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- Publisher Website: 10.1002/ijc.11704
- Scopus: eid_2-s2.0-1342267077
- PMID: 14961573
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Article: Chromosome 13q12 region critical for the viability and growth of nasopharyngeal carcinoma hybrids
Title | Chromosome 13q12 region critical for the viability and growth of nasopharyngeal carcinoma hybrids |
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Authors | |
Keywords | References (40) View In Table Layout |
Issue Date | 2004 |
Publisher | John Wiley & Sons, Inc.. The Journal's web site is located at http://www3.interscience.wiley.com/journal/29331/home |
Citation | International Journal Of Cancer, 2004, v. 109 n. 3, p. 357-362 How to Cite? |
Abstract | Allelic losses of chromosome 13 are often detected in nasopharyngeal carcinoma (NPC) and other cancers, implicating the presence of possible tumor suppressor genes (TSGs) on this chromosome. To identify candidate regions from larger and multiple lost areas observed from direct tumor studies, the technique of monochromosome transfer was utilized to provide functional evidence to verify and define these deletion findings. An intact chromosome 13 was transferred into the NPC HONE1 cell line. Resultant hybrids were used to map putative TSG activity. A critical region at 13q12 was non-randomly eliminated in all surviving microcell hybrids around the marker D13S893; these hybrids were uniformly tumorigenic. Although a known TSG, BRCA2, is mapped close to this critical region, no aberrant expression of this gene was detected in microcell hybrids and other NPC cell lines. These results suggest that at least one novel growth control gene on chromosome 13q12, which is not the BRCA2 gene, is essential for hybrid selection and may play a critical role in tumorigenicity. © 2004 Wiley-Liss, Inc. |
Persistent Identifier | http://hdl.handle.net/10722/91275 |
ISSN | 2023 Impact Factor: 5.7 2023 SCImago Journal Rankings: 2.131 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
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dc.contributor.author | Cheng, Y | en_HK |
dc.contributor.author | Lung, HL | en_HK |
dc.contributor.author | Wong, PS | en_HK |
dc.contributor.author | Hao, DC | en_HK |
dc.contributor.author | Man, CS | en_HK |
dc.contributor.author | Stanbridge, EJ | en_HK |
dc.contributor.author | Lungi, ML | en_HK |
dc.date.accessioned | 2010-09-17T10:16:03Z | - |
dc.date.available | 2010-09-17T10:16:03Z | - |
dc.date.issued | 2004 | en_HK |
dc.identifier.citation | International Journal Of Cancer, 2004, v. 109 n. 3, p. 357-362 | en_HK |
dc.identifier.issn | 0020-7136 | en_HK |
dc.identifier.uri | http://hdl.handle.net/10722/91275 | - |
dc.description.abstract | Allelic losses of chromosome 13 are often detected in nasopharyngeal carcinoma (NPC) and other cancers, implicating the presence of possible tumor suppressor genes (TSGs) on this chromosome. To identify candidate regions from larger and multiple lost areas observed from direct tumor studies, the technique of monochromosome transfer was utilized to provide functional evidence to verify and define these deletion findings. An intact chromosome 13 was transferred into the NPC HONE1 cell line. Resultant hybrids were used to map putative TSG activity. A critical region at 13q12 was non-randomly eliminated in all surviving microcell hybrids around the marker D13S893; these hybrids were uniformly tumorigenic. Although a known TSG, BRCA2, is mapped close to this critical region, no aberrant expression of this gene was detected in microcell hybrids and other NPC cell lines. These results suggest that at least one novel growth control gene on chromosome 13q12, which is not the BRCA2 gene, is essential for hybrid selection and may play a critical role in tumorigenicity. © 2004 Wiley-Liss, Inc. | en_HK |
dc.language | eng | en_HK |
dc.publisher | John Wiley & Sons, Inc.. The Journal's web site is located at http://www3.interscience.wiley.com/journal/29331/home | en_HK |
dc.relation.ispartof | International Journal of Cancer | en_HK |
dc.subject | References (40) View In Table Layout | en_HK |
dc.subject.mesh | Animals | en_HK |
dc.subject.mesh | Cell Division | en_HK |
dc.subject.mesh | Cell Survival | en_HK |
dc.subject.mesh | Chromosome Deletion | en_HK |
dc.subject.mesh | Chromosomes, Human, Pair 13 - physiology | en_HK |
dc.subject.mesh | Gene Dosage | en_HK |
dc.subject.mesh | Gene Transfer Techniques | en_HK |
dc.subject.mesh | Genes, Tumor Suppressor | en_HK |
dc.subject.mesh | Humans | en_HK |
dc.subject.mesh | Hybrid Cells | en_HK |
dc.subject.mesh | In Situ Hybridization, Fluorescence | en_HK |
dc.subject.mesh | Karyotyping | en_HK |
dc.subject.mesh | Mice | en_HK |
dc.subject.mesh | Microsatellite Repeats - genetics | en_HK |
dc.subject.mesh | Nasopharyngeal Neoplasms - genetics - pathology | en_HK |
dc.subject.mesh | Tumor Cells, Cultured | en_HK |
dc.title | Chromosome 13q12 region critical for the viability and growth of nasopharyngeal carcinoma hybrids | en_HK |
dc.type | Article | en_HK |
dc.identifier.email | Cheng, Y:yuecheng@hku.hk | en_HK |
dc.identifier.email | Lung, HL:hllung2@hku.hk | en_HK |
dc.identifier.authority | Cheng, Y=rp01320 | en_HK |
dc.identifier.authority | Lung, HL=rp00299 | en_HK |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.1002/ijc.11704 | en_HK |
dc.identifier.pmid | 14961573 | - |
dc.identifier.scopus | eid_2-s2.0-1342267077 | en_HK |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-1342267077&selection=ref&src=s&origin=recordpage | en_HK |
dc.identifier.volume | 109 | en_HK |
dc.identifier.issue | 3 | en_HK |
dc.identifier.spage | 357 | en_HK |
dc.identifier.epage | 362 | en_HK |
dc.identifier.isi | WOS:000189245300007 | - |
dc.publisher.place | United States | en_HK |
dc.identifier.scopusauthorid | Cheng, Y=36131038300 | en_HK |
dc.identifier.scopusauthorid | Lung, HL=6603819904 | en_HK |
dc.identifier.scopusauthorid | Wong, PS=7403979959 | en_HK |
dc.identifier.scopusauthorid | Hao, DC=7005159211 | en_HK |
dc.identifier.scopusauthorid | Man, CS=7005722366 | en_HK |
dc.identifier.scopusauthorid | Stanbridge, EJ=7103249410 | en_HK |
dc.identifier.scopusauthorid | Lungi, ML=6506293498 | en_HK |
dc.identifier.issnl | 0020-7136 | - |