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Conference Paper: Gain of 6p and 20p and loss of 10p and 10q in esophageal squamous cell carcinoma associated with lymph node metastasis
Title | Gain of 6p and 20p and loss of 10p and 10q in esophageal squamous cell carcinoma associated with lymph node metastasis |
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Authors | |
Issue Date | 2004 |
Publisher | American Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/ |
Citation | The 95th Annual Meeting of the American Association of Cancer Research (AACR 2004), Orlando FL., 27-31 March 2004. In Cancer Research, 2004, v. 64 n. 7 suppl., p. 744, abstract no. 3214 How to Cite? |
Abstract | To understand the genetic mechanisms underlying the progression of esophageal squamous cell carcinoma (ESCC) metastasis, differences of genomic alterations between 15 pairs of primary ESCC tumors and their matched metastatic lymph nodes were analyzed by comparative genomic hybridization (CGH). Chromosomal alterations including loss of 10p, 10q, 17p, 18q, 4p, 13q and gain of 3q, 8q, 6p, 20p, 5p, 18p, 2p, 2q, 1q were detected frequently. The most significant finding was that the gains of chromosome 6p with a minimum high-level amplification region at 6p12-6q12 were found in 7 metastatic lymph nodes but only in 2 corresponding primary tumors (p=0.05) and 20p with a minimum high-level amplification region at 20p12 was found in 11 metastatic lymph nodes but only in 5 corresponding primary tumors (p<0.05). Another interesting finding was the loss of chromosome 10p and 10q which was found in 8 (10p) and 7 (10q) metstatic lymph nodes but only in 2 corresponding primary tumors (p<0.05), respectively. These results suggest that the gains of chromosome 6p and 20p and deletion of chromosome 10 might contribute to the development of ESCC metastasis. The present results provide a candidate amplification region in ESCC for further study to identify oncogenes and tumor suppressor genes related to the development or progression of ESCC. (Supported by Chinese National Outstanding Young Scientists Foundation 30025016 and NCI CA65871; Correspondence to: Dr. Li Dong Wang, Lab. for Cancer Res., College of Medicine, Zhengzhou University, Zhengzhou, Henan, 450052, China. E-mail: lidong0823@sina.com) |
Persistent Identifier | http://hdl.handle.net/10722/95447 |
ISSN | 2023 Impact Factor: 12.5 2023 SCImago Journal Rankings: 3.468 |
DC Field | Value | Language |
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dc.contributor.author | Wang, LD | en_HK |
dc.contributor.author | Qin, Y | en_HK |
dc.contributor.author | Fan, Z | en_HK |
dc.contributor.author | Kwong, DLW | en_HK |
dc.contributor.author | He, X | en_HK |
dc.contributor.author | Chang, ZW | en_HK |
dc.contributor.author | Li, JL | en_HK |
dc.contributor.author | Guan, XY | en_HK |
dc.contributor.author | Tsao, GSW | en_HK |
dc.contributor.author | Sham, JST | en_HK |
dc.contributor.author | Zheng, S | en_HK |
dc.contributor.author | Yang, CS | en_HK |
dc.contributor.author | Li, J | en_HK |
dc.date.accessioned | 2010-09-25T16:02:33Z | - |
dc.date.available | 2010-09-25T16:02:33Z | - |
dc.date.issued | 2004 | en_HK |
dc.identifier.citation | The 95th Annual Meeting of the American Association of Cancer Research (AACR 2004), Orlando FL., 27-31 March 2004. In Cancer Research, 2004, v. 64 n. 7 suppl., p. 744, abstract no. 3214 | en_HK |
dc.identifier.issn | 0008-5472 | - |
dc.identifier.uri | http://hdl.handle.net/10722/95447 | - |
dc.description.abstract | To understand the genetic mechanisms underlying the progression of esophageal squamous cell carcinoma (ESCC) metastasis, differences of genomic alterations between 15 pairs of primary ESCC tumors and their matched metastatic lymph nodes were analyzed by comparative genomic hybridization (CGH). Chromosomal alterations including loss of 10p, 10q, 17p, 18q, 4p, 13q and gain of 3q, 8q, 6p, 20p, 5p, 18p, 2p, 2q, 1q were detected frequently. The most significant finding was that the gains of chromosome 6p with a minimum high-level amplification region at 6p12-6q12 were found in 7 metastatic lymph nodes but only in 2 corresponding primary tumors (p=0.05) and 20p with a minimum high-level amplification region at 20p12 was found in 11 metastatic lymph nodes but only in 5 corresponding primary tumors (p<0.05). Another interesting finding was the loss of chromosome 10p and 10q which was found in 8 (10p) and 7 (10q) metstatic lymph nodes but only in 2 corresponding primary tumors (p<0.05), respectively. These results suggest that the gains of chromosome 6p and 20p and deletion of chromosome 10 might contribute to the development of ESCC metastasis. The present results provide a candidate amplification region in ESCC for further study to identify oncogenes and tumor suppressor genes related to the development or progression of ESCC. (Supported by Chinese National Outstanding Young Scientists Foundation 30025016 and NCI CA65871; Correspondence to: Dr. Li Dong Wang, Lab. for Cancer Res., College of Medicine, Zhengzhou University, Zhengzhou, Henan, 450052, China. E-mail: lidong0823@sina.com) | - |
dc.language | eng | en_HK |
dc.publisher | American Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/ | - |
dc.relation.ispartof | Cancer Research | en_HK |
dc.title | Gain of 6p and 20p and loss of 10p and 10q in esophageal squamous cell carcinoma associated with lymph node metastasis | en_HK |
dc.type | Conference_Paper | en_HK |
dc.identifier.email | Qin, Y: yanruqin@sohu.com | en_HK |
dc.identifier.email | Kwong, DLW: dlwkwong@hkucc.hku.hk | en_HK |
dc.identifier.email | Guan, XY: xyguan@hkucc.hku.hk | en_HK |
dc.identifier.email | Tsao, GSW: gswtsao@hkucc.hku.hk | en_HK |
dc.identifier.email | Sham, JST: jstsham@hku.hk | en_HK |
dc.identifier.authority | Kwong, DLW=rp00414 | en_HK |
dc.identifier.authority | Guan, XY=rp00454 | en_HK |
dc.identifier.authority | Tsao, GSW=rp00399 | en_HK |
dc.identifier.hkuros | 95691 | en_HK |
dc.identifier.volume | 64 | en_HK |
dc.identifier.issue | 7 suppl. | - |
dc.identifier.spage | 744, abstract no. 3214 | en_HK |
dc.identifier.epage | 744, abstract no. 3214 | - |
dc.identifier.issnl | 0008-5472 | - |