion, and cellular metabolism. Reverse transcription (RT)‐polymerase chain reaction (PCR) analysis of 15 OSCCs and matched nonmalignant oral tissues provided the first evidence that 14‐3‐3‐zeta, melanoma metastasizing clone D (MEMD), KIAA0471, sperm protein 17 (SP17), TC21, and anti‐TNF α antibody are upregulated in OSCCs. Immunohistochemical analysis confirmed overexpression of 14‐3‐3‐zeta and TC21 protein, a member of the Ras family, in OSCCs as compared to histologically normal oral tissues validating the differential display analysis. Identification of six novel differentially expressed genes in oral tumors adds to the repertoire of genes associated with oral carcinogenesis and provides candidate potential biological targets for diagnosis and/or therapy. Further characterization of the 14 unknown differentially expressed cDNAs identified in this study may provide significant clues for understanding the molecular mechanisms underlying oral tumorigenesis. © 2004 Wiley‐Liss, Inc.</div></front></TEI><affiliations><list><country><li>Inde</li></country></list><tree><country name="Inde"><noRegion><name sortKey="Arora, Shilpi" sort="Arora, Shilpi" uniqKey="Arora S" first="Shilpi" last="Arora">Shilpi Arora</name></noRegion><name sortKey="Deo, S V S" sort="Deo, S V S" uniqKey="Deo S" first="S. V. S." last="Deo">S. V. S. Deo</name><name sortKey="Matta, Ajay" sort="Matta, Ajay" uniqKey="Matta A" first="Ajay" last="Matta">Ajay Matta</name><name sortKey="Ralhan, Ranju" sort="Ralhan, Ranju" uniqKey="Ralhan R" first="Ranju" last="Ralhan">Ranju Ralhan</name><name sortKey="Ralhan, Ranju" sort="Ralhan, Ranju" uniqKey="Ralhan R" first="Ranju" last="Ralhan">Ranju Ralhan</name><name sortKey="Shukla, Nootan Kumar" sort="Shukla, Nootan Kumar" uniqKey="Shukla N" first="Nootan Kumar" last="Shukla">Nootan Kumar Shukla</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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