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- Scopus: eid_2-s2.0-67651153099
- PMID: 16732964
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Article: Study on mismatch repair genes of chronic myeloid leukemia
Title | Study on mismatch repair genes of chronic myeloid leukemia |
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Authors | |
Keywords | Chemicals And Cas Registry Numbers |
Issue Date | 2006 |
Citation | Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi, 2006, v. 27 n. 2, p. 103-106 How to Cite? |
Abstract | OBJECTIVE: To investigate the expression and regulation mechanism of mismatch repair (MMR) genes in chronic myeloid leukemia (CML). METHODS: Expression of MMR genes hMSH2, hMSH3, hMSH6, hMLH1 and hPMS2 mRNAs in 62 CML patients and K562 cell line were detected by semi-quantitative reverse transcription polymerase chain reaction (RT-PCR). Expression of bcr-abl mRNA and MMR genes mRNA were detected by RT-PCR in 26 CML patients with allogeneic peripheral blood stem cell transplantation (allo-PBSCT) and 4 CML patients on imatinib treatment. Expression of bcr-abl mRNA was detected by RT-PCR and tyrosine phosphorylation of BCR-ABL fusion protein by Western blot. RESULTS: Expression of hMSH2, hMSH3 and hMLH1 mRNA was significantly lower in CML and K562 cells than in normal control (P < 0.05). In 26 CML with allo-PBSCT and 4 CML patients on imatinib treatment, expressions of hMSH2, hMSH3 and hMLH1 mRNA was enhanced while expression of bcr-abl mRNA decreased. In CML MNC after imatinib treatment and in K562 cells, expression of hMSH2, hMSH3 and hMLH1 mRNA was enhanced while tyrosine phosphorylation of BCR-ABL fusion protein decreased. CONCLUSION: Expressions of hMSH2, hMSH3 and hMLH1 mRNA were down-regulated by bcr-abl fusion gene. |
Persistent Identifier | http://hdl.handle.net/10722/92020 |
ISSN | 2023 SCImago Journal Rankings: 0.179 |
DC Field | Value | Language |
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dc.contributor.author | Luo, J | en_HK |
dc.contributor.author | Peng, ZG | en_HK |
dc.contributor.author | Chen, Y | en_HK |
dc.contributor.author | Lai, YR | en_HK |
dc.contributor.author | Lu, YY | en_HK |
dc.contributor.author | Song, SJ | en_HK |
dc.date.accessioned | 2010-09-17T10:33:42Z | - |
dc.date.available | 2010-09-17T10:33:42Z | - |
dc.date.issued | 2006 | en_HK |
dc.identifier.citation | Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi, 2006, v. 27 n. 2, p. 103-106 | en_HK |
dc.identifier.issn | 0253-2727 | en_HK |
dc.identifier.uri | http://hdl.handle.net/10722/92020 | - |
dc.description.abstract | OBJECTIVE: To investigate the expression and regulation mechanism of mismatch repair (MMR) genes in chronic myeloid leukemia (CML). METHODS: Expression of MMR genes hMSH2, hMSH3, hMSH6, hMLH1 and hPMS2 mRNAs in 62 CML patients and K562 cell line were detected by semi-quantitative reverse transcription polymerase chain reaction (RT-PCR). Expression of bcr-abl mRNA and MMR genes mRNA were detected by RT-PCR in 26 CML patients with allogeneic peripheral blood stem cell transplantation (allo-PBSCT) and 4 CML patients on imatinib treatment. Expression of bcr-abl mRNA was detected by RT-PCR and tyrosine phosphorylation of BCR-ABL fusion protein by Western blot. RESULTS: Expression of hMSH2, hMSH3 and hMLH1 mRNA was significantly lower in CML and K562 cells than in normal control (P < 0.05). In 26 CML with allo-PBSCT and 4 CML patients on imatinib treatment, expressions of hMSH2, hMSH3 and hMLH1 mRNA was enhanced while expression of bcr-abl mRNA decreased. In CML MNC after imatinib treatment and in K562 cells, expression of hMSH2, hMSH3 and hMLH1 mRNA was enhanced while tyrosine phosphorylation of BCR-ABL fusion protein decreased. CONCLUSION: Expressions of hMSH2, hMSH3 and hMLH1 mRNA were down-regulated by bcr-abl fusion gene. | en_HK |
dc.language | eng | en_HK |
dc.relation.ispartof | Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi | en_HK |
dc.subject | Chemicals And Cas Registry Numbers | en_HK |
dc.title | Study on mismatch repair genes of chronic myeloid leukemia | en_HK |
dc.type | Article | en_HK |
dc.identifier.email | Chen, Y:ychenc@hkucc.hku.hk | en_HK |
dc.identifier.authority | Chen, Y=rp1318 | en_HK |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.pmid | 16732964 | - |
dc.identifier.scopus | eid_2-s2.0-67651153099 | en_HK |
dc.identifier.volume | 27 | en_HK |
dc.identifier.issue | 2 | en_HK |
dc.identifier.spage | 103 | en_HK |
dc.identifier.epage | 106 | en_HK |
dc.identifier.issnl | 0253-2727 | - |